Eagle syndrome

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"Eagle syndrome" styloid process

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Eagle Syndrome

Definition and History

Eagle syndrome is a condition in which an elongated styloid process (>2.5-3 cm, generally accepted as elongated if >4 cm) or a calcified/ossified stylohyoid ligament produces a characteristic pain syndrome. It was first described by W.W. Eagle in 1937, originally in the context of post-tonsillectomy pain, though subsequent studies established that tonsillectomy is not always an aetiological factor.
  • Scott-Brown's Otorhinolaryngology, Vol 2, p. 6843
  • K.J. Lee's Essential Otolaryngology, p. 7844

Epidemiology

  • An elongated styloid process is found incidentally in approximately 4% of the general population
  • Only about 4% of those with an elongated styloid process actually develop symptoms
  • More common in women; usually presents in the 4th-5th decade

Anatomy and Pathophysiology

The styloid process is a bony projection from the inferior surface of the temporal bone, with the stylohyoid ligament running from its tip to the lesser cornu of the hyoid bone. When elongated or calcified, it can:
  1. Compress the hypoglossal nerve
  2. Impinge on or irritate the carotid vessels (internal or external carotid artery) - this is the vascular variant
  3. Cause inflammatory changes at the insertion of the stylohyoid ligament
  4. Irritate cranial nerves V, VII, IX, or X passing nearby
Scott-Brown's, p. 6845

Clinical Variants

Eagle originally described two clinical variants:
VariantMechanismKey Features
Classic (stylohyoid) syndromeNerve/soft tissue irritationThroat pain, foreign body sensation, dysphagia, otalgia
Carotid artery syndromeStyloid compresses carotid artery/periarterial sympatheticsNeck/face pain on head turning, pre-syncopal episodes, TIA risk
The vascular variant is now recognized as potentially serious - it can cause carotid artery dissection and stroke by direct compression or microtrauma to the internal carotid artery. A 2024 review in Frontiers in Neurology [PMID 39440251] specifically addresses this neurological risk.

Clinical Features

Classic symptoms:
  • Dull, aching pharyngeal pain - typically in the tonsillar fossa
  • Radiation to the ipsilateral ear (otalgia)
  • Foreign body sensation in the throat (like a fish bone)
  • Odynophagia (pain on swallowing)
  • Pain on jaw movement or head turning
  • Unilateral headaches and neck pain
Physical examination findings:
  • The elongated styloid process may be palpable in the tonsillar fossa
  • Palpation of the tonsillar fossa may reproduce and aggravate symptoms
  • Local anaesthetic injection into this area provides temporary relief (diagnostic and therapeutic)
Cummings Otolaryngology, p. 1918; Scott-Brown's, p. 6848

Diagnostic Criteria (ICHD-based, per Cummings)

Radiographic evidence of a calcified or elongated stylohyoid ligament, plus at least 2 of the following:
  1. Pain provoked or worsened by digital palpation of the stylohyoid ligament
  2. Pain provoked or worsened by head turning
  3. Pain significantly improved by local anaesthetic injection into the ligament, or by styloidectomy
  4. Pain is ipsilateral to the inflamed stylohyoid ligament
Cummings Otolaryngology, p. 1918-1926
Note: The International Headache Society has previously described this syndrome as "not sufficiently demonstrated," which reflects the ongoing controversy around its diagnosis.

Imaging

  • Orthopantomogram (OPG/panoramic X-ray): First-line, shows elongated styloid process
  • CT scan (with 3D reconstruction): Preferred for accurate measurement, surgical planning, and to assess vascular proximity
  • Normal styloid length: ~2.5 cm; >3 cm is often considered abnormal; >4 cm is generally accepted as "elongated"

Management

Conservative (Medical)

  • NSAIDs - first-line
  • Anticonvulsants (e.g., carbamazepine) - used for neuropathic pain component
  • Antidepressants (amitriptyline)
  • Corticosteroid + local anaesthetic injection into the tonsillar fossa - both diagnostic and therapeutic, but effects are temporary
  • Results are variable; surgery is generally considered definitive
Cummings, p. 1927; Scott-Brown's, p. 6851

Surgical (Styloidectomy)

The only curative treatment is surgical shortening of the styloid process. Two approaches:
ApproachNotes
Transoral (via tonsillar fossa)Less invasive, avoids external scar, limited exposure
External transcervicalBetter exposure and visualization, preferred for vascular variant
A 2024 systematic review [PMID 38290994] specifically examined transoral robotic styloidectomy (TORS) as an emerging minimally invasive option.
"The only effective treatment for Eagle syndrome is surgical shortening of the styloid process." - K.J. Lee's Essential Otolaryngology, p. 457
In carefully selected patients, surgical management provides high rates of lasting symptomatic improvement. (Cummings, p. 1927)

Recent Evidence (2023-2024)

StudyFinding
Hassani et al., 2024 - Systematic Review/Meta-Analysis (PMID 38948209)Neurological phenotypes in Eagle syndrome; meta-analyzed treatment outcomes
Campisi et al., 2024 (PMID 38290994)Transoral robotic styloidectomy is feasible with good outcomes
Tadjer & Béjot, 2024 (PMID 39440251)Vascular variant carries significant stroke/TIA risk; warrants early surgical intervention
Pagano et al., 2023 (PMID 38053694)Updated comprehensive review of pathophysiology and management

Key Points Summary

  • Eagle syndrome = elongated styloid process (>4 cm) or calcified stylohyoid ligament
  • Affects ~0.16% of population (4% have elongation, 4% of those are symptomatic)
  • Classic: throat/ear pain, foreign body sensation, odynophagia
  • Vascular variant: carotid compression - can cause stroke/TIA
  • Diagnose with OPG or CT; palpation in tonsillar fossa reproduces pain
  • Conservative treatment (NSAIDs, carbamazepine, steroid injections) offers partial relief
  • Definitive treatment: styloidectomy (transoral or transcervical)

Oro antral fistula

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"oroantral fistula" treatment closure

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oroantral fistula classification causes repair techniques buccal flap palatal flap

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Oro-Antral Fistula (OAF)

Definition

An oro-antral fistula is a pathological, epithelium-lined communication between the oral cavity and the maxillary sinus. It is distinguished from an oro-antral communication (OAC) - which is an acute, non-epithelialized opening - by the presence of epithelial lining, which indicates persistence (typically >48-72 hours without treatment).
Terminology: An acute, fresh opening is called an oro-antral communication (OAC); once epithelialized and chronic, it becomes an oro-antral fistula (OAF).

Anatomy - Why It Happens

The roots of the upper posterior teeth (particularly upper 1st and 2nd molars, and occasionally premolars) are in close proximity to - or may project into - the floor of the maxillary sinus. In some individuals, only a thin layer of bone (or even just periosteum/mucosa) separates the root apex from the sinus. When these teeth are extracted, the antral floor may be breached.
Key anatomical point: The maxillary sinus floor is lowest in the region of the 1st molar, making it the most common site.

Aetiology / Causes

CategorySpecific Causes
Iatrogenic (most common)Tooth extraction (upper molars/premolars), dental implant failure, apicectomy, endodontic overfill
InfectivePeriapical abscess, periodontitis, osteomyelitis of maxilla, actinomycosis
PathologicalMaxillary cyst (dentigerous, radicular) erosion into sinus, tumours (including maxillary antral carcinoma - important cause of OAF that must not be missed)
TraumaticFacial fractures (Le Fort I), gunshot wounds
Iatrogenic - ENTCaldwell-Luc procedure, sinus surgery
RadiationOsteoradionecrosis
Dental extraction is the most common single cause, accounting for ~60-70% of cases. The 1st molar is the tooth most frequently involved.
Scott-Brown's Otorhinolaryngology, Vol 1 | Bailey & Love's Short Practice of Surgery, p. 8918
Maxillary antral carcinoma presenting through an oro-antral fistula
Maxillary antral carcinoma presenting through an oro-antral fistula - Bailey & Love's Short Practice of Surgery

Clinical Features

Symptoms:
  • Nasal regurgitation of fluids - pathognomonic; fluid taken orally passes into the nose
  • Nasal voice (hyper-nasal speech)
  • Unpleasant taste or smell (due to sinus secretions entering the mouth)
  • Halitosis
  • Pain/pressure over the cheek (associated sinusitis)
  • Sense of air passing between mouth and nose on blowing
  • Unilateral mucopurulent nasal discharge (odontogenic sinusitis)
  • Reduced sense of smell
Signs:
  • Visible opening in the alveolar socket or mucosa
  • Nose-blowing test (Valsalva): air passes from mouth into nose through the fistula
  • Probe test: a blunt probe passes freely from the oral cavity into the sinus
  • CT: loss of sinus floor continuity ± mucosal thickening or opacification of maxillary sinus
Scott-Brown's Otorhinolaryngology, Vol 1, p. 1756

Investigations

  1. Clinical exam + probe test - identifies communication
  2. OPG (Orthopantomogram) - shows bone loss, relation of roots to sinus floor
  3. CT scan (fine-cut coronal) - gold standard for imaging; shows sinus floor defect, mucosal thickening, bony involvement; rules out malignancy
  4. Biopsy - mandatory if malignancy is suspected (carcinoma can present as OAF)

Classification (by size)

SizeManagement
Small (<5 mm)May close spontaneously with conservative measures
Medium (5-10 mm)Surgical closure usually required
Large (>10 mm)Definitive surgical repair mandatory

Management

Step 1: Manage Associated Sinusitis

Before or during OAF repair, the maxillary sinus must be treated:
  • Antibiotics - broad-spectrum (amoxicillin-clavulanate; metronidazole for anaerobic coverage)
  • Nasal decongestants - to improve ostial drainage
  • Antral washout or FESS (functional endoscopic sinus surgery) if established chronic sinusitis is present
  • Failure to treat sinusitis leads to flap failure

Step 2: Surgical Closure

A. Buccal Advancement Flap (Rehrmann Flap) - Most Common

  • A trapezoidal mucoperiosteal flap is raised from the buccal (cheek) side
  • Periosteum is incised at the base to allow advancement and tension-free closure
  • Fistula edges are freshened, and the flap is advanced and sutured to the palatal mucosa
  • Indications: Small to medium OAFs in lateral/anterior position
  • Disadvantage: Reduces vestibular depth (may need vestibuloplasty later)
  • Success rate: ~90%

B. Buccal Fat Pad (BFP) Flap - Increasingly Preferred

  • The buccal fat pad (Bichat's fat pad) is mobilized through a small incision in the upper buccal sulcus
  • Fat is laid into the defect and sutured to the margins; epithelializes in ~3-4 weeks
  • Indications: Defects in the central/posterior alveolar crest; OAF >5 mm
  • Advantages: Rich blood supply, abundant tissue, no donor site morbidity, does not reduce vestibular depth
  • Success rate: ~98% (highest of all techniques)
  • Can be combined with buccal advancement flap for large defects (double-layer closure)

C. Palatal Rotation-Advancement Flap

  • A posteriorly-based palatal mucoperiosteal flap is rotated to cover the defect
  • Based on the greater palatine artery
  • Indications: Defects in the premolar region; posterior/palatal OAF location; when buccal flap is unsuitable
  • Disadvantages: Leaves a raw donor area on hard palate (heals by secondary intention); technically demanding
  • Success rate: ~86%

D. Other / Distant Flaps (for large/complex defects)

  • Tongue flap (anteriorly or posteriorly based)
  • Nasolabial flap
  • Temporalis muscle flap
  • Free flaps (radial forearm, anterolateral thigh) - for post-oncologic large defects
  • Zygomatic implants - for post-maxillectomy oroantral defects
Surgical technique selection summary from PMC6538900 (147-patient retrospective analysis):
  • Buccal flap: 40.1% of cases, 89.8% success
  • Buccal fat pad: 28.6% of cases, 98.3% success
  • Palatal flap: 19% of cases, 85.7% success

Flap Selection Algorithm

OAF identified
     │
     ├── Size <5 mm → Conservative (gelatin sponge, suture, observe)
     │
     ├── Size 5-10 mm
     │       ├── Lateral/anterior location → Buccal advancement (Rehrmann) flap
     │       ├── Central alveolar crest → Buccal fat pad flap
     │       └── Palatal side / premolar → Palatal rotation flap
     │
     └── Size >10 mm
             └── Buccal fat pad ± buccal advancement (double layer)
                 or distant/free flap for very large defects

Post-Operative Care

  • Antral precautions: Avoid nose blowing, sneezing with closed mouth, use of straws, smoking for 2-4 weeks
  • Antibiotics + nasal decongestants for 1-2 weeks
  • Soft diet
  • Follow-up to confirm closure at 3 months

Complications of Untreated OAF

  1. Chronic odontogenic sinusitis - most common; unilateral, anaerobic-predominant
  2. Antral polyp formation
  3. Ascending spread to other sinuses or orbit (rare)
  4. Persistent halitosis and social disability
Scott-Brown's, Vol 1: "In approximately 10% of cases [of unilateral sinusitis], the cause will be odontogenic. Therefore, all unilateral cases should include an oral examination and a careful review of the maxillary sinus floor on the CT scan to look for signs of an oro-antral fistula." - Scott-Brown's Otorhinolaryngology, Vol 1, p. 1756

Important: Always Exclude Malignancy

An OAF presenting spontaneously (without preceding dental extraction or surgery), or one that fails to heal after repair, should raise suspicion for maxillary antral carcinoma. Biopsy of the fistula edges is mandatory in atypical cases.

Recent Evidence

StudyFinding
Alomari et al., 2025 (PMID 41091334)Clinical decision-making algorithm for OAF management - comprehensive guide
Kheiri et al., 2025 (PMID 40301851)Systematic review of dental implant outcomes at OAC sites
Kwon et al., 2020 (PMC7049762)Review of local flap techniques: BFP has highest success rate for defects >5 mm

Key Points Summary

  • OAC = acute, non-epithelialized; OAF = chronic, epithelialized communication
  • Most common cause: upper molar extraction (1st molar most at risk)
  • Classic symptom: nasal regurgitation of fluids + nasal voice
  • Diagnosis: clinical probe test + CT scan; always biopsy to exclude carcinoma
  • Small (<5 mm): may close spontaneously
  • Surgical repair: buccal fat pad flap has the highest success rate (~98%); choice guided by defect size and location
  • Always treat associated sinusitis before/during repair

Radioactive thyroid scanning

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"thyroid scintigraphy" radionuclide

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Radioactive Thyroid Scanning (Thyroid Scintigraphy)

Overview

Radioactive thyroid scanning (thyroid scintigraphy) uses radiotracers that are taken up by thyroid follicular cells to produce a functional image of the gland. It assesses how much radiotracer the thyroid (or a nodule within it) takes up relative to the rest of the gland, revealing areas of hyperfunction, hypofunction, or absent function.
Key distinction: Thyroid scintigraphy (the image of the gland) is different from but adjunctive to the radioactive iodine uptake (RAIU) test (which simply measures the fraction of dose taken up at 24 hours as a number).

Radiotracers Used

RadiotracerTypeHalf-lifeMechanismNotes
Tc-99m pertechnetateGamma emitter6 hoursTrapped by thyroid (transport only, NOT organified)Most commonly used; scan within 20-30 min of IV injection; less radiation; cheaper; one-day test; does NOT penetrate sternum - cannot assess substernal goiter
I-123Gamma/beta emitter13.2 hoursTrapped AND organified (full iodine pathway)Oral administration; images at 4h and 24h; tests both transport and organification; more expensive, 2-day test; preferred for accurate RAIU measurement
I-131Beta + gamma emitter~8 daysSame as I-123Longer half-life; higher radiation dose; used for post-thyroidectomy remnant ablation and differentiated thyroid cancer staging; diagnostic dose 1-5 mCi; therapeutic dose 30-150 mCi
Important: Any "hot" nodule identified on Tc-99m must be confirmed with I-123 scanning, because Tc-99m tests only iodine transport, not organification - a small number of nodules that trap Tc-99m may not organify iodine ("discordant nodule"), and these have a higher malignancy risk.
  • Cummings Otolaryngology, p. 3649; Mulholland & Greenfield's Surgery, p. 4030

Normal Scan Appearance

A normal scan shows uniform, symmetric uptake across both thyroid lobes with a characteristic butterfly shape. The isthmus may be faintly visible.

Nodule Classification

CategoryDefinitionMalignancy Risk
Hot nodule (hyperfunctioning)Uptake greater than surrounding thyroid tissue - autonomous function suppresses the rest of the glandVery low (~4%); rarely malignant
Warm / isofunctioning noduleUptake equal to surrounding tissueLow
Cold nodule (hypofunctioning/non-functioning)Uptake less than surrounding thyroid tissue (photopenic area)~10-15% malignancy risk
"In a meta-analysis of patients with scanned nodules that were surgically removed, 95% of all nodules were cold. The incidence of malignancy in cold nodules was 10% to 15% compared with only 4% in 'hot' nodules."
  • Cummings Otolaryngology, p. 3647
Autonomously functioning (hot) nodules do not require biopsy because the risk of malignancy is very low. Hypo- and isofunctional nodules warrant FNA biopsy if they meet size/sonographic criteria.
  • Goldman-Cecil Medicine, p. 3322

Scan Patterns in Thyrotoxicosis

The thyroid scan is most useful for differentiating causes of hyperthyroidism / thyrotoxicosis. The key principle:
Thyrotoxicosis uptake classification
  • True hyperthyroidism (thyroid overproducing hormone) = INCREASED RAI uptake
  • Thyrotoxicosis without hyperthyroidism (hormone released from destruction) = DECREASED RAI uptake

Pattern 1: Diffuse Increased Uptake

Graves' disease scan pattern - diffuse uniform uptake
Graves' disease - diffuse, homogeneous, symmetric increased uptake throughout the entire gland. The gland appears enlarged and uniformly active.

Pattern 2: Focal Increased Uptake (Single "Hot" Area)

Solitary toxic nodule scan pattern
Toxic adenoma (solitary hyperfunctioning nodule) - focal intense uptake in the nodule, with suppressed/absent uptake in the rest of the gland (because normal thyroid is TSH-suppressed). "A thyroid scan provides a definitive diagnostic test, demonstrating focal uptake in the hyperfunctioning nodule and diminished uptake in the remainder of the gland." - Harrison's, p. 528

Pattern 3: Multiple "Hot" Foci

Toxic multinodular goiter scan pattern
Toxic multinodular goiter (TMNG) - multiple focal areas of increased uptake scattered throughout the gland, with relatively normal or suppressed uptake between nodules.

Pattern 4: Absent / Markedly Reduced Uptake

Thyroiditis (subacute/De Quervain's, silent/painless thyroiditis, post-partum thyroiditis) - near-total absence of uptake. Thyrotoxicosis arises from destruction/leakage of pre-formed hormone, not new synthesis. "Thyroid scintigraphy with 99mTc or I-131 shows a complete absence of uptake." - Scott-Brown's, Vol 1, p. 5363-5364
Also seen in: thyrotoxicosis factitia (exogenous T4/T3 ingestion), iodine-induced hyperthyroidism (Jod-Basedow effect), amiodarone-induced thyrotoxicosis type 2.

Summary Table: Scan Patterns in Common Conditions

ConditionRAIUScan Pattern
Graves' diseaseIncreasedDiffuse uniform uptake, enlarged gland
Toxic adenomaIncreasedSingle hot nodule; rest of gland suppressed
Toxic multinodular goiterIncreasedMultiple focal hot areas
Subacute thyroiditisDecreased/absentNear-zero uptake throughout
Silent/post-partum thyroiditisDecreased/absentNear-zero uptake
Thyrotoxicosis factitiaDecreased/absentNear-zero uptake
HashitoxicosisNormal/increased (variable)Variable (exception to the rule)
Struma ovariiDecreased in neckUptake in pelvis
Post-thyroidectomy residualVariableResidual uptake in neck/possible metastases
Frameworks for Internal Medicine, p. 7864-7900; Cummings, p. 3647

Indications for Thyroid Scanning

  1. Hyperthyroid patient with thyroid nodule - to distinguish toxic nodule from Graves' disease with co-existing cold nodule (Marine-Lenhart syndrome)
  2. Thyrotoxicosis workup - to differentiate causes (see table above)
  3. After indeterminate FNA cytology - an I-123 scan should be considered; if a concordant autonomously functioning nodule is found, surgery may be deferred
  4. Post-thyroidectomy differentiated thyroid cancer - I-131 whole-body scan for remnant ablation and detection of metastases
  5. Suspected substernal/ectopic thyroid - I-123 or I-131 (Tc-99m cannot penetrate sternum)
  6. Congenital hypothyroidism - to identify thyroid aplasia, ectopia, or dyshormonogenesis in neonates
Cummings Otolaryngology, p. 3655-3663; Schwartz's Principles of Surgery, p. 2874

When Thyroid Scanning is NOT Indicated / Limitations

  • Routine evaluation of a thyroid nodule in a euthyroid patient: NOT recommended. FNA (fine-needle aspiration biopsy) guided by ultrasound has largely replaced scintigraphy here, as 95% of nodules are cold and the cold nodule classification is not specific enough.
  • Pregnancy and breastfeeding: I-131 is absolutely contraindicated. I-123 is relatively contraindicated. Tc-99m pertechnetate is excreted in breast milk; breastfeeding should be suspended for 24 hours.
  • Cannot assess anatomy (size, margins, vascularity) - use ultrasound for that
  • Cold lesions may be obscured by overlying normal thyroid tissue; oblique views help
"With the evolution of FNAC, radionuclide scanning is not routinely performed in the evaluation of a thyroid nodule." - Cummings Otolaryngology, p. 3654

I-131 in Differentiated Thyroid Cancer

  • Post-thyroidectomy, I-131 is used for remnant ablation (30-100 mCi) to destroy residual normal thyroid tissue and facilitate future serum thyroglobulin monitoring
  • Diagnostic whole-body scan with a low dose (1-5 mCi) at 6-12 months post-ablation to detect functioning metastases
  • Therapeutic doses (100-200 mCi or more) for known metastatic disease
  • Requires TSH stimulation (either thyroid hormone withdrawal OR recombinant TSH/Thyrogen) to maximize I-131 uptake
  • Poorly differentiated thyroid cancers and medullary carcinoma do not take up iodine - FDG-PET is used instead
Mulholland & Greenfield's Surgery, p. 4030, 4047

Key Points

  • Tc-99m pertechnetate: one-day test, low radiation, tests iodine trapping only; confirm hot nodules with I-123
  • I-123: two-day test, tests transport + organification, preferred for RAIU measurement; best for scintigraphy
  • I-131: therapeutic isotope; diagnostic whole-body scanning for differentiated thyroid cancer
  • Hot nodules: rarely malignant (~4%); no FNA needed
  • Cold nodules: 10-15% malignancy risk; FNA warranted if meets criteria
  • 95% of all scanned nodules are cold
  • Most useful clinical role today: differentiating causes of thyrotoxicosis and post-thyroidectomy cancer management
  • Scan NOT needed for routine nodule evaluation in euthyroid patients - ultrasound + FNA is preferred

Powered instruments in ENT

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Powered Instruments in ENT

Overview

Powered instruments in ENT encompass a range of motorized, electrically or pneumatically driven surgical tools that provide controlled, precise tissue removal, cutting, or drilling. They can be broadly divided into:
  1. Microdebrider (powered shaver system) - used in rhinology, laryngology, and head & neck
  2. Powered drills (high-speed drills with burrs) - used in otology, skull base, and sinonasal surgery
  3. Other powered instruments - coblation, ultrasonic aspirator, etc.

1. The Microdebrider (Powered Shaver System)

Mechanism of Action

The microdebrider consists of:
  • A powered handpiece connected to a console
  • A disposable hollow rotating blade at the tip
  • Integrated suction that aspirates tissue into the port as the blade rotates
  • Irrigation system in some configurations
The inner blade rotates inside a fixed outer window, shearing tissue that is aspirated into the opening. The cut tissue is simultaneously removed via suction. The blade can rotate in oscillating (back-and-forth) or continuous mode.
Key settings: 300-700 rpm for delicate work (e.g., laryngeal papillomas); higher speeds for bulk tissue removal.

Applications in Rhinology (FESS)

The microdebrider is a core instrument in Functional Endoscopic Sinus Surgery (FESS):
ProcedureHow microdebrider is used
UncinectomyInitial cut/removal of uncinate process
Anterior ethmoidectomyRemoval of bulla ethmoidalis and anterior ethmoid cells
Posterior ethmoidectomy"A microdebrider, Kerrison's punch or through-biting instruments can be used to remove the partitions between the posterior ethmoid cells" - Scott-Brown's, Vol 1, p. 5217
Nasal polypectomyRapid debulking of polyp tissue
Frontal recess dissectionAngled (40-90°) microdebrider blades used to remove fronto-ethmoidal cells; curved blades for supraorbital ethmoid cells
Maxillary antrostomyEnlargement of the natural ostium
SphenoidotomyEnlargement of sphenoid ostium
"40- to 90-degree microdebrider blades [are used] to expand the neostium [in frontal sinus surgery]. It is often safer to work anteriorly..." - Cummings Otolaryngology, p. 1948
"Care must be taken to avoid a circumferential injury to the mucosa [in the frontal recess] as this will undoubtedly result in stenosis of the frontal recess and recurrent frontal sinusitis." - Scott-Brown's, Vol 1, p. 5264
Advantages over cold forceps:
  • Simultaneous cutting and suctioning keeps the surgical field clear
  • Precise, controlled tissue removal
  • Reduces mucosal trauma and bleeding
  • Faster dissection
  • Reduces risk of polyp/tissue fragment dropping into the airway

Applications in Inferior Turbinate Surgery

The mini-microdebrider (2 mm oscillating blade) is used for submucosal turbinate reduction:
  • A submucosal tunnel is created via a small anterior incision
  • The erectile tissue is partially resected from the medial and inferior turbinate
  • Post-operative nasal packing is not necessary
  • The microdebrider can be controlled to preserve all overlying mucosa - a key advantage
"This technique is effective, carries minimal risk, and the microdebrider can be controlled to preserve all of the overlying mucosa." - Scott-Brown's, Vol 1, p. 3710
In turbinoplasty, the microdebrider removes the lateral mucosa while the medial mucosa is repositioned laterally to form a "neoturbinate."

Applications in Adenoidectomy

The microdebrider under direct endoscopic vision is an effective adenoidectomy technique:
  • 20% faster than traditional curettage technique (RCT evidence)
  • Precise removal under visual control; avoids the blind nature of traditional curette adenoidectomy
  • Lower risk of velopharyngeal insufficiency when partial adenoidectomy is performed
  • Reduced risk of inadvertent eustachian tube orifice trauma
  • Disadvantage: High unit cost (microdebrider blade is expensive and single-use)
"Of the direct-vision techniques, those with the largest clinical experience are the suction coagulator and the microdebrider. In a randomized controlled trial, the microdebrider was 20% faster than the curettage technique." - Scott-Brown's, Vol 2, p. 6323

Applications in Tonsillectomy / Intracapsular Tonsillectomy

The microdebrider is the instrument of choice for intracapsular tonsillectomy (tonsillotomy):
  • The tonsil is debulked inside the capsule, leaving the capsule intact
  • Preserves the fibrous capsule as a barrier against secondary haemorrhage
  • Lower post-operative pain and faster return to normal activities vs. electrocautery
  • Lower bleeding rates
  • Risk of tonsil regrowth - especially in younger children
"The microdebrider group were more likely to get back to normal activities and diet quicker than the electrocautery group." - Scott-Brown's, Vol 2, p. 8073-8076

Applications in Laryngology

The laryngeal microdebrider is now the gold standard for recurrent respiratory papillomatosis (RRP):
"The use of the powered microdebrider... has become the gold standard for papilloma removal in the larynx." - Scott-Brown's, Vol 2, p. 3040
Advantages over CO₂ laser for laryngeal papillomas:
  • No thermal trauma to surrounding tissue
  • No laser plume - eliminates risk of viral aerosol transmission to operating room staff
  • No risk of airway fire
  • Shorter operative times
  • Less post-operative pain
  • Precise removal with minimal mucosal damage
Setting: Non-serrated laryngeal blade at 300-700 rpm - papillomas are suctioned into the debrider with minimal cutting trauma to surrounding normal tissue.
Blade types (Cummings, p. 3410):
  • Round window (skimmer) blade - for soft, bulky lesions (papillomas, tracheal papilloma)
  • Subglottic/tracheal blade - for fibrous scar (subglottic/tracheal stenosis)
  • Smaller skimmer laryngeal blade - for true vocal fold lesions
Other laryngeal indications (Box 67.2, Cummings):
  • Internal laryngoceles
  • Tumour debulking
  • Removal of PTFE granulomas
  • Subglottic and tracheal stenosis
  • Tracheostomal granulation tissue
  • Laryngeal cysts
  • Reinke's oedema
Relative contraindication: Vascular lesions (risk of bleeding)
Cummings Otolaryngology, p. 3385-3410; Scott-Brown's, Vol 2, p. 3035-3055

2. Powered Drills in Otology and Skull Base Surgery

Types of Burrs

The high-speed otological drill uses interchangeable burrs:
Burr TypePropertiesUses
Cutting burrSerrated/fluted; removes bone rapidlyInitial cortical drilling, large area bone removal; zygomatic root and attic opening
Diamond burrSmooth surface; safer near vital structures; generates heat (requires continuous irrigation)Near facial nerve, dura, sigmoid sinus, ossicular chain, cochlea; haemostasis in bone
"Drilling out the zygomatic root and opening the attic is often better accomplished with a 3-mm cutting burr... A smaller diamond burr is used for more medial dissection, especially if the ossicular chain is intact. The 3-mm diamond burr offers better control in this tight area and is less likely to skip." - Shambaugh Surgery of the Ear, p. 2324
"Diamond burr to reduce haemorrhage" from mastoid bone marrow - Cummings, p. 2490

Applications in Ear Surgery

ProcedureRole of Powered Drill
Cortical/simple mastoidectomyCortical bone removal, opening mastoid air cell system
Canal wall up mastoidectomyAttic dissection, posterior tympanomeatal flap
Canal wall down (radical/modified) mastoidectomyLowering facial ridge, meatoplasty
Cochlear implant surgeryPosterior tympanotomy, cochleostomy
Stapedectomy/stapedotomyOval window drilling (small diamond burr)
Exostoses removal"Cases of severe exostoses may require meticulous surgical removal via a postaural approach using a high-speed drill." - Scott-Brown's, Vol 2, p. 9598
Facial nerve decompressionDiamond burr to skeletonize fallopian canal
Cholesteatoma dissectionBone removal to access and exteriorize disease

Applications in Rhinology and Skull Base

  • Endoscopic skull base surgery: High-speed drill for removal of bony partitions, sella turcica, clivus, orbital apex
  • Frontal sinus trephine / drill-out (Lothrop procedure): Powered drill for bony frontal floor removal
  • Orbital decompression: Orbital apex decompression using high-speed drill for optic neuropathy in compressive thyroid eye disease
  • Sinonasal tumour surgery: Bone removal for access and resection margins

3. Other Powered Instruments

InstrumentMechanismENT Use
Coblation (bipolar RF)Bipolar radiofrequency creates cold plasma field (85°C) - dissolves tissue then induces fibrosisTonsillotomy/tonsillectomy, turbinate reduction, adenoidectomy, RRP
Endoscopic ultrasonic aspirator (CUSA)Ultrasonic fragmentation + irrigation + suctionSkull base tumour removal (endoscopic)
Powered laryngeal shaverSame principle as microdebrider, adapted for larynxRRP, laryngeal tumour debulking

Advantages of Powered Instruments - Summary

FeatureBenefit
Simultaneous cutting + suctionClear operative field; faster surgery
Controlled tissue removalPrecise; preserves adjacent structures
No thermal spread (microdebrider)Less collateral mucosal damage vs. diathermy/laser
No airway fire risk (vs. laser)Safer in oxygen-rich airway
No laser plumeProtects OR staff from viral/tumour aerosol
Oscillating blade controlAdjustable rpm for different tissue types
Angled/curved blades availableAccess to difficult anatomical sites (frontal recess, subglottis)

Disadvantages

  • High unit cost - blades are single-use and expensive (limits use as sole technique for adenoidectomy)
  • Learning curve - especially for angled blades
  • Suction removes all tissue - no specimen for histology in some techniques (important in tonsillotomy)
  • Risk of mucosal stripping if not used carefully - can cause adhesions, stenosis (especially in frontal recess)
  • Relative contraindication near vascular structures (laryngeal microdebrider)
  • Drill heat generation (diamond burr) - requires continuous suction-irrigation to prevent thermal bone/nerve injury

Key Points Summary

  • Microdebrider = cutting + suction in one instrument; gold standard for laryngeal papillomatosis (RRP) and widely used in FESS and turbinate surgery
  • In FESS: straight and angled (40-90°) blades for different sinus regions; circumferential frontal recess injury must be avoided
  • In adenoidectomy: 20% faster than curette; preserves direct vision
  • Intracapsular tonsillectomy with microdebrider: less pain, faster recovery, but risk of regrowth
  • Drill in otology: cutting burr for rapid cortical bone removal; diamond burr near vital structures (facial nerve, ossicles, dura, sigmoid)
  • Diamond burr also achieves haemostasis from mastoid bone marrow
  • Coblation: alternative powered technique operating at lower temperature (85°C), less thermal spread than diathermy

Intra tympanic therapy

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Intratympanic (IT) Therapy

Concept and Rationale

Intratympanic therapy involves the direct injection of a pharmacological agent through the tympanic membrane into the middle ear, from where it diffuses across the round window membrane (RWM) into the inner ear (perilymph and, to a lesser extent, endolymph).
The key rationale is to bypass the blood-labyrinth barrier - analogous to the blood-brain barrier - which severely limits the entry of systemically administered drugs into the inner ear. IT delivery achieves perilymph concentrations far higher than systemic administration while minimizing systemic side effects.
"The concentration of steroids in perilymph is much higher after intratympanic (IT) application than after oral administration." - Cummings Otolaryngology, p. 4903

Anatomical Basis: The Round Window Membrane

The round window membrane (RWM) is the primary route for drug entry after IT injection:
  • It is a three-layered, dynamic biological structure capable of both active and passive transport
  • The three layers: outer epithelium (middle ear side), middle fibrous connective tissue layer, inner epithelium (perilymph side)
  • It is semipermeable - allows selective passage based on molecular size, charge, and lipid solubility
Key factors affecting RWM drug delivery:
  1. Method of delivery (injection vs. sustained release vs. catheter)
  2. Permeability of the substance applied (lipid-soluble agents penetrate better)
  3. Rate of clearance from the perilymph (Eustachian tube drainage)
  4. Adhesions over the RWM - can significantly reduce drug delivery; some surgeons advocate microscopic removal of adhesions (e.g., round window plug) before therapy
  5. Patient head position after injection - affects pooling near the RWM
"The round window also participates in absorption and secretion of the perilymph by virtue of a semipermeable membrane. This has opened up possibilities for intratympanic drug delivery through the round window to achieve effective intralabyrinthine concentrations." - Scott-Brown's Otorhinolaryngology, Vol 2, p. 2335
The oval window and micro-pores in the otic capsule bone are secondary routes.

Drugs Used in Intratympanic Therapy

DrugMechanismPrimary Indication
DexamethasoneAnti-inflammatory, immunomodulatorySSNHL (salvage), Meniere's disease (vertigo control)
MethylprednisoloneAnti-inflammatory, immunomodulatorySSNHL (primary or salvage)
GentamicinVestibulotoxic aminoglycosideMeniere's disease (vertigo ablation)
StreptomycinVestibulotoxic (historical)Meniere's (now rarely used due to cochleotoxicity)

IT Technique (Procedure)

Steps:

  1. Patient reclined with head turned ~45° to the treated side (to fill the inferior middle ear near the RWM)
  2. Topical anaesthesia applied to the TM (e.g., EMLA cream, phenol, or iontophoresis)
  3. Injection with a fine-gauge needle (25-27 gauge) through the anteroinferior or posteroinferior quadrant of the TM
  4. Drug is slowly instilled into the middle ear (~0.3-0.5 mL)
  5. A separate ventilation hole is sometimes made in the anterosuperior quadrant for pressure equalization as the drug is injected
  6. Patient asked to remain still with head tilted for 20-30 minutes to maximize drug contact with the RWM; should avoid swallowing (closes Eustachian tube temporarily)
  7. Patient instructed not to blow the nose immediately after

Delivery Variants:

  • Single injection - most common outpatient approach
  • Repeated injections - multiple sessions (e.g., 3-4 injections over 2 weeks for SSNHL)
  • Tympanostomy tube-based delivery - drug instilled through an existing grommet (no injection needed; can be done by patient at home)
  • Silverstein MicroWick - a thin wick placed through a myringotomy tube to the RWM niche for continuous drug delivery
  • Microcatheter / round window catheter - placed surgically at the RWM for continuous or controlled drug release; used in trials for severe SSNHL
  • Sustained-release formulations (gel-based, e.g., hyaluronic acid or poloxamer gels) - under development; prolongs contact time at the RWM

1. IT Steroids

For Sudden Sensorineural Hearing Loss (SSNHL)

Agents: Dexamethasone (10-24 mg/mL) or methylprednisolone (30-62.5 mg/mL)
Roles:
  • Primary treatment - when systemic steroids are contraindicated (diabetes, hypertension, peptic ulcer, immunocompromised patients)
  • Salvage/rescue treatment - when SSNHL has not responded to initial oral/IV steroid course (most common indication; administered 2-6 weeks after onset)
Evidence:
  • RCT evidence shows IT methylprednisolone improves hearing in patients who failed oral steroids for SSNHL (Cummings, p. 70)
  • "Strong data support the use of IT steroids as salvage therapy after failure to respond to oral steroids. Results are best when steroids are applied as early as possible." - Cummings, p. 4905
  • A 2025 systematic review (PMID 40734818) confirms IT steroids as the leading salvage strategy for refractory SSNHL
Mechanism in SSNHL:
  • Reduces endocochlear inflammation
  • Upregulates Na-K-ATPase in stria vascularis (maintains endocochlear potential)
  • Immunomodulation if autoimmune aetiology
  • Possible anti-apoptotic effects on cochlear hair cells

For Meniere's Disease (Vertigo Control)

Agent: Dexamethasone (10 mg/mL most typical; range 2-24 mg/mL)
Indication: Intractable vertigo attacks with preserved hearing (when patient still has functional hearing and medical therapy has failed)
Evidence:
  • Small RCT: 82% complete resolution of vertigo with dexamethasone vs. 57% with saline (Cummings, p. 144)
  • Scott-Brown's (recommendation grade A): "Repetitive intratympanic injections of dexamethasone enable substantial and long-term vertigo control in 80% of refractory cases without significant hearing loss." - Scott-Brown's, Vol 2, p. 6344
Dosing: May need repeating every 3 months; optimal frequency is unknown
Advantage over IT gentamicin: Does not carry risk of sensorineural hearing loss - preferred when the patient still has useful hearing
Mechanism: Unclear; possible autoimmune modulation; possible regulation of endolymph ion transport

2. IT Gentamicin

Mechanism

Gentamicin is an aminoglycoside with preferential vestibulotoxicity relative to its cochleotoxicity. It selectively destroys type I vestibular hair cells (which are more sensitive than type II cells and cochlear hair cells), ablating the pathological labyrinthine signalling that drives Meniere's vertigo attacks.
"Installation of aminoglycosides into the middle ear was described by Schuknecht in 1957 with streptomycin injection through a microcatheter placed through the tympanic membrane." - Cummings, p. 129
"The term 'chemical labyrinthectomy' is often applied to intratympanic gentamicin treatment, but it may not be an appropriate assessment of the effect of gentamicin on the labyrinth in titrated therapy." - Cummings, p. 129

Indications

  1. Meniere's disease - refractory to medical therapy AND after failure of IT dexamethasone
  2. End-stage / Tumarkin crises (drop attacks) - even in patients with poor hearing, as hearing preservation is less of a concern
  3. Recommendation grade A (Scott-Brown's): Used when IT dexamethasone has failed

Protocols (Titration vs. Fixed)

Several protocols exist; there is no consensus on the best approach:
ProtocolApproachNotes
Fixed-dose1 injection/week × 4 weeksSimple; higher cumulative dose; higher hearing loss risk
Titration (as-needed)Single injections given at intervals until vertigo controlledLower total dose; preferred by most to minimize HL risk
Low-doseSingle or few injections, wait for responsePreserves more hearing; may need repeat
Key principle: Complete ablation of caloric response is NOT required for vertigo control - "they found that it was not [needed], and that this end point led to severe to profound hearing loss in 58% of patients." - Cummings, p. 140

Efficacy

  • Meta-analysis (Huon et al., 2012): 87.5% Class A and B vertigo control
  • RCT (intratympanic gentamicin vs. dexamethasone): 93.5% vs. 61% substantial vertigo control at 2-year follow-up (Scott-Brown's, p. 6334)
  • Effective for drop attacks (Tumarkin crises): IT gentamicin has demonstrated effectiveness (Scott-Brown's, p. 6341)

Risks

  • Sensorineural hearing loss: 0-38.7% across series (highly variable; dependent on dose and protocol)
  • Vestibular hypofunction / oscillopsia post-ablation
  • Imbalance - patient may develop chronic disequilibrium
"Sensorineural hearing loss is a potential complication of this treatment and should be considered in the evaluation of the individual patient." - Scott-Brown's, p. 6360

Decision Algorithm for Meniere's Disease

Meniere's disease - medical treatment failure
         │
         ▼
IT Dexamethasone (Grade A recommendation)
    → 80% vertigo control; no significant HL risk
         │
    If refractory
         ▼
IT Gentamicin (Grade A recommendation) - "as-needed" titration
    → 87-93% vertigo control; risk of SNHL
         │
    If bilateral or further failure
         ▼
Surgical options: Endolymphatic sac surgery / Vestibular nerve section

Complications of IT Injection Procedure

ComplicationNotes
Persistent TM perforationUsually heals spontaneously; rare persistent perforation (<1%)
Dizziness/vertigoTransient; especially if cold solution used
Tinnitus exacerbationTemporary
PainUsually mild with topical anaesthesia
Infection / otitis mediaRare; sterile technique important
Drug-specific: SNHLWith IT gentamicin (see above)
Round window membrane adhesionsMay impair drug delivery; identifiable on otoendoscopy

Emerging and Future Directions

  • Sustained-release IT formulations (gel-based dexamethasone, OTO-104/OTO-313) - prolonged drug contact at RWM; in clinical trials
  • Nano-formulations - nanoparticles for targeted cochlear drug delivery
  • Gene therapy via IT route - delivery of vectors (AAV) to cochlea via round window; neurotrophins and hair cell regeneration genes
  • IT aminoglycosides for tinnitus - investigational
  • IT gels: A 2024 scoping review (PMID 38308599) documents growing clinical trial data for intratympanic gel formulations

Key Points Summary

  • IT therapy bypasses the blood-labyrinth barrier; RWM is the primary drug entry route
  • RWM is three-layered, semipermeable; adhesions over it reduce drug entry
  • IT steroids: first-line for SSNHL in contraindications to systemic steroids; gold standard salvage for SSNHL after failed systemic steroids; dexamethasone for Meniere's vertigo (80% control, no HL risk)
  • IT gentamicin: selective vestibulotoxic; 87-93% vertigo control in Meniere's; used after IT dexamethasone failure; risk of SNHL; titration protocol preferred over fixed dosing
  • Complete caloric ablation is NOT the endpoint - associated with high SNHL rates
  • IT dexamethasone is preferred when hearing is still useful; IT gentamicin for end-stage or refractory cases
  • Drug delivery methods: single injection, grommet instillation, MicroWick, catheter, sustained-release gels

Direct laryngoscopy

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Direct Laryngoscopy (DL) / Microlaryngoscopy

Definition and Terminology

  • Direct laryngoscopy (DL): Visualization of the larynx by direct line-of-sight using a rigid laryngoscope, with the patient's oral, pharyngeal, and laryngeal axes aligned. Can be performed under general anaesthesia (operative/suspension DL) or with topical anaesthesia.
  • Microlaryngoscopy (MLB / suspension laryngoscopy): Direct laryngoscopy under general anaesthesia with the laryngoscope suspended on a chest support, leaving both hands of the surgeon free to use microsurgical instruments or an operating microscope.
  • Panendoscopy: Combined direct laryngoscopy + rigid oesophagoscopy + bronchoscopy performed under the same anaesthetic.
"Endoscopy includes diagnostic and operative laryngoscopy and microlaryngoscopy (laryngoscopy aided by an operating microscope), esophagoscopy, and bronchoscopy." - Morgan & Mikhail's Clinical Anaesthesiology, p. 758
Endoscopic view of the larynx as seen during direct laryngoscopy - vocal fold injection being performed
Direct laryngoscopic view of the larynx during vocal fold injection - Cummings Otolaryngology

Historical Development

  • Chevalier Jackson (1865-1958): Father of endoscopy; developed the tubular laryngoscope and systematic approach to laryngoscopy
  • Kleinsasser (1968): Developed the wide-bore suspension laryngoscope and microlaryngoscopic technique
  • Jako and Strong (1972): First described CO₂ laser surgery of the larynx using microlaryngoscopy
  • Dedo: Developed the Dedo laryngoscope widely used for suspension microlaryngoscopy

Types of Laryngoscopes

For Intubation (Anaesthesia)

BladeShapeMechanismUse
Macintosh (curved)CurvedTip placed in vallecula; indirectly lifts epiglottis by traction on hyoepiglottic ligamentStandard adult intubation
Miller (straight)StraightTip placed posterior to epiglottis; directly lifts itChildren; anterior larynx; difficult airways; paraglossal technique
McCoyHinged tipTip flexes to improve viewDifficult airways

For ENT/Operative Laryngoscopy

LaryngoscopeFeaturesUse
KleinsasserWide bore; oval cross-section; slotted designStandard suspension microlaryngoscopy
DedoLong, slender, anterior commissure typeSuspension MLB; good for anterior commissure
Hollinger (anterior commissure)Narrow neck with distal anterior flareAnterior commissure lesions; difficult larynges
LindholmWider bore; good for instrumentsSubglottic and tracheal access
Benjamin-LindholmPaediatric variantPaediatric laryngoscopy
Ossoff-KarlanSlotted; designed for laser useCO₂ laser microlaryngoscopy

Patient Positioning

"Sniffing Position" (Jackson Position)

The classic position for DL:
  • Neck flexed on the thorax (pillow under occiput, ~8-10 cm)
  • Head extended at the atlanto-occipital joint
  • This aligns the three axes: oral axis, pharyngeal axis, and laryngeal axis into one straight line of sight
"Panendoscopy is generally done while the patient is under general anesthesia with the patient's neck flexed and the head extended, usually employing a shoulder roll and a head ring (Jackson position)." - Miller's Anaesthesia, p. 803
"Successful direct laryngoscopy with a Macintosh or Miller blade requires appropriate alignment of the oral, pharyngeal, and laryngeal structures to visualize the glottis." - Morgan & Mikhail, p. 5352

BURP Manoeuvre

Backward Upward Rightward Pressure on the thyroid cartilage - improves the laryngeal view during DL by moving the larynx into the line of sight.

Cormack-Lehane Grading of Laryngoscopic View

A grading system developed in 1984 to describe the laryngoscopic view obtained during DL:
GradeViewClinical Significance
Grade IEntire glottis (vocal cords) visibleEasy intubation
Grade IIAPartial view of glottisUsually easy
Grade IIBArytenoids or posterior vocal cords only visibleIncreased difficulty
Grade IIIEpiglottis only visible; no glottic structures seenDifficult intubation
Grade IVNo laryngeal structures visible (not even epiglottis)Failed intubation; requires alternative
"Intubation is rarely difficult when a grade I or IIA view is achieved; grades IIB and III are associated with a significantly higher incidence of failed intubation. A grade IV laryngoscopic view requires an alternate method of intubation." - Miller's Anaesthesia, p. 1929
POGO scale (Percentage of Glottic Opening): An alternative scoring system with higher inter-observer reliability - measures what % of the vocal cords from anterior commissure to arytenoid notch is visible.

Anaesthesia for Operative Microlaryngoscopy

Goals (Morgan & Mikhail, p. 776)

  1. Immobile surgical field - profound neuromuscular blockade
  2. Adequate masseter muscle relaxation for laryngoscope introduction
  3. Adequate oxygenation and ventilation
  4. Cardiovascular stability despite rapidly varying stimulation levels

Premedication

  • Glycopyrrolate (0.2-0.3 mg IM): Minimises secretions to facilitate airway visualization; given 1 hour before surgery
  • Avoid heavy sedation in patients with threatened airway obstruction

Neuromuscular Blockade

  • Profound paralysis required until end of procedure
  • Intermediate-duration agents: rocuronium, vecuronium, cisatracurium
  • Sugammadex now allows reversal of profound rocuronium blockade → largely replaced succinylcholine infusions
  • Morgan & Mikhail, p. 781

Ventilation Techniques

MethodDescriptionProsCons
MLT (Microlaryngeal tube)Small-diameter (5.0-5.5 mm) long ETT with high-volume low-pressure cuff (Mallinckrodt MLT)Protects airway; ETCO₂ monitoring; safePartially obscures posterior commissure / vocal folds; requires laser-safe tube if CO₂ laser used
Intermittent apnoeaPatient ventilated between surgical episodes; apnoeic during surgeryNo tube in fieldHypercarbia risk; shorter operative windows (2-3 min)
Supraglottic jet ventilation (Venturi/Sanders)High-pressure O₂ jet (30-50 psi) through laryngoscope side port; entrains room air (Venturi effect)Best laryngeal exposureRisk of barotrauma if expiration inadequate; CO₂ monitoring unreliable; risk of aspiration
Subglottic jet ventilation (Hunsacker Mon-Jet)Small tube in posterior commissure below glottis; controlled jet ventilationBetter CO₂ monitoring; stable ventilation; good laryngeal exposureMore invasive; not for posterior commissure lesions
High-frequency jet ventilation (HFJV)80-300 breaths/min via small cannulaQuiet, still fieldComplex; ETCO₂ unreliable
"Jet ventilation should not be used in cases where bleeding is expected as there is no barrier for aspiration of the blood." - Scott-Brown's Otorhinolaryngology, p. 889
"The endotracheal tube with the smallest outer diameter that can offer safe respirations should be utilized. The authors rarely utilize endotracheal tubes larger than size 5.0 during phonosurgery." - Scott-Brown's, p. 889

Laser Precautions (when CO₂ laser used)

  • Use a laser-resistant ETT (e.g., Laser-Flex, Lasertubus)
  • Fill tracheal cuff with saline (not air) - saline acts as heat sink; add methylene blue to detect cuff puncture
  • Pack throat with wet gauze to protect infraglottic structures
  • Protect patient's eyes with wet gauze and tape
  • Use minimum FiO₂ to support SpO₂ (minimize airway fire risk - avoid FiO₂ >0.3 with flammable gases)

Indications for Operative Direct Laryngoscopy / Microlaryngoscopy

Diagnostic

  • Suspicious laryngeal lesion on flexible laryngoscopy requiring biopsy
  • Assessment of dysplasia / carcinoma in situ with mapping biopsies
  • Failure of indirect/flexible laryngoscopy to adequately visualize larynx
  • Staging of laryngeal/hypopharyngeal malignancy (palpation of cricoarytenoid mobility, tumour extent)

Therapeutic / Operative

IndicationNotes
Vocal fold polyps, nodules, cystsExcision by microflap/cold instruments
Reinke's oedema (polypoid corditis)Microsuction + microdebrider
Recurrent respiratory papillomatosis (RRP)Microdebrider (gold standard); ± KTP/CO₂ laser
Laryngeal carcinoma (early T1/T2)Transoral laser microsurgery (TLM)
Vocal fold granulomaExcision (with acid reflux treatment)
Leukoplakia / dysplasiaExcision biopsy ± CO₂ laser
Subglottic/laryngotracheal stenosisCold instruments, laser, microdebrider; dilation
Laryngeal webDivision; keel insertion
Arytenoid granuloma, laryngoceleExcision
Subglottic cystsSuspension MLB with excision/marsupialization
Vocal fold injection augmentationFor paralysis/paresis; Cymetra, fat, Restylane injection
Foreign body removalFrom larynx, subglottis, trachea
Airway tumour debulkingPalliation of obstruction
Interarytenoid injectionMay be performed at initial DL as diagnostic + therapeutic
K.J. Lee's Essential Otolaryngology; Cummings Otolaryngology; Scott-Brown's

Procedure: Suspension Microlaryngoscopy

Step-by-step:
  1. Anaesthesia induction with TIVA (propofol/remifentanil) ± inhalational agents; profound NMB
  2. Patient positioned in Jackson (sniffing) position - shoulder roll, head ring
  3. Tooth guard applied to protect upper teeth/gums
  4. Laryngoscope introduced via the right side of the mouth, advanced along the right paraglossal gutter
  5. Tongue displaced to the left; laryngoscope advanced to visualize epiglottis
  6. Tip positioned in vallecula (Macintosh technique) or under epiglottis (Miller technique)
  7. Suspension apparatus attached to chest support - hands-free
  8. Operating microscope or 0°/30°/70° Hopkins rod telescopes used for magnification
  9. Systematic assessment: supraglottis → glottis → anterior commissure → posterior commissure → subglottis
  10. Arytenoid mobility palpated with a spatula
  11. Biopsies/operative procedures performed with cold instruments, laser, or microdebrider
  12. For discrete lesion: excision biopsy preferred over incisional biopsy (microflap technique for vocal cord lesions)
  13. For diffuse changes: representative biopsy from area that minimises voice impact (e.g., superior-lateral surface)
"The patient's larynx is assessed using 0, 30 and 70 degree rod lens endoscopes so that the type and extent of any lesion or lesions can be determined. If the lesion is discrete then excision biopsy, if at all possible, should be carried out." - Scott-Brown's, p. 3804

Microflap Technique (for Vocal Fold Surgery)

For benign vocal fold lesions (polyps, cysts, Reinke's oedema):
  • A mucosal microflap is raised using a sickle knife
  • The lesion is dissected from the superficial lamina propria
  • The mucosa is replaced/trimmed conserving as much epithelium as possible
  • Avoids injury to the vocalis muscle and preserves vibration of the vocal cord
  • Minimises scarring and preserves voice quality

Post-operative Care

  • Voice rest: 48 hours absolute voice rest; 7-10 days strict vocal rest (no control studies, but widely accepted practice) - Scott-Brown's, p. 892-899
  • Gradual return to voicing under voice therapy guidance
  • Proton pump inhibitors if laryngopharyngeal reflux suspected (reduces granuloma recurrence)
  • Follow-up flexible laryngoscopy at 4-6 weeks

Complications

ComplicationNotes
Dental damageMost common; chipped/avulsed upper teeth; tooth guard mandatory
Lip/tongue lacerationFrom laryngoscope pressure
Temporomandibular joint injuryFrom forced mouth opening
Tongue numbness (lingual nerve injury)From compression
Vocal fold scarring/adhesionEspecially anterior commissure - avoid bilateral anterior commissure resection
Laryngeal oedemaPost-operative; may cause airway compromise
LaryngospasmOn recovery from anaesthesia
Airway fireWith laser; prevented by wet throat packs, laser-safe tube, minimising FiO₂
HaemorrhageIntra/post-operative
Failure to visualizeDifficult anatomy; short neck, limited mouth opening; micrognathia
Cervical spine injuryRare; extreme hyperextension in osteoporotic patients
Broken laryngoscope suspensionPatient must never be left unattended
Important: "Knowing that the glottic opening was not easily visualized with the Dedo laryngoscope is significant for future airway management." - Cummings, p. 3647-3651

Contraindications / Predictors of Difficult DL (LEMON Assessment)

  • Look externally - micrognathia, prognathism, short neck, large tongue, obesity
  • Evaluate the 3-3-2 rule - mouth opening <3 fingers; hyoid-chin distance <3 fingers; thyroid-floor of mouth <2 fingers
  • Mallampati class III/IV
  • Obstruction / Obesity
  • Neck mobility - cervical spine disease, trauma, ankylosing spondylitis

Key Points Summary

  • Direct laryngoscopy = direct line-of-sight visualization; microlaryngoscopy = DL + operating microscope with suspension
  • Jackson (sniffing) position: neck flexed, head extended - aligns oral, pharyngeal, laryngeal axes
  • Cormack-Lehane Grade I/IIA = easy; IIB/III = difficult; IV = failed - requires alternative
  • BURP manoeuvre improves grade
  • Anaesthesia: TIVA preferred; profound NMB; MLT tube (size 5.0-5.5) most common; jet ventilation when posterior commissure/vocal fold exposure needed
  • Laser surgery requires laser-safe ETT + saline-filled cuff + minimum FiO₂
  • Cold instrument microsurgery preferred for benign vocal fold lesions to preserve voice
  • Microdebrider = gold standard for RRP
  • Excision biopsy preferred over incisional for discrete lesions
  • 48 hours absolute voice rest post-phonosurgery; 7-10 days strict rest
  • Most common complication: dental trauma - always use tooth guard

Epiphora

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Epiphora

Definition

Epiphora is the overflow of tears at the eyelid margin onto the cheek. It results from an imbalance between tear production and drainage.
"Epiphora is the overflow of tears at the eyelid margin." - Kanski's Clinical Ophthalmology, p. 4390

Anatomy of the Lacrimal Drainage System

Anatomy of the lacrimal drainage system
Anatomy of the lacrimal drainage system - Kanski's Clinical Ophthalmology
The lacrimal drainage pathway (proximal to distal):
StructureSizeNotes
Punctum (upper + lower)~0.3 mm diameterLocated on medial lid margin, ~6 mm from medial canthus
Ampulla~2 mmVertical dilated segment just below punctum
Canaliculus (upper + lower)~8 mmTurns medially after ampulla
Common canaliculusShortUpper + lower canaliculi merge; enters lacrimal sac
Valve of Rosenmuller-Mucosal fold at canalicular-sac junction; prevents reflux
Lacrimal sac~10 mmLies in lacrimal fossa of lacrimal bone
Nasolacrimal duct (NLD)~12 mmRuns through bony canal into inferior meatus
Valve of Hasner-Mucosal fold at distal NLD opening into inferior meatus

Physiology of Tear Drainage (Lacrimal Pump)

  • With each blink, the pretarsal orbicularis oculi compresses the ampullae and canaliculi and moves the puncta medially
  • Contraction of the lacrimal part of orbicularis creates positive pressure, forcing tears down the NLD into the nose
  • On eye opening, the canaliculi and sac expand creating negative pressure that draws tears from the canaliculi into the sac
  • Kanski's, p. 4371-4373

Pathophysiology - Two Mechanisms of Epiphora

1. Hypersecretion (Overproduction)

  • Secondary to anterior segment disease: dry eye (paradoxical watering), blepharitis, conjunctivitis, keratitis, foreign body, entropion
  • Paradox: Dry eye stimulates reflex hypersecretion via the trigeminal-lacrimal reflex - the most common cause of watering eye overall
  • Treatment is usually medical (addressing the underlying cause)

2. Defective Drainage (Lacrimal Outflow Failure)

More clinically significant; due to:
  • Malposition of puncta: ectropion, entropion, punctal eversion - "punctal abnormality is the most common cause of lacrimal drainage failure" - Kanski's, p. 4415
  • Obstruction at any level from punctum to valve of Hasner
  • Lacrimal pump failure: lower lid laxity, orbicularis weakness (facial nerve palsy)
Clinical tip: Drainage failure is exacerbated by cold/windy environments and least evident in warm, dry rooms. Tears overflowing onto the cheek = drainage failure (vs. hypersecretion which causes tears on the lower lid margin). - Kanski's, p. 4410

Causes at Each Level

LevelCause
PunctumPunctal stenosis (primary - blepharitis, idiopathic; secondary - drugs [5-FU, docetaxel], radiation, cicatrizing conjunctivitis, HSV/HZV), punctal atresia, punctal ectropion, eyelash obstructing punctum, large caruncle
CanaliculusCanaliculitis (Actinomyces israelii - most common cause), canalicular obstruction (scarring post-HSV, trachoma, pemphigoid), trauma
Common canaliculusDacryolith (lacrimal stone), trauma, post-radiation stenosis
Lacrimal sacDacryocystitis (acute/chronic), lacrimal sac tumour, dacryolith
Nasolacrimal ductIdiopathic stenosis (most common acquired cause), trauma, nasal/sinus surgery, granulomatous disease (GPA, sarcoidosis), nasopharyngeal tumour infiltration, dacryolith, congenital obstruction (valve of Hasner)
FunctionalLacrimal pump failure (facial palsy, lid laxity), conjunctivochalasis

Evaluation

History

  • Unilateral vs. bilateral
  • Age of onset (congenital vs. acquired)
  • Discharge character (watery vs. mucoid vs. mucopurulent)
  • Exacerbating factors (cold/wind → drainage failure)
  • History of: trauma, nasal/sinus surgery, eye drops (especially glaucoma drops), systemic drugs, radiotherapy, granulomatous disease

Examination

  1. Slit-lamp examination of puncta (before any instrumentation - syringing temporarily dilates and masks stenosis)
  2. Assess for ectropion, entropion, lid laxity
  3. Fluorescein dye disappearance test (FDDT): Instil fluorescein; normal drainage = dye disappears from tear meniscus within 5 minutes; retained dye = drainage failure
  4. Tear meniscus height - elevated in drainage failure
  5. Regurgitation test: Digital pressure over lacrimal sac - if mucopurulent material regurgitates, indicates chronic dacryocystitis with NLD obstruction

Investigations

1. Lacrimal Syringing (Diagnostic Irrigation)

  • Cannulate lower punctum → instil saline
  • Normal: Saline tasted in throat = patent system
  • Soft stop: Cannula meets resistance before entering sac = canalicular obstruction
  • Hard stop: Cannula enters sac but fluid does not pass to nose; reflux through opposite punctum = NLD obstruction
  • Reflux through the same punctum = lower canalicular obstruction; through upper punctum = common canalicular obstruction
  • Kanski's, p. 4485-4498

2. Jones Dye Tests (for partial/functional obstruction)

  • Jones I: Primary dye test - fluorescein instilled; recovered from nose on blowing = patent, functional drainage
  • Jones II: Secondary dye test - after Jones I failure; syringe with saline; fluorescein in saline = punctum/canaliculus drains but pump fails; clear saline = canalicular obstruction

3. Dacryocystography (DCG)

  • Contrast injection into canalicular system + X-ray/CT
  • Shows site and extent of obstruction, sac size, filling defects (dacryoliths, tumour)

4. Lacrimal Scintigraphy (Nuclear DCG)

  • Physiological test - radiolabelled technetium-99m drops instilled; gamma camera images
  • Shows functional drainage (assesses pump mechanism as well as patency)
  • "Nuclear lacrimal scintigraphy showing passage of tracer via the right lacrimal system but obstructed drainage in the left nasolacrimal duct" - Kanski's, Fig. 3.10

5. Nasal Endoscopy

  • Assesses inferior meatus, valve of Hasner, septal deviation, nasal polyps, turbinate hypertrophy - important pre-DCR assessment

Dacryocystitis

Acute Dacryocystitis

  • Sudden painful swelling at medial canthus below medial canthal tendon
  • Red, tender, hot swelling in the region of the lacrimal sac
  • Organisms: Staphylococcus aureus, Streptococcus pneumoniae
  • Management: Systemic antibiotics (IV if severe); warm compresses; do NOT incise acutely (risk of fistula formation); DCR once infection resolved

Chronic Dacryocystitis

  • Persistent epiphora + mucopurulent discharge
  • Regurgitation of pus on pressure over lacrimal sac
  • May present as a medial canthal swelling (mucocele/pyocele)
  • Management: DCR is definitive

Congenital Nasolacrimal Duct Obstruction (CNLDO)

  • Present in up to 20% of neonates
  • Due to persistent membranous obstruction at valve of Hasner (last part to canalize)
  • Natural history: Spontaneous resolution in majority; rapid in first year, continues beyond
  • Presentation: epiphora + sticky eye from first month of life; increased tear meniscus; mucocele may develop

Treatment - Stepwise

  1. Conservative (< 12 months): Observation; Crigler massage (lacrimal sac massage) - 2-3x daily; topical antibiotics for infection
  2. Probing (12-24 months): Under GA; stepwise probing from punctum to Hasner valve; success rate ~90%
  3. Probing + silicone intubation: For failed probing or older children; stent left for 3-6 months
  4. Balloon dacryoplasty: For failed probing
  5. DCR: Rarely required in children - for persistent epiphora despite probing, bony atresia, upper NLD involvement
"Congenital nasolacrimal duct obstruction has a very high rate of spontaneous resolution, so observation is recommended until the child is at least 1 year old. Under 1 year of age, probing is no better than observation." - Scott-Brown's, p. 5726-5729

Dacryocystorhinostomy (DCR)

DCR creates a new communication between the lacrimal sac and the nasal cavity (middle meatus), bypassing the obstructed NLD.
DCR - anastomosis of lacrimal sac to nasal mucosa
DCR - anastomosis between lacrimal sac and nasal mucosa - Kanski's Clinical Ophthalmology
Indication: Obstruction distal to the medial opening of the common canaliculus (i.e., at or below the lacrimal sac/NLD junction)

Three DCR Approaches (Success Rates - Cummings Table 49.1)

ApproachImmediate Success~5-year Success
Endoscopic (endonasal)84-94%92%
External65-100%94%
Laser-assisted47-100%38% (poor long-term)

A. External DCR

  • Incision: vertical skin incision 10 mm medial to the inner canthus (avoiding angular vein)
  • Medial canthal tendon and lacrimal sac exposed and reflected
  • Intervening bone (anterior lacrimal crest + lacrimal fossa bone) removed
  • Sac incised in an H-shaped manner to create anterior and posterior flaps
  • Nasal mucosa incised; anterior and posterior flaps sutured together
  • Silicone stents passed through canaliculi and NLD into nose (optional, 3-6 months)
  • Success >90%
  • Complications: Cutaneous scar, haemorrhage, angular vein injury, medial canthal structure injury, infection, CSF rhinorrhoea (if subarachnoid space entered), sump syndrome (ostium too high/small)

B. Endoscopic (Endonasal) DCR

  • No skin incision → no external scar
  • A light pipe through the canalicular system guides the endonasal approach
  • Bone removed endoscopically; lacrimal sac marsupialized into middle meatus
  • Transcanalicular laser/drill variants also exist
  • Advantages: Less blood loss, no scar, shorter operative time, lower CSF risk, simultaneous nasal pathology addressed
  • Disadvantages: Slightly lower success rate in some series; requires rhinological expertise; ~50% need additional nasal procedures
  • "This concept allows outcomes of endonasal DCR to be equal or better than those of external DCR." - Cummings, p. 3776

C. Laser-Assisted DCR

  • Laser (KTP, holmium, diode) creates ostium transcanalicularly
  • Poor long-term results (38% at 5 years) - not recommended as primary approach
  • Cummings, p. 3969

Adjunctive Measures

  • Silicone stenting: Standard post-DCR; may be optional; little added benefit per recent data
  • Mitomycin C / 5-FU: Antimetabolites to prevent scarring; evidence is mixed
  • Grommet through medial sac wall / vertical slit without marsupialization: >65% failure rates - to be avoided

Management of Specific Situations

ConditionTreatment
Punctal ectropion/stenosisPunctoplasty (one/two/three-snip), mini-Monoka stent
Canaliculitis (Actinomyces)Canaliculotomy + curettage + antibiotics (penicillin)
Lower canalicular obstructionJones tube (conjunctivodacryocystorhinostomy - CDCR)
Functional epiphora (pump failure)Jones tube if severe; treat lid laxity; treat facial palsy
ConjunctivochalasisTopical steroids; surgical excision/fixation
DacryolithRemoval via DCR
NLD obstruction (acquired, adult)Endoscopic or external DCR
Total canalicular obstructionLester Jones tube (CDCR)
Congenital NLD obstruction <12 moConservative + massage
Congenital NLD obstruction >12 moProbing ± intubation

Causes of Failed DCR / Recurrent Epiphora after DCR

  1. Sump syndrome - ostium too small and too high; lacrimal sac below the stoma retains secretions
  2. Unrecognized common canalicular obstruction (pre-existing, not addressed)
  3. Ostium stenosis/closure - scar tissue formation
  4. Inadequate sac marsupialization
  5. Nasal synechiae blocking ostium
  6. Residual functional failure - lacrimal pump dysfunction (ongoing despite patent system)

Key Points Summary

  • Epiphora = tear overflow; two mechanisms: hypersecretion (dry eye, inflammation) vs. defective drainage
  • Punctal abnormality = most common cause of lacrimal drainage failure
  • Paradoxical watering from dry eye is the most common cause of a watering eye overall
  • Lacrimal syringing is the key diagnostic test: hard stop + reflux = NLD obstruction; soft stop = canalicular obstruction
  • Jones dye tests for functional/partial obstruction
  • CNLDO: 20% neonates; observation until 12 months; probing after 1 year; DCR rarely needed
  • DCR is definitive for NLD obstruction; external and endoscopic approaches have equivalent ~92-94% long-term success; laser DCR has poor long-term results (38%)
  • Post-DCR failure: sump syndrome, canalicular obstruction, ostial scarring
  • Canaliculitis (Actinomyces) presents with medial eyelid discharge, pouting punctum - treat with canaliculotomy

Photodynamic therapy

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Photodynamic Therapy (PDT)

Definition

Photodynamic therapy (PDT) is a treatment modality that combines three essential components to achieve selective tissue destruction:
  1. A photosensitizing agent (photosensitizer)
  2. Light of a specific wavelength
  3. Molecular oxygen (O₂)
When the photosensitizer is activated by appropriate light in the presence of oxygen, it generates reactive oxygen species (ROS), principally singlet oxygen (¹O₂), which cause oxidative cellular damage and death of the target tissue.
"PDT is a subset of photochemotherapy where, in addition to an administered drug and the application of light, oxygen is required to complete the process." - Scott-Brown's Otorhinolaryngology, Vol 1, p. 3548
"Photodynamic therapy (PDT) involves the activation of a photosensitizer by visible light in the presence of oxygen, resulting in the creation of reactive oxygen species, which selectively destroy the target tissue." - Andrews' Diseases of the Skin, p. 2625

Mechanism of Action

PDT mechanism - photosensitizer delivery, photoactivation, acute photodynamic injury, and target cell death via apoptosis and ischemia
PDT mechanism: photosensitizer delivery → photoactivation → ROS generation → apoptosis and ischemic necrosis - Dermatology 2-Volume Set 5e

Photochemical Steps (Jablonski Diagram)

  1. Photosensitizer delivered to target tissue (topically or systemically) - exists in ground state
  2. Light of appropriate wavelength absorbed → photosensitizer excited to singlet excited state (nanoseconds)
  3. Intersystem crossing → more stable triplet excited state (microseconds)
  4. Excited triplet photosensitizer transfers energy to molecular O₂ (Type II photochemical reaction):
Triplet PS + ³O₂ → Ground state PS + ¹O₂ (singlet oxygen)
  1. Singlet oxygen reacts with cellular biomolecules: lipids, proteins, nucleic acids
Dermatology 2-Volume Set 5e, p. 3998

Two Pathways of Cell Death

PathwayMechanismDominant in
Direct cellular injurySinglet O₂ damages mitochondrial membranes, plasma membrane, endoplasmic reticulum → apoptosisTopical PDT (ALA/mALA)
Vascular injuryROS damages endothelial cells of tumour vasculature → thrombus formation → vascular collapse → ischemic necrosisSystemic PDT (porfimer sodium)
"Singlet oxygen causes oxidative damage to cellular membranes (mitochondria and other cellular organelles) and direct cell death, the key mechanism of action in topical PDT. In comparison, PDT using systemic photosensitizers predominantly causes destruction of target sites through vascular injury that leads to tissue ischaemia." - Andrews' Diseases of the Skin, p. 2633

Why Is PDT Selective?

The photosensitizer accumulates preferentially in tumour tissue due to:
  • Increased vascular permeability of tumour vessels (EPR effect)
  • Tumour cells have abnormal metabolism with higher PpIX accumulation
  • Reduced lymphatic drainage - photosensitizer not cleared quickly
  • ALA/mALA penetrate better through abnormal stratum corneum overlying tumour
  • Selectivity ratio: >10:1 (tumour vs. surrounding normal tissue) for ALA/mALA

Photosensitizers

First Generation (Systemic)

AgentNotes
Hematoporphyrin derivative (HpD)First used (1970s); systemic IV administration
Porfimer sodium (Photofrin®)Purified HpD; FDA-approved; systemic; activated at 630 nm; prolonged skin photosensitivity (4-6 weeks) - major disadvantage
Dihematoporphyrin ether (DHE)Similar to porfimer; used in early head/neck trials

Second Generation

AgentNotes
Temoporfin (mTHPC, Foscan®)Meta-tetrahydroxyphenylchlorin; IV systemic; activated at 652 nm; more selective; shorter photosensitivity (2-4 weeks); used in head/neck cancer in Europe
Verteporfin (Visudyne®)Benzoporphyrin derivative; IV; activated at 690 nm; photosensitivity ≤72 hours; primarily used in ophthalmology (age-related macular degeneration)

Third Generation / Topical Prodrugs

AgentNotes
5-Aminolevulinic acid (ALA)Topical prodrug; converted intracellularly to protoporphyrin IX (PpIX) (active photosensitizer); naturally occurring intermediate in heme biosynthesis; activated at 417 nm (blue) or 630 nm (red)
Methyl aminolevulinate (mALA / Metvix®)Methyl ester of ALA; more lipophilic → better skin penetration; greater selectivity for neoplastic cells

ALA/mALA Mechanism:

  • ALA bypasses the rate-limiting step (ALA synthase, feedback-inhibited by heme)
  • Pharmacological ALA → overwhelming accumulation of PpIX in mitochondria → PpIX leaks to plasma membrane, ER
  • Tumour cells: iron-deficient + rapidly proliferating → produce more PpIX than normal cells
"The ideal photosensitizer for PDT should meet: (1) chemical purity, (2) high singlet-oxygen quantum yield, (3) significant light absorption at wavelengths that penetrate tissue deeply, (4) high tissue selectivity, (5) efficacy after topical application." - Fitzpatrick's Dermatology, p. 5052

Light Sources

SourceWavelengthTissue PenetrationUse
Blue light (417-420 nm)Soret band of PpIXSuperficial (<1 mm)Actinic keratoses (epidermis)
Red light (630-635 nm)Minor absorption peak of PpIX / porfimerDeeper (up to 3 mm)Dermal lesions, BCC, SCC, oesophageal/airway tumours
Near-infrared (652 nm)Temoporfin activationDeeper stillHead/neck tumours (Foscan)
690 nmVerteporfin activation-Choroidal neovascularization
Light delivery methods:
  • Surface illumination: LED panels, lamp heads, diode lasers
  • Optical fibres through flexible endoscope: For oesophageal, bronchial, bladder tumours
  • Interstitial light propagation: Optical fibre needles inserted into tumour bulk - extends PDT to deeper tumours
  • Diffuser tip fibres: For tubular structures (trachea, oesophagus)
"Light penetration in tissue is only up to 3 mm [at 400-700 nm], limiting PDT to superficial tumours unless interstitial light propagation is used." - Fitzpatrick's Dermatology, p. 5060

Drug-Light Interval

The time between photosensitizer administration and light delivery - critical for selective targeting:
  • Systemic agents (porfimer, temoporfin): Drug-light interval 3-96 hours (allows washout from normal tissue)
  • Topical ALA/mALA: Incubation 1-18 hours (allows selective accumulation in target cells)
"The drug uptake period (drug-light interval) may last between 3 and 96 hours. The tumour is then irradiated with a measured light dose." - Scott-Brown's, p. 3572

PDT in ENT / Head and Neck Surgery

1. Early Laryngeal Cancer (T1/T2)

  • Biel treated 25 patients with early SCC of the larynx using PDT; achieved complete response in all - notably in 17 patients in whom prior radiotherapy had failed
  • Advantages: organ-preserving; repeatable; not compromised by prior RT, surgery, or chemotherapy

2. Oral Cavity and Oropharynx

  • Karakullukcu et al. (170 patients, early-stage oral cavity/oropharynx): 90% response rate, 70% complete response (cure) rate
  • Gluckman: oral cavity/oropharynx - 11/13 complete response, 2/13 partial response with dihematoporphyrin ether + 630 nm light
  • "The endoscopic access to squamous tumours of the upper aerodigestive tract combined with the tendency to develop field cancerisation make these tumours good candidates for PDT" - Scott-Brown's, p. 3606-3610

3. Oesophageal Cancer

  • Phase II RCT (218 patients): palliative PDT (porfimer sodium) vs. Nd:YAG laser
    • Equivalent improvement in dysphagia
    • Fewer perforations with PDT (1% vs. 7%, p<0.05)
  • Barrett's oesophagus with dysplasia/early adenocarcinoma: PDT showed ablation in 43/55 patients
    • Oesophageal stricture in 53% - significant complication
  • Scott-Brown's, p. 3599-3604

4. Recurrent Respiratory Papillomatosis (RRP)

  • Biel reported results of PDT for laryngeal papillomatosis with durable disease control
  • Red Book 2021: photodynamic therapy listed as an adjuvant treatment option for RRP alongside interferon, indole-3-carbinol, bevacizumab

5. Endobronchial / Tracheobronchial Tumours

  • PDT is an established bronchoscopic intervention for primary or metastatic tracheobronchial neoplasms
  • Indications: malignant central airway obstruction, carcinoma in situ of bronchus
  • Listed alongside laser, electrocautery, cryotherapy, brachytherapy in bronchoscopic armamentarium
  • Fishman's Pulmonary Diseases, p. 3987 (Table 34-1)

6. Nasopharyngeal Carcinoma

  • PDT trials for squamous carcinoma of the nasopharynx reported

7. Sinonasal Inverted Papilloma

  • Non-malignant application; targeted due to recurrent nature

8. Oral Dysplasia / Leukoplakia (Pre-malignant)

  • ALA/mALA-based PDT used for oral epithelial dysplasia

PDT in Ophthalmology

Verteporfin (Visudyne®) PDT is the standard treatment for wet age-related macular degeneration (AMD) with predominantly classic choroidal neovascularisation (CNV):
  • IV verteporfin → selectively accumulates in neovascular endothelium
  • Activated at 689 nm via low-power diode laser directed at CNV
  • Causes thrombosis of choroidal new vessels without damaging overlying retina
  • Kanski's Clinical Ophthalmology (dedicated section)

PDT in Dermatology

IndicationEvidence
Actinic keratosesALA/mALA; clearance 50-70% single tx; up to 90% with repeat
Basal cell carcinoma (superficial)FDA/EMA approved; 87-95% clearance
Bowen disease (SCC in situ)mALA approved; high clearance rates
Superficial SCCApproved in Europe
Acne vulgarisALA-PDT; reduces sebaceous gland activity
PhotorejuvenationALA/mALA; cosmetic improvement of photoaged skin
Localised sclerodermaSystemic PDT
Cutaneous leishmaniasisPDT trials

Advantages of PDT

  • Organ preservation - no ablative surgery needed for early lesions
  • Selectivity - photosensitizer preferentially retained in tumour tissue
  • No effect from prior treatments - not affected by prior radiotherapy, chemotherapy, or surgery (Scott-Brown's, p. 3562)
  • Repeatable - can be given multiple times without cumulative toxicity
  • Minimal long-term side effects
  • Minimal scarring compared to surgery
  • Can treat field cancerisation (wide area treatment)
  • Suitable for patients on anticoagulation
  • No dark toxicity - photosensitizer harmless without light activation

Limitations and Side Effects

LimitationDetails
Skin phototoxicityMajor disadvantage of systemic agents; porfimer = 4-6 weeks sun avoidance; temoporfin = 2-4 weeks; verteporfin ≤72 hours
Limited tissue penetrationLight penetrates only 3 mm at 630 nm; limits treatment to superficial lesions without interstitial delivery
Intraoperative painOften intense at light exposure site; significant patient disincentive
Oesophageal stricture53% after PDT for Barrett's/oesophageal cancer
Tumour oedemaPost-treatment swelling can compromise airway
CostCommercial PDT systems are expensive
Variable drug-light dosimetryDifficult to standardise; multiple permutations of dose/light
Requires oxygenHypoxic tumour cores may be resistant
"The principle shortcomings of PDT have been the limited depth of tissue penetration and extensive skin phototoxicity." - Scott-Brown's, p. 3563

Key Points Summary

  • PDT requires three components: photosensitizer + light + oxygen
  • Mechanism: photosensitizer → excited triplet state → energy transfer to O₂ → singlet oxygen → cell death by apoptosis (topical) or vascular thrombosis/ischaemia (systemic)
  • First-generation: porfimer sodium (Photofrin) - systemic; long phototoxicity; 630 nm
  • Second-generation: temoporfin (Foscan) for head/neck; verteporfin for AMD
  • Third-generation: ALA/mALA topical prodrugs → PpIX; used in dermatology
  • Depth of light penetration: blue light (417 nm) = superficial (<1 mm); red light (630 nm) = deeper (up to 3 mm)
  • Drug-light interval (3-96 h for systemic) allows normal tissue washout → selectivity
  • ENT applications: early laryngeal SCC, oral cavity/oropharynx carcinoma, oesophageal cancer (palliative), RRP, endobronchial tumours
  • PDT is not compromised by prior RT, surgery, or chemotherapy
  • Major limitations: skin phototoxicity, limited penetration depth, pain, oesophageal stricture risk

Faucial diphtheria

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Bat ear

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I now have comprehensive content from Cummings and Shambaugh. I have enough for a thorough structured answer. Let me compile it now:

Bat Ear (Prominent Ear / Prominauris / Protruding Ear)

Definition

A bat ear (prominauris) is a congenital auricular deformity in which the ear protrudes excessively away from the side of the head, causing a cosmetically unacceptable appearance. It is the most common congenital ear deformity requiring surgical correction.
Normal auriculocephalic angle: 20-35 degrees. Protruding ears typically exceed 40-45 degrees. - Cummings Otolaryngology, p. 2582

Anatomy of the Normal Ear

Anatomical landmarks of the normal ear including helix, antihelix, scapha, concha, tragus, fossa triangularis, and lobule
Normal auricular anatomy - Cummings Otolaryngology

Key anatomical norms

MeasurementNormal Value
Ear length (adult)5.5 - 6.5 cm
Ear width50-60% of length
Long-axis posterior rotation15-30 degrees
Superior helix levelLevel of eyebrow
Lobule levelLevel of subnasale (columella base)
Auriculocephalic angle20-35° (>40° = abnormal)
Scalp-helix distance: superior10-12 mm
Scalp-helix distance: mid-helix16-18 mm
Scalp-helix distance: caudal helix20-22 mm
Conchal bowl depth≤1.5 cm
Helix rim lateral to antihelix2-5 mm

Embryology and Development

  • The auricle develops from six hillocks of His on the first and second branchial arches, fusing during weeks 6-12 of gestation
  • The antihelix furls during weeks 12-16; failure to do so results in protruding scapha (the most common cause of bat ear)
  • The helix furls during the 6th month of gestation
  • By age 3: 85% of auricular growth is complete
  • By age 5: cartilaginous growth is nearly complete - suitable age for surgery
"By the time a person is 3 years old, 85% of auricular growth is complete, and the cartilaginous growth is almost complete by 5 years of age. Because of these growth characteristics, surgical intervention can be accomplished at the age of 5 or 6 years without hindering additional growth." - Cummings Otolaryngology, p. 2554

Aetiology (Anatomic Causes)

The two main anatomical abnormalities causing bat ear are:

1. Underdeveloped (absent/poorly formed) antihelical fold - MOST COMMON

  • Failure of the antihelix to furl produces a flat, featureless ear
  • The scapha (flat area between helix and antihelix) flares outward
  • Conchoscaphal angle >90° (normal = 90°)

2. Deep/large conchal bowl (conchal hypertrophy)

  • A deep conchal bowl pushes the entire auricle laterally away from the head
  • Conchal depth >1.5 cm is abnormal
  • Conchomastoid angle >90° (normal = 90°)

3. Combination (both)

  • Most patients have elements of both antihelical underdevelopment and conchal excess

4. Prominent lobule

  • An inferiorly protruding lobule may accompany the above
"The most common underlying anatomic abnormalities are either an insufficiency in the furl at the antihelix (conchal-scaphal angle is >90°) or an increase in the depth of the conchal bowl (conchomastoid angle >90°), with the former being more common." - Cummings Otolaryngology, p. 2586

Psychosocial Impact

  • Significant psychological impact on children from teasing and bullying by peers, particularly after starting school (~age 5)
  • "The entity has no significant otologic ramifications; rather, its importance is determined by the psychological disturbance endured by the patient." - Shambaugh Surgery of the Ear, p. 1725
  • May lead to low self-esteem, social withdrawal, anxiety

Assessment

Clinical Evaluation

  • Document both ears separately - asymmetry is common; each ear may need a different corrective plan
  • Measure auriculocephalic angle and scalp-helix distance
  • Identify whether the problem is: antihelix deficiency / conchal excess / both / lobule
  • Preoperative photography is mandatory

Surgical Planning Priorities

  1. Correct protrusion of helix and lobe
  2. Create a smooth, natural-looking antihelical fold
  3. Avoid overcorrection (helix should remain visible lateral to antihelix on frontal view)
  4. Create bilateral symmetry

Treatment

1. Non-Surgical / Ear Moulding (Neonates)

  • Indicated within the first few weeks of life while auricular cartilage is still pliable (maternal oestrogen maintains cartilage plasticity for 4-6 weeks post-birth)
  • External splints, foam moulding devices, or adhesive tape applied to reshape the ear
  • Most effective if started within the first 72 hours of birth
  • By 3-4 months, the cartilage hardens and moulding becomes ineffective
  • Does not require anaesthesia; avoids surgical risks

2. Surgical Otoplasty

Timing: Age 5-6 years (cartilage growth near-complete; before school bullying begins)

Surgical Techniques

A. Suture-Based Techniques (Cartilage-Sparing)

Mustardé Technique (Most Widely Used)

  • Principle: Horizontal mattress sutures placed through cartilage and anterior perichondrium to recreate the antihelical fold by rolling the scaphoid fossa toward the concha
  • Approach: Postauricular (posterior auricular skin excision + mattress sutures)
  • Steps:
    1. Preoperative ink markings define the crest of the new antihelix; marking sutures placed through anterior skin with ear folded into correct position
    2. Elliptical skin incision in postauricular sulcus
    3. Posterior auricular skin elevated to helical rim and triangular fossa (avoid nicking cartilage)
    4. Tissues elevated from conchal cartilage toward mastoid periosteum; intrinsic/extrinsic muscles divided
    5. 3-4 Mustardé sutures (5-0 or 6-0 non-absorbable, taper needle) placed as horizontal mattress sutures through cartilage and anterior perichondrium
    6. Each suture temporarily tightened to fold antihelix; all placed before tying
    7. Helix should remain visible lateral to new antihelix
    8. Conchomastoid sutures (4-0 or 5-0, >1 stitch): conchal cartilage tacked to mastoid periosteum to reduce conchal depth if needed
    9. Conchal cartilage may be thinned or excised if excessive
    10. Upper pole: stitch between triangular fossa and deep temporal fascia if needed
    11. Redundant posterior skin excised; wound closed
    12. Ear dressed with cotton packing in contours + mastoid pressure dressing
Shambaugh Surgery of the Ear, p. 1746-1771

Incisionless Otoplasty (Fritsch / Merck Technique)

  • Suture loop passed through small puncture sites - no skin incision
  • 4-pass needle technique: horizontal pass through posterior skin and cartilage → under postauricular skin → second horizontal pass → exit through initial entry point
  • Advantages: minimal scarring, faster recovery
  • Suitable for mild-moderate deformity

B. Cartilage-Cutting / Scoring Techniques

TechniqueDescription
Luckett (1910)Single incision through posterior cartilage to recreate antihelical fold; first described technique
Converse-Wood-SmithParallel cartilage incisions (creates tube effect for antihelix)
Stenstrom scoringAnterior surface cartilage abrasion/scoring to cause cartilage to curve away from scored side (Gibson's principle)
  • Gibson's principle: When one surface of cartilage is scored/abraded, it bends away from the scored surface (intrinsic cartilage memory released)
  • Cartilage-cutting techniques have higher hematoma rates (~3%) than suture-only techniques

C. Conchal Reduction Techniques

  • Conchal bowl shaving/excision: Direct excision of posterior conchal cartilage to reduce depth
  • Conchomastoid (Furnas) sutures: Conchal cartilage sutured to mastoid periosteum - brings concha closer to head without excision
  • Suitable when conchal hypertrophy is the main cause

Summary of Technique Selection

DeformityPreferred Technique
Absent/poor antihelical foldMustardé sutures ± scoring
Deep conchal bowlFurnas (conchomastoid) sutures ± conchal excision
BothCombined: Mustardé + Furnas
Prominent lobuleCauda-concha suture or soft tissue excision
Neonatal (age <6 weeks)Ear moulding splint

Postoperative Care

  • Dressing removed at postoperative day 1 to check for haematoma and pressure injury
  • Dressing replaced for a few days
  • Headband worn for 3-4 months post-surgery to maintain ear position during healing
  • Frequent post-op review to check ear position

Complications

Early

ComplicationNotes
HaematomaMost serious early complication; ~3% incidence (higher with cutting techniques); leads to cauliflower ear if untreated; treat by immediate drainage + pressure dressing + IV antibiotics
PainWorsening pain post-op = suspect haematoma
InfectionOrganisms: S. aureus, E. coli, Pseudomonas; treat with drainage + antibiotics
PerichondritisFollows infection/haematoma; IV antibiotics + debridement
Cartilage necrosisFrom infection, haematoma, excess cautery, or tight dressings

Late

ComplicationNotes
Suture extrusion/granulomaBraided > monofilament; remove suture + granuloma
Relapse/recurrenceCartilage overcomes suture fixation; use multiple redundant sutures + scoring
OvercorrectionHelix not visible behind antihelix on frontal view ("pinned-back" appearance)
Telephone deformityMid-ear over-corrected; upper and lower poles protrude; due to inadequate pole correction or excess conchal removal
Hypertrophic scar / keloidPostauricular (less visible); risk in predisposed patients
HypoaesthesiaSensory loss due to nerve injury
Cold susceptibilityAltered circulation
AsymmetryFrom different techniques applied to each ear
"Overcorrection results when the sutures are too tight, causing the helix to be invisible behind the new antihelix in the frontal view. Telephone deformity occurs if the upper and lower poles of the ear are not addressed or if too much conchal cartilage is removed." - Shambaugh Surgery of the Ear, p. 1780

Key Points Summary

  • Bat ear = prominent ear = prominauris; most common congenital auricular deformity
  • Two causes: absent antihelical fold (most common) + deep conchal bowl
  • Auriculocephalic angle >40-45° is abnormal (normal 20-35°)
  • Ear reaches 85% adult size by age 3; surgery safe at age 5-6
  • Non-surgical: ear moulding within first few weeks of life
  • Gold standard surgical technique: Mustardé horizontal mattress sutures to recreate antihelical fold (posterior approach, cartilage-sparing)
  • Conchal excess: Furnas conchomastoid sutures ± conchal excision
  • Most dreaded early complication: haematoma → cauliflower ear
  • Most common late complication: relapse (suture failure)
  • Notorious aesthetic complications: overcorrection (pinned-back ear) and telephone deformity
  • Post-op headband worn for 3-4 months

Now delivering the full answer above - here is the compiled response:


Bat Ear (Prominent Ear / Prominauris)

Definition

A bat ear (prominauris) is a congenital auricular deformity where the pinna protrudes excessively from the side of the head. It is the most common congenital ear deformity requiring surgical correction. The normal auriculocephalic angle is 20-35°; protruding ears typically exceed 40-45°. It has no significant otologic (hearing) consequence - its importance lies in the psychological disturbance it causes, particularly from peer teasing after starting school. - Shambaugh Surgery of the Ear, p. 1725; Cummings, p. 2582

Anatomy of the Normal Auricle

Anatomical landmarks of the normal ear - helix, antihelix, scapha, concha, fossa triangularis, lobule and more

Normal measurements

ParameterNormal
Auriculocephalic angle20-35°
Scalp to superior helix10-12 mm
Scalp to mid helix16-18 mm
Scalp to caudal helix20-22 mm
Helix lateral to antihelix2-5 mm
Conchal bowl depth≤1.5 cm
Superior helix levelLevel of eyebrow
Inferior lobule levelLevel of subnasale
Long axis posterior rotation15-30°
Cummings Otolaryngology, p. 2582-2584

Embryology and Development

  • Auricle arises from six hillocks of His (1st and 2nd branchial arches), fusing during gestation weeks 6-12
  • Antihelix furls at weeks 12-16; failure causes protruding scapha - the most common cause of bat ear
  • Helix furls at 6 months gestation
  • 85% of auricular growth complete by age 3; cartilage growth nearly complete by age 5
  • Surgery is safe at age 5-6 without hindering growth

Causes (Anatomic Defects)

CauseAngle AbnormalityFrequency
Absent/underdeveloped antihelical foldConchoscaphal angle >90°Most common
Deep/hypertrophic conchal bowlConchomastoid angle >90° / conchal depth >1.5 cmSecond
Combination of bothBoth angles abnormalCommon
Prominent lobule-Less common, often co-exists

Treatment

1. Ear Moulding (Non-surgical - Neonates)

  • Window: First few weeks of life (maternal oestrogen keeps cartilage pliable; best results within 72 hours of birth)
  • External foam/silicone splints reshape the cartilage painlessly
  • By 3-4 months, cartilage hardens and moulding becomes ineffective
  • No anaesthesia, no scarring

2. Surgical Otoplasty

Optimal timing: Age 5-6 years (cartilage near-mature; before school-related bullying)

Surgical Techniques

A. Mustardé Suture Technique (Gold Standard)

Target: Absent/deficient antihelical fold
Approach: Postauricular
Steps:
  1. Marking sutures through anterior skin with ear manually folded into position to define new antihelix crest
  2. Elliptical postauricular skin incision and excision
  3. Posterior skin elevated to helical rim and triangular fossa; conchal cartilage elevated to mastoid periosteum
  4. Intrinsic/extrinsic auricular muscles divided
  5. 3-4 horizontal mattress sutures (5-0 or 6-0 non-absorbable monofilament, taper needle) placed through cartilage and anterior perichondrium - rolls the scaphoid fossa toward the concha, recreating the antihelical fold
  6. All sutures placed before tying; tied sequentially with repeated assessment
  7. After setting the antihelix, assess residual conchal depth
  8. Conchomastoid (Furnas) sutures added if needed: 4-0 or 5-0 non-absorbable stitch tacking conchal cartilage to mastoid periosteum
  9. Upper pole addressed with fossa triangularis-temporalis fascia stitch if prominent
  10. Lobule addressed if needed
  11. Redundant posterior skin excised; wound closed
  12. Pressure dressing with cotton conforming to auricular contours
Shambaugh Surgery of the Ear, p. 1746-1770; Cummings Otolaryngology, p. 2594-2620

B. Cartilage-Scoring / Cutting Techniques

TechniquePrinciple
Luckett (1910)Single full-thickness cartilage incision posteriorly to recreate antihelical fold; first historical technique
Converse-Wood-SmithTwo parallel cartilage incisions creating a tube for the antihelix
Stenstrom / anterior scoringAbrasion of anterior cartilage surface → Gibson's principle (cartilage curls away from scored surface)
  • Gibson's principle: Cartilage bends away from a scored surface due to release of intrinsic stress
  • Cutting techniques have higher haematoma rates (~3%) vs. suture-only

C. Incisionless Otoplasty

  • No skin incision - sutures passed through puncture sites only
  • 4-pass needle loop technique through posterior auricular skin and cartilage
  • Suitable for mild-to-moderate deformity
  • Minimal scarring, faster recovery

D. Conchal Reduction

  • Furnas (conchomastoid) sutures: conchal cartilage sutured to mastoid periosteum
  • Direct conchal bowl excision/shaving: for severe conchal hypertrophy
  • Indicated when conchal depth >1.5 cm is the dominant problem

Technique Selection Summary

Dominant DefectPreferred Technique
Absent antihelical foldMustardé mattress sutures
Deep conchal bowlFurnas conchomastoid sutures ± excision
BothCombined Mustardé + Furnas
Neonatal (<6 weeks)Ear moulding splint
Mild, any ageIncisionless suture technique

Postoperative Care

  • Dressing removed at day 1 to inspect for haematoma and pressure injury
  • Dressing re-applied for a few days
  • Headband worn for 3-4 months post-surgery to hold ear in position during healing
  • Frequent follow-up to assess position

Complications

Early

ComplicationKey Points
Haematoma (~3%)Most serious early complication; worsening pain is the first symptom; must be drained immediately; if untreated → cauliflower ear (fibrocartilaginous organisation)
InfectionS. aureus, Pseudomonas, E. coli; treat with drainage + broad-spectrum antibiotics
PerichondritisSecondary to infection/haematoma; IV antibiotics + debridement
Cartilage necrosisFrom infection, haematoma, excess cautery, or tight dressings

Late

ComplicationKey Points
Relapse/recurrenceCartilage spring overcomes sutures; use multiple redundant sutures + scoring to reduce
OvercorrectionHelix hidden behind antihelix on frontal view ("pinned-back" appearance) - sutures too tight
Telephone deformityUpper and lower poles remain prominent while middle is over-corrected; due to inadequate pole treatment or excess mid-conchal removal
Suture granuloma / extrusionBraided > monofilament; remove suture + granuloma
Keloid / hypertrophic scarPostauricular location; less visible but problematic in susceptible patients
HypoaesthesiaNerve injury (great auricular nerve most at risk)
Cold susceptibilityImpaired circulation
AsymmetryDifferent techniques used on each ear; different cartilage stiffness
"Overcorrection results when the sutures are too tight, causing the helix to be invisible behind the new antihelix. Telephone deformity occurs if the upper and lower poles are not addressed or if too much conchal cartilage is removed." - Shambaugh Surgery of the Ear, p. 1780

Key Points

  • Bat ear = prominauris; auriculocephalic angle >40-45°; normal is 20-35°
  • Two mechanisms: absent antihelical fold (most common) + deep conchal bowl
  • Antihelix failure to furl (weeks 12-16 gestation) is the root cause in most cases
  • No hearing impairment; psychological impact (bullying) drives treatment
  • Surgery at age 5-6; non-surgical ear moulding if neonate (<6 weeks)
  • Mustardé technique (posterior horizontal mattress sutures) is the gold standard for antihelical fold reconstruction
  • Furnas technique (conchomastoid sutures) addresses conchal bowl excess
  • Most serious early complication: haematoma (→ cauliflower ear)
  • Classic late aesthetic complications: overcorrection (helix hidden) and telephone deformity (poles prominent, mid-ear flat)
  • Headband worn for 3-4 months post-operatively

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Monoclonal Antibodies (mAbs) and Their Applications in ENT

What Is a Monoclonal Antibody?

A monoclonal antibody (mAb) is a laboratory-produced antibody derived from a single B-cell clone, designed to bind with high specificity to a single target antigen (epitope). Unlike polyclonal antibodies (which target multiple epitopes), mAbs offer precision targeting with predictable pharmacological effects.
"The molecular biology of HNSCC guides therapeutic approaches. The monoclonal antibody cetuximab targets the epidermal growth factor receptor (EGFR), overexpressed in nearly 90% of HNSCCs." - Cummings Otolaryngology, p. 3389

Nomenclature

mAb names follow a standardized WHO suffix system:
SuffixSourceExample
-omabMurine (mouse)Ibritumomab
-ximabChimeric (mouse + human)Cetuximab, Rituximab
-zumabHumanized (mostly human)Bevacizumab, Pembrolizumab
-umabFully humanPanitumumab, Dupilumab
Prefix indicates target:
  • -ci- = cardiovascular
  • -li- = immune/inflammatory
  • -tu- = tumour
  • -ki- = interleukin

Classification by Target / Mechanism

ClassMechanismExamples
Anti-IgEBlocks free IgE, prevents mast cell/basophil degranulationOmalizumab
Anti-IL-4/IL-13Blocks Type 2 Th2 inflammatory cytokinesDupilumab
Anti-IL-5 / Anti-IL-5RαReduces eosinophil production and survivalMepolizumab, Benralizumab, Reslizumab
Anti-TSLPBlocks upstream epithelial alarminTezepelumab
Anti-EGFRBlocks epidermal growth factor receptor → inhibits tumour proliferationCetuximab, Panitumumab
Anti-PD-1Checkpoint inhibitor - restores T-cell anti-tumour immunityPembrolizumab, Nivolumab
Anti-CTLA-4Checkpoint inhibitor - prevents T-cell suppressionIpilimumab
Anti-VEGFInhibits angiogenesis (tumour/papilloma vascularity)Bevacizumab

ENT Application 1: Chronic Rhinosinusitis with Nasal Polyps (CRSwNP)

Background

  • CRSwNP is driven by Type 2 (Th2) inflammation with elevated IL-4, IL-5, IL-13, and IgE
  • Key cells: eosinophils, mast cells, innate lymphoid cells type 2 (ILC2)
  • Biologics target this eosinophilic/Th2 inflammatory cascade
  • Indicated for: severe, refractory CRSwNP that fails topical steroids and/or surgery (or recurs post-surgery)

1. Dupilumab (Dupixent®) - FIRST-LINE BIOLOGIC

FeatureDetail
TargetIL-4Rα (shared receptor for IL-4 and IL-13) → blocks both IL-4 and IL-13 simultaneously
RouteSubcutaneous injection every 2 weeks (300 mg)
FDA approvalCRSwNP (2019); asthma (2018); atopic dermatitis (2017)
Key trialsLIBERTY NP SINUS-24 and SINUS-52: significant reduction in nasal polyp score, nasal congestion, loss of smell; reduced need for systemic steroids and revision surgery
ENT effectsReduces polyp burden, improves nasal patency and smell, reduces systemic steroid use
Side effectsInjection site reactions, conjunctivitis, transient eosinophilia (hypereosinophilia paradox)
"Dupilumab (anti-IL-4 with anti-IL-13 activity) has been approved by the FDA for treatment of CRS with nasal polyps... Concerns related to cost and requirement for continued therapy may limit the clinical utility of this medication." - Murray & Nadel's, p. 3979

2. Omalizumab (Xolair®)

FeatureDetail
TargetFree IgE - binds to Fc region of IgE, preventing binding to FcεRI on mast cells/basophils
RouteSubcutaneous every 2-4 weeks (dose based on IgE level and body weight)
FDA approvalAllergic asthma (2003); chronic idiopathic urticaria; CRSwNP (2020)
MechanismReduces free IgE by 90-95%; downregulates FcεRI expression; reduces mast cell/basophil activation
ENT effectsReduces nasal polyp size, improves symptom scores, reduces need for surgery; also benefits allergic rhinitis
SelectionHigh baseline IgE (30-700 IU/mL), elevated blood eosinophils, high FeNO → best predictors of response
Side effectsInjection site reactions; rare anaphylaxis (must observe 30 min post-dose)
"Omalizumab targets the FcER1 receptor-binding portion of IgE, preventing it from interacting with immune cells to cause degranulation. Treatment reduces unbound IgE capable of binding to its receptor by 90-95%." - Murray & Nadel's, p. 450

3. Mepolizumab (Nucala®)

FeatureDetail
TargetIL-5 (anti-IL-5 antibody)
RouteSubcutaneous 100 mg every 4 weeks
FDA approvalSevere eosinophilic asthma; eosinophilic granulomatosis with polyangiitis (EGPA)
ENT effectsReduces eosinophilic CRSwNP polyp burden; reduces blood and tissue eosinophils; efficacy in EGPA (a granulomatous vasculitis affecting ENT - sinonasal involvement, subglottic stenosis)
EvidencePhase III trials showing polyp size reduction and symptom improvement in eosinophilic CRSwNP

4. Benralizumab (Fasenra®)

FeatureDetail
TargetIL-5Rα (receptor for IL-5 on eosinophils and basophils) - produces ADCC-mediated eosinophil depletion
RouteSubcutaneous 30 mg every 4 weeks x3, then every 8 weeks
Unique mechanismDirect eosinophil depletion (near-complete) via antibody-dependent cell cytotoxicity (ADCC) - faster and more complete than anti-IL-5 antibodies
ENT effectsReduces eosinophilic CRSwNP; studied in EGPA

5. Tezepelumab (Tezspire®)

FeatureDetail
TargetTSLP (thymic stromal lymphopoietin) - an upstream epithelial "alarmin" that initiates the entire Type 2 cascade
RouteSubcutaneous 210 mg every 4 weeks
SignificanceBlocks the most upstream trigger of Th2 inflammation; effective in both eosinophilic and non-eosinophilic asthma/CRS; broader mechanism than IL-5/IL-4/IL-13 targeting
ENTEmerging evidence for CRSwNP (PMID 39636450 - 2024 review confirms role in CRSwNP)

Biologic Selection for CRSwNP

BiomarkerPreferred Agent
Elevated IgE + allergic sensitizationOmalizumab
Elevated blood eosinophils (>300/μL)Mepolizumab or Benralizumab
High FeNO + eosinophiliaDupilumab
Comorbid atopic dermatitis/asthmaDupilumab
Non-eosinophilic endotypeTezepelumab
EGPAMepolizumab
"Biologics offer improved symptoms, endoscopic scores, and reduced polyp burden. Drugs under investigation/approved: reslizumab, mepolizumab, benralizumab, dupilumab, and omalizumab." - Cummings Otolaryngology Table 42.1

ENT Application 2: Head and Neck Squamous Cell Carcinoma (HNSCC)

1. Cetuximab (Erbitux®) - Anti-EGFR

PD-1/PD-L1 pathway and anti-PD1 monoclonal antibody blockade restoring T-cell anti-tumour activity
Immune checkpoint inhibition - anti-PD1 mAb blocks PDL1-PD1 interaction allowing T-cell tumour killing - Cummings Otolaryngology
FeatureDetail
TypeChimeric IgG1 monoclonal antibody
TargetEGFR (epidermal growth factor receptor) - overexpressed in >90% of HNSCCs
MechanismCompetitively inhibits EGF and TGF-α binding to EGFR → inhibits downstream RAS/MAPK and PI3K/Akt signalling → reduced proliferation, invasion, angiogenesis + ADCC
FDA approvalHNSCC (locoregionally advanced and recurrent/metastatic)
Key trial - Bonner (2006)Radiation vs. radiation + cetuximab in locally advanced HNSCC: cetuximab improved locoregional control (24.4 vs 14.9 months) and OS (49 vs 29.3 months); established cetuximab + RT as standard
Key trial - EXTREMECetuximab + platinum/5-FU vs. chemotherapy alone in recurrent/metastatic HNSCC: improved OS (10.1 vs 7.4 months); established EXTREME regimen as first-line standard
HPV statusHPV-positive HNSCC derives less benefit from cetuximab monotherapy; HPV-negative patients respond better
Monotherapy response rate<10% as single agent
Side effectsAcneiform rash (severity correlates with treatment response), hypomagnesaemia, infusion reactions (severe in <3%), fatigue
"The monoclonal antibody cetuximab targets the EGFR, overexpressed in nearly 90% of HNSCCs... as a monotherapy, cetuximab has very low efficacy and induces a response in less than 10% of HNSCC patients." - Cummings Otolaryngology, p. 2639

2. Pembrolizumab (Keytruda®) - Anti-PD-1 Checkpoint Inhibitor

FeatureDetail
TypeHumanized IgG4 antibody
TargetPD-1 (programmed cell death protein 1) on T cells
MechanismBlocks PD-1 from binding PD-L1 on tumour cells → prevents T-cell exhaustion → restores cytotoxic T-cell tumour killing
FDA approvalFirst-line treatment of recurrent/metastatic HNSCC (2019, as monotherapy for PD-L1 CPS ≥1, and in combination with chemotherapy)
Key trialsKEYNOTE-012 (Phase Ib), KEYNOTE-055, KEYNOTE-040, KEYNOTE-048
KEYNOTE-048Pembrolizumab + chemotherapy vs. EXTREME regimen: superior OS for PD-L1 CPS ≥1 patients; pembrolizumab monotherapy superior for CPS ≥20
PD-L1 biomarkerCPS (combined positive score) ≥1 required for first-line monotherapy; ≥20 predicts best response
HNSCC PD-L1 expression45-80% of HNSCCs express PD-L1
Side effectsImmune-related adverse events (irAEs): pneumonitis, colitis, hepatitis, endocrinopathies (hypothyroidism, adrenal insufficiency), skin rash; pseudoprogression can occur

3. Nivolumab (Opdivo®) - Anti-PD-1 Checkpoint Inhibitor

FeatureDetail
TypeHuman IgG4 antibody
TargetPD-1
FDA approvalRecurrent/metastatic HNSCC after platinum failure (2016)
Key trial - CheckMate 141Nivolumab vs. investigator's choice (cetuximab/methotrexate/docetaxel) in platinum-refractory r/m-HNSCC: OS 7.5 vs 5.1 months (p<0.01); grade 3-4 toxicities 13% vs 35%
AdvantageMarkedly lower toxicity than chemotherapy while achieving superior OS
"Approval of nivolumab and pembrolizumab for HNSCC followed landmark trials... Overall survival in the intention to treat population of 361 patients was 7.5 months for nivolumab compared to 5.1 months for investigator's choice. Severe grade 3-4 toxicities were less for nivolumab (13% vs 35%)." - Cummings Otolaryngology, p. 3715

4. Panitumumab - Anti-EGFR (Fully Human)

  • Fully human IgG2 anti-EGFR antibody (less ADCC than cetuximab due to IgG2 isotype)
  • Phase III trial (657 patients): panitumumab + cisplatin/5-FU vs. chemotherapy alone: improved PFS (5.8 vs 4.6 months, p=0.004) but no significant OS improvement
  • Less infusion reaction risk than cetuximab (fully human)
  • Better OS in HPV-negative (p16-negative) HNSCC (11.6 vs 8.6 months)

5. Ipilimumab (Yervoy®) - Anti-CTLA-4

  • Blocks CTLA-4 on regulatory T cells → promotes T-cell activation against tumour
  • Used in combination with nivolumab in recurrent/metastatic HNSCC (investigational)
  • CTLA-4 inhibition = more systemic, broader immune activation than PD-1 blockade
  • Higher irAE rates than PD-1 inhibitors

ENT Application 3: Recurrent Respiratory Papillomatosis (RRP)

Bevacizumab (Avastin®) - Anti-VEGF

FeatureDetail
TargetVEGF (vascular endothelial growth factor)
MechanismInhibits VEGF-driven angiogenesis; HPV-driven papillomas depend on neovascularisation for growth; bevacizumab disrupts this
Route in RRPIntralesional injection (25-50 mg per session, subepithelial injection after KTP/angiolytic laser ablation)
Half-life~1 month
Systemic routeIV infusion also used for aggressive/disseminated RRP
EvidenceMultiple case series showing reduced frequency of surgery and extent of recurrence; some patients achieve disease remission
TechniqueAfter office-based angiolytic laser ablation, bevacizumab injected into superficial lamina propria at papilloma sites (25 mg/mL, 25-50 mg)
BenefitReduces number of procedures per year; some patients have total disease eradication
"Bevacizumab (Avastin®), a vascular endothelial growth factor inhibitor, appears to reduce the angiogenesis critical to papilloma regrowth, and can reduce the frequency of procedures and extent of papilloma recurrence. In some patients, the disease has remained in remission." - Scott-Brown's ORL, p. 3368-3372

ENT Application 4: Allergic Rhinitis

Omalizumab (Additional Role)

  • Anti-IgE mechanism is directly applicable to allergic rhinitis (IgE-mediated)
  • Reduces mast cell and basophil response to allergen
  • Useful in patients with severe allergic rhinitis comorbid with asthma and/or CRSwNP
  • Not first-line for isolated allergic rhinitis (antihistamines + nasal steroids preferred), but relevant in step-up/refractory disease
  • The EXTRA study showed greatest benefit in patients with high FeNO, high serum eosinophils, and elevated periostin

ENT Application 5: Eosinophilic Granulomatosis with Polyangiitis (EGPA / Churg-Strauss)

  • ENT manifestations: nasal polyps, sinusitis, granulomatous nasal obstruction, subglottic stenosis
  • Mepolizumab (anti-IL-5): FDA-approved for EGPA; reduces eosinophilic inflammation; reduces steroid dependence; reduces ENT flares
  • IL-5 drives eosinophil survival in EGPA - blocking it is pathophysiologically logical

Application 6: Nasopharyngeal Carcinoma (NPC)

  • NPC overexpresses EGFR and PD-L1
  • Cetuximab studied in combination with radiotherapy and chemotherapy
  • Pembrolizumab and nivolumab evaluated in recurrent/metastatic NPC (PD-L1 highly expressed)
  • EBV-associated NPC shows immune evasion through PD-L1 upregulation - rationale for checkpoint inhibitors

Key Concepts: Immune Checkpoints in HNSCC

PD-1 / PD-L1 Pathway:
  • PD-1 is expressed on activated T cells; its ligand PD-L1 is on tumour cells and APCs
  • Tumour cells upregulate PD-L1 (stimulated by IFN-γ) → binds PD-1 on T cells → T-cell exhaustion → tumour immune escape
  • Anti-PD-1 antibodies (pembrolizumab, nivolumab) block this interaction → restore T-cell killing
CTLA-4 Pathway:
  • CTLA-4 expressed on regulatory T cells; binds B7 on APCs → downregulates T-cell activation
  • Ipilimumab blocks CTLA-4 → removes T-cell suppression → more potent but more toxic immune activation
Tumour Microenvironment:
  • MDSCs, tolerogenic DCs, TGF-β, IL-6 secretion all contribute to immune evasion
  • Immunoediting: elimination → equilibrium → escape (tumour evades immune system)
  • Pseudoprogression: tumour appears larger initially due to immune infiltration - must confirm progression 4 weeks later before stopping therapy (irRC criteria)

Adverse Effects - Summary

DrugKey Adverse Effects
CetuximabAcneiform rash, hypomagnesaemia, infusion reactions, paronychia
Pembrolizumab/NivolumabirAEs: pneumonitis, colitis, hepatitis, thyroiditis, hypophysitis, skin rash; rarely myocarditis
DupilumabConjunctivitis, injection site reactions, paradoxical eosinophilia
OmalizumabInjection site reactions; rare anaphylaxis (observe 30 min post-injection)
Mepolizumab/BenralizumabGenerally well tolerated; injection site reactions; headache
BevacizumabHypertension, proteinuria, wound healing impairment, thromboembolic events, nasal septal perforation (systemic)

Summary Table: mAbs in ENT

DrugTargetENT IndicationRouteApproval
DupilumabIL-4Rα (IL-4/IL-13)CRSwNPSC q2wFDA approved (CRSwNP 2019)
OmalizumabIgE (FcεRI binding site)CRSwNP, allergic rhinitisSC q2-4wFDA approved (CRSwNP 2020)
MepolizumabIL-5CRSwNP, EGPASC q4wFDA approved (EGPA 2017)
BenralizumabIL-5RαCRSwNP (eosinophilic)SC q4-8wInvestigational for CRSwNP
TezepelumabTSLPCRSwNP (emerging)SC q4wInvestigational
CetuximabEGFRHNSCC (oropharynx, larynx, NPC)IVFDA approved
PembrolizumabPD-1Recurrent/metastatic HNSCCIV q3wFDA approved (2016/2019)
NivolumabPD-1Recurrent/metastatic HNSCCIVFDA approved (2016)
PanitumumabEGFRHNSCC (r/m)IVInvestigated
BevacizumabVEGFRRP (intralesional)Intralesional / IVOff-label in RRP

Key Points

  • mAbs are single-clone antibodies targeting one specific epitope; named by source suffix (-ximab = chimeric, -zumab = humanized, -umab = fully human)
  • In CRSwNP: Type 2/eosinophilic inflammation drives disease; dupilumab (anti-IL-4/IL-13) is FDA-approved first-line biologic; omalizumab (anti-IgE) also approved; mepolizumab/benralizumab target IL-5 pathway; tezepelumab targets upstream TSLP
  • Biomarker-guided biologic selection: IgE → omalizumab; eosinophilia → mepolizumab/benralizumab; Th2/mixed → dupilumab
  • In HNSCC: EGFR overexpressed in >90% - cetuximab (chimeric anti-EGFR) used with RT (Bonner trial) and chemotherapy (EXTREME trial)
  • Checkpoint inhibitors: PD-L1 expressed on 45-80% of HNSCCs; pembrolizumab + chemotherapy now first-line for r/m-HNSCC (KEYNOTE-048); nivolumab approved post-platinum failure (CheckMate 141: OS 7.5 vs 5.1 months)
  • RRP: bevacizumab (anti-VEGF, 25-50 mg intralesional) reduces papilloma angiogenesis, decreases surgical frequency, can achieve remission
  • EGPA: mepolizumab approved; addresses eosinophilic ENT manifestations including nasal polyps and subglottic stenosis
  • irAEs from checkpoint inhibitors are distinct from cytotoxic chemotherapy toxicities and require early recognition and steroid treatment
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