Intubation Granuloma

Epidemiology

• May occur after brief or prolonged intubation.
• More common in females when caused by intubation (in contrast to contact/hyperfunctional granulomas, which are more common in men).
• Develops typically 4-6 weeks after intubation.

Pathophysiology

• Sessile initially, later forming a large pedunculated lesion
• Unilateral or bilateral (frequently bilateral)
• Associated with sclerosis of the arytenoid (visible on CT scan)

• Tissue loss with posterior glottic incompetence
• Partial or complete fixation of one or both arytenoid cartilages
• Interarytenoid synechia

Clinical Features

Endoscopic Appearance

Diagnosis

1. History - recent intubation or laryngeal instrumentation
2. Laryngoscopy / videostroboscopy - visual diagnosis is usually sufficient; biopsy generally not needed unless diagnosis is uncertain, carcinoma must be excluded, or the lesion is atypical
3. Vocal Capability Battery - speaking voice may be surprisingly normal as the membranous vocal folds can vibrate unimpeded
4. CT scan - may show arytenoid sclerosis; useful in assessing for arytenoid fixation in prolonged intubation cases
5. Assessment of vocal fold motion - mandatory for recent injuries to guide management intensity

Management

Normal vocal fold motion (conservative approach)

• Antireflux therapy (PPIs/H2 blockers) - treats the co-factor impairing healing
• Inhaled corticosteroids - reduce inflammation
• Voice therapy - reduce hyperfunctional behaviors, throat clearing
• Smoking cessation, vocal hygiene
• Voice rest (relative)
• Watchful waiting - the lesion is best thought of as an exuberant healing response; spontaneous maturation and detachment can occur

Impaired vocal fold motion (more aggressive)

• Direct microlaryngoscopy + excision of granuloma
• Intralesional steroid injection at the time of surgery
• Surgery is a last resort because:
  • Postoperative recurrence is predictable
  • Spontaneous resolution is expected
  • Excision should be limited, leaving the base/pedicle undisturbed

Adjunct / refractory options

• Botulinum toxin injection - reduces mechanical trauma by temporarily weakening the ipsilateral thyroarytenoid muscle
• Antibiotics (if secondary infection)
• Systemic corticosteroids

Key Differentials

Sources

• Cummings Otolaryngology Head and Neck Surgery, Chapter 60 (Benign Vocal Fold Mucosal Disorders)
• Scott-Brown's Otorhinolaryngology Head & Neck Surgery, Chapter 63 (Specific Inflammatory Conditions)
• Fishman's Pulmonary Diseases and Disorders, Chapter 47 (Endotracheal Tube-Related Trauma)
• Miller's Anesthesia, 10th ed., Chapter 66

Contact Granuloma (Contact Ulcer / Vocal Process Granuloma)

• Contact ulcer / contact granuloma
• Vocal process granuloma
• Peptic granuloma
• Intubation granuloma (when caused by endotracheal tube)
• Contact pachydermia

Epidemiology

• Primarily affects men (in contrast to intubation granuloma, which is more common in women)
• Associated with demanding vocal occupations (clergy, teachers, lawyers, salespeople)
• Strong association with laryngopharyngeal reflux (LPR) / gastroesophageal reflux
• Psychological stress and conflict have also been suggested as contributing factors

Aetiology / Causes

Pathophysiology

Clinical Features

• Unilateral discomfort or pain over the mid-thyroid cartilage, often with referred otalgia (to the ipsilateral ear)
• Foreign body sensation ("something stuck in the throat")
• Frequent throat clearing and/or chronic cough
• Voice changes - may be subtle; habitual low-pitched, monotone, or gravelly voice
• Hoarseness when the lesion becomes large
• Symptoms of LPR: morning sore throat with sour taste, acid eructations, low gravelly morning voice

Laryngoscopic Appearance

• Depressed, ulcerated area with whitish exudate or a bilobed, heaped-up lesion at the vocal process
• Surrounding erythema extending up the medial arytenoid surface
• Contralateral vocal process fits into the cleft of a bilobed granuloma during phonation (characteristic)
• Mature lesion: pedunculated, flips above and below the vocal fold plane with breathing/phonation
• Stroboscopy useful to identify glottal incompetence as a contributing factor

Diagnosis

1. History - behavioral patterns (caffeine, alcohol, late-night eating), LPR symptoms, voice use habits, stress
2. Laryngoscopy - visual diagnosis is usually sufficient; biopsy is generally not required for a classic-appearing lesion
3. Rigid telescope or distal-chip camera - may be needed to detect ulcers
4. Stroboscopy - identifies glottal incompetence contributing to compensatory hyperfunction
5. pH monitoring / barium swallow - role remains controversial; empiric antireflux treatment is the standard approach

Management

1. Antireflux therapy (first-line, empiric)

• PPIs (e.g., omeprazole, lansoprazole twice daily) - started empirically even without reflux symptoms
• Lifestyle modifications: avoid late meals, caffeine, alcohol, spicy foods, elevate head of bed
• Effective even in patients without overt GERD symptoms

2. Voice therapy

• Address hyperfunctional behaviors: eliminate throat clearing, raise average speaking pitch, reduce glottal attack
• Role is somewhat indeterminate given high rate of spontaneous resolution, but worthwhile in patients with clear vocal abuse patterns

3. Corticosteroids

• Intralesional depot corticosteroid injection (e.g., triamcinolone) - can be done in the office/videoendoscopy suite; lesions tend to diminish in size and symptoms resolve
• Inhaled corticosteroids (triamcinolone, mometasone) - effective alternative that avoids systemic side effects
• Patients reassessed every 6-8 weeks; treatment continued if there is size reduction and symptom improvement

4. Watchful waiting

• Spontaneous maturation and detachment occurs in 3-6 months in many cases
• The natural history shown in the image sequence above is not uncommon

5. Botulinum toxin injection (refractory cases)

• Injection into the thyroarytenoid-lateral cricoarytenoid muscle complex
• Reduces the mechanical force of arytenoid apposition
• Should be considered for refractory cases or as an adjunct to surgical removal
• Patients must be counselled that significant (temporary) dysphonia results from the injection

6. Surgery - last resort only

• Indicated for: symptomatic lesions failing conservative therapy, or when malignancy cannot be excluded
• Microlaryngoscopy with excision - removal should be limited, leaving the base/pedicle undisturbed
• Surgery alone carries a very high recurrence rate; recurrent lesions are often more recalcitrant than the original
• Postoperative recurrence of the ulcer or granuloma is predictable if underlying causes are not addressed
• Biopsy is justified if the lesion persists despite adequate conservative management (to exclude carcinoma)

Comparison: Contact Granuloma vs. Intubation Granuloma

Differential Diagnosis

Contact Granuloma - Summary

Key Points

Management (stepwise)

1. PPIs - empiric antireflux therapy (even without overt reflux symptoms)
2. Voice therapy - eliminate throat clearing, raise pitch, reduce glottal attack
3. Inhaled / intralesional corticosteroids - triamcinolone or mometasone
4. Watchful waiting - spontaneous maturation and detachment in 3-6 months is common
5. Botulinum toxin (thyroarytenoid-LA muscle complex) - for refractory cases; causes temporary dysphonia
6. Surgery - last resort only; high recurrence rate; leave base/pedicle undisturbed; biopsy if carcinoma cannot be excluded

Tuning Fork Tests for Malingering (Pseudohypacusis)

Terminology

Why Tuning Fork Tests Catch Malingerers

1. Biophysics of bone conduction - sound transmitted via the skull reaches both cochleas simultaneously; a claimed "dead" ear still receives bone-conducted sound
2. The Stenger principle - when two identical tones differ only in intensity, perception is referred entirely to the louder ear

Tuning Fork Tests for Malingering

1. Chimani-Moos Test (Modified Weber)

• Place the vibrating tuning fork on the vertex (midline)
• The malingerer claims to hear it only in the "good" ear
• Now occlude the good ear (external canal) with a finger
• Normal response / true deafness: Sound still heard only in the good (occluded) ear or disappears
• Malingerer's response: They now report hearing the tone - revealing the "deaf" ear can in fact hear bone-conducted sound that is now louder on that side

• True total SNHL: No response (cochlea genuinely dead)
• Malingerer: Either responds (revealing the ear hears) or gives an exaggerated "no" that is itself inconsistent with normal audiometry

2. Stenger Tuning Fork Test

• Hold one vibrating tuning fork close to the "good" ear (suprathreshold, clearly audible)
• Hold a second identical vibrating tuning fork farther away from the "bad" ear (below the patient's claimed threshold but above their true threshold)
• Negative Stenger (genuine loss): Patient responds - they hear the tone in the good ear; the tone at the bad ear is genuinely below threshold and does not interfere
• Positive Stenger (malingering): Patient does NOT respond - the tone at the "bad" ear is actually audible to them and, being the dominant signal, cancels out perception of the good-ear tone. Because the patient doesn't want to admit hearing in the bad ear, they choose silence - but silence proves the bad ear heard the louder tone

Positive Stenger = the patient heard the "bad" ear tone = feigned loss confirmed

3. Absolute Bone Conduction (ABC) Test / Schwabach Comparison

• Place a vibrating tuning fork on the mastoid of the examiner (who has known normal hearing)
• When the examiner can no longer hear it, immediately transfer it to the mastoid of the claimed "deaf" ear
• True deafness: Patient cannot hear it
• Malingering: Patient perceives the tone (because bone-conducted vibration still reaches a functioning cochlea), revealing the ear is not dead

4. Forehead/Vertex Weber Paradox

• In a malingerer claiming bilateral total deafness, the vibrating fork placed on the forehead/vertex should not be heard at all - but patients frequently instinctively respond, revealing intact bone conduction

5. Transcranial Bone Conduction (Dead Ear) Test

• If the patient truly has a dead ear, bone-conduction thresholds on the "dead" side should match the true bone-conduction threshold of the good ear (within 5-10 dB)
• If claimed bone-conduction loss on the bad side greatly exceeds the actual bone-conduction threshold of the good ear, pseudohypacusis is unmasked

Summary of Key Tests

Supporting (Non-Tuning Fork) Behavioral Clues to Malingering

• PTA-SRT discrepancy >10 dB (the two should agree within 5-10 dB) - one of the most common inconsistencies
• Poor test-retest reliability (>5 dB variation)
• Lombard test: Patient's voice gets louder when masking noise is played (proves they hear the noise)
• Delayed Auditory Feedback (DAF): Patient shows speech disturbances when hearing own voice with a delay, proving auditory self-monitoring
• Acoustic reflexes present with audiometric air-bone gaps that should have prevented them
• Good word recognition at claimed SRT level (should be impossible)

Objective Confirmation

• Otoacoustic Emissions (OAEs) - present = cochlear function is intact, regardless of claimed thresholds
• Auditory Brainstem Response (ABR) - objective threshold estimation not dependent on voluntary cooperation
• Acoustic reflexes (stapedial reflex) - present at levels below the claimed hearing threshold = functional loss

Horner Syndrome (Oculosympathetic Palsy)

Anatomy of the Sympathetic Pathway (3-Neuron Arc)

Clinical Features

• Inferior ptosis (upward displacement of the lower lid) - "reverse ptosis" from loss of inferior tarsal muscle - gives the false impression of enophthalmos
• Apparent enophthalmos - actually an illusion from narrowing of the palpebral fissure on both sides
• Dilation lag - the miotic Horner pupil dilates slowly when lights are dimmed; anisocoria is most obvious in the dark (distinguishes it from CN III palsy where anisocoria is worse in light)
• Hypochromic heterochromia iridis - lighter-coloured iris on the affected side; seen in congenital or long-standing cases (loss of sympathetic melanin stimulation)
• Pupillary light and near reflexes are preserved (parasympathetics are intact)
• Loss of ciliospinal reflex on the affected side (painful pinch of neck normally causes pupil dilation via sympathetics)

Clinical Photographs

Causes by Neuron Order

First-order (central) lesions

• Lateral medullary (Wallenberg) infarction - most classic
• Brainstem tumour or haemorrhage
• Demyelinating disease (multiple sclerosis)
• Syringomyelia / syringobulbia
• Cervical cord trauma or tumour
• Diabetic autonomic neuropathy

Second-order (preganglionic) lesions

• Pancoast tumour (apical lung carcinoma) - classic; associated with T1 pain, wasting of hand intrinsics
• Aortic or carotid aneurysm / dissection
• Thoracic spinal cord lesion
• Cervical rib
• Neck surgery (carotid endarterectomy, thyroidectomy, cervical lymph node dissection)
• Thyroid tumour, enlarged lymph nodes, brachial plexus trauma

Third-order (postganglionic) lesions

• Internal carotid artery dissection - acute painful Horner; urgent diagnosis (no anhidrosis because sudomotor fibres run with external carotid)
• Cavernous sinus thrombosis, tumour, or aneurysm
• Nasopharyngeal carcinoma
• Cluster headache (migrainous neuralgia) - transient Horner
• Otitis media / petrous apicitis
• Microvascular (most common isolated cause)

Painful Horner syndrome of acute onset = carotid dissection until proven otherwise

Pharmacological Testing

Step 1: Confirm Horner syndrome

• Cocaine blocks norepinephrine reuptake → dilates a normal pupil; Horner pupil does not dilate (depleted norepinephrine in denervated terminals). Anisocoria ≥0.8 mm after cocaine = diagnostic.
• Apraclonidine (weak alpha-agonist): normally no dilation effect, but causes reversal of anisocoria in Horner syndrome due to denervation hypersensitivity of the supersensitive dilator muscle. The Horner pupil dilates and may become larger than the fellow pupil; ptosis also improves. Now the preferred confirmatory test.

Step 2: Localise the lesion (pre- vs. postganglionic)

• Preganglionic (1st or 2nd order) lesion: postganglionic neurons are intact → still contain norepinephrine → hydroxyamphetamine causes dilation of the Horner pupil (normal response)
• Postganglionic (3rd order) lesion: terminal axons degenerate → norepinephrine depleted → hydroxyamphetamine fails to dilate the Horner pupil

Key Distinguishing Features: Horner vs. CN III Palsy

Workup

1. Acute painful Horner (neck/face pain) → immediate MRI/MRA to exclude carotid/vertebral dissection
2. Newly discovered Horner without clear cause → CT chest (Pancoast), neck/mediastinal imaging
3. Horner + ipsilateral CN involvement → cavernous sinus or skull base lesion
4. Horner + Wallenberg signs (dysphagia, ipsilateral facial numbness, contralateral limb sensory loss, vertigo, ataxia) → lateral medullary infarction; brain MRI
5. Isolated Horner, no pain → pharmacologic localisation; if postganglionic, less urgent; if preganglionic or central, full workup
6. Congenital Horner in neonates → birth trauma to cervical sympathetic chain; also consider neuroblastoma