Sequence of Ossicular Erosion by Cholesteatoma

Classic Sequence

Mnemonic: "I Love Seeing My Students" - Incus (LPI) -> Lenticular process -> (incus body) -> Stapes superstructure -> Malleus -> Stapes footplate

Why the Incus First?

• The long process of the incus has a single terminal nutrient artery (unlike the malleus, which has a rich blood supply from the mucoperiosteum)
• It lies in direct contact with epitympanic cholesteatoma expanding in Prussak's space
• It is the most exposed ossicle and least protected by surrounding structures

Epidemiological Data (Scott-Brown's, Table 85.1 - 1211 consecutive chronic middle ear cases)

Pars Flaccida vs Pars Tensa Cholesteatoma - Differences

• Pars flaccida (attic/epitympanic) cholesteatoma: keratin accumulates in Prussak's space, displaces ossicles medially, erodes scutum. Causes early erosion of the long process of incus.
• Pars tensa (posterosuperior marginal) cholesteatoma: lies medial to the ossicular chain (displaces ossicles laterally), causes early erosion of LPI and stapes superstructure, and tends to cause more erosion of inner ear structures.

Key Points for Exams

1. Most commonly eroded ossicle: Incus (long process) - due to end-arterial blood supply
2. Most commonly preserved ossicle: Malleus handle
3. Stapes footplate is the most resistant structure to erosion
4. Despite severe ossicular erosion, hearing is often preserved until late stage because the cholesteatoma itself can conduct sound (contact between tympanic membrane and stapes footplate via the cholesteatoma mass = "pseudo-ossiculoplasty")
5. On CT imaging: erosion of scutum + incus is characteristic; stapes erosion prompts concern for labyrinthine fistula

Jaundice and Its Clinical Relevance to ENT Disease

1. Jaundice causing ENT disease
2. ENT/Head-neck disease causing jaundice
3. Jaundice as part of a systemic disease with ENT manifestations
4. Jaundice as a preoperative/perioperative concern in ENT surgery

1. Neonatal Jaundice Causing Sensorineural Hearing Loss (Most Important ENT Link)

• Unconjugated (indirect) bilirubin is lipid-soluble and crosses the blood-brain barrier
• It preferentially deposits in the cochlear nuclei, inferior colliculus, and auditory brainstem (these nuclei are particularly vulnerable due to their high metabolic activity)
• This leads to auditory neuropathy spectrum disorder (ANSD) - the inner hair cells may be spared but the spiral ganglion cells and auditory nerve fibers are damaged
• In severe cases, kernicterus (bilirubin encephalopathy) causes permanent neurological damage including SNHL

• Sensorineural hearing loss (SNHL) - typically bilateral
• Abnormal or absent Auditory Brainstem Response (ABR) with preserved otoacoustic emissions (OAEs) - classic ANSD pattern
• Associated with: cerebral palsy, upward gaze palsy, choreoathetosis (the tetrad of kernicterus)

• Bilirubin levels even 12-15 mg/dL can cause hearing loss when associated with other risk factors
• Risk significantly elevated when bilirubin is ≥10 mg/dL above exchange transfusion threshold, or absolute level ≥35 mg/dL
• Premature infants are more susceptible at lower bilirubin levels

• Neonatal hyperbilirubinemia is a JCIH (Joint Committee on Infant Hearing) high-risk indicator for hearing loss - mandates audiological follow-up even if newborn hearing screen is passed
• OAE + ABR must both be performed; OAE alone may be falsely reassuring in ANSD

2. ENT/Head-Neck Conditions Causing Jaundice

• Advanced head and neck cancers (nasopharynx, thyroid, salivary gland) can metastasize to the liver, causing hepatic jaundice
• Lymphoma (including Waldeyer's ring lymphoma, cervical lymphadenopathy) can compress the bile duct or involve the liver directly causing obstructive or hepatocellular jaundice
• Lymph node enlargement at the porta hepatis from metastatic cervical/pharyngeal malignancy can cause obstructive jaundice

• Severe parapharyngeal/retropharyngeal abscess or Ludwig's angina with septicemia can cause sepsis-related hepatic dysfunction and jaundice (part of multiorgan failure)
• Lemierre's syndrome (internal jugular vein thrombophlebitis from oropharyngeal infection, usually Fusobacterium necrophorum) can cause septic emboli to the liver, producing jaundice

3. Systemic Diseases with Both Jaundice and ENT Manifestations

Congenital TORCH infections are a key shared link - they present with neonatal jaundice AND cause permanent SNHL.

4. Perioperative Relevance in ENT Surgery

• Obstructive jaundice (due to any cause) indicates coagulopathy risk - vitamin K-dependent clotting factors (II, VII, IX, X) are reduced due to poor fat absorption and hepatic dysfunction
• This is relevant before any ENT surgery involving significant vascularity: total thyroidectomy, neck dissection, parotidectomy, tonsillectomy
• Halothane hepatitis (now rare) was a historic concern with older anaesthetic agents used in ENT procedures; modern agents (sevoflurane, desflurane) carry minimal hepatotoxic risk

5. Jaundice as a Sign in the ENT Physical Examination

• Scleral icterus (yellowing of the sclera) is examined as part of a full head and neck examination
• May be the first sign of occult malignancy (e.g., liver metastases from an unknown primary in the head and neck)
• In a patient presenting with cervical lymphadenopathy + jaundice, lymphoma or metastatic disease must be urgently excluded

Summary Table