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5 Pediatric Otology andCochlear Implants

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Further Reading

Huang BY, Zdanski C, Castillo M.Pediatric sensorineural hearing loss, Part 1: Practical aspects for

neuroradiologists. AJNR Am J Neuroradiol. 2012;33(2):211–7.

Mori T, Westerberg BD, Atashband S, Kozak FK.Natural history of hearing loss in children with

enlarged vestibular aqueduct syndrome. J Otolaryngol Head Neck Surg. 2008;37(1):112–8.

Gluth MB.Rhabdomyosarcoma and other pediatric temporal bone malignancies. Otolaryngol Clin

N Am. 2015;48(2):375–90.

Neff MJ, American Academy of Pediatrics; American Academy of Family Physicians. AAP, AAFP

release guideline on diagnosis and management of acute otitis media. Am Fam Physician. 2004;69(11):2713–5.

Rosenfeld RM, Culpepper L, Doyle KJ, etal. Clinical practice guideline: otitis media with effu-

sion. Otolaryngol Head Neck Surg. 2004;130(5 Suppl):S95–118.

Liming BJ, Carter J, Cheng A, Choo D, Curotta J, Carvalho D, Germiller JA, Hone S, Kenna

MA, Loundon N, Preciado D.International Pediatric Otolaryngology Group (IPOG) consensus recommendations: hearing loss in the pediatric patient. Int J Pediatr Otorhinolaryngol. 2016;90:251–8.

Anne S, Schwartz S, Ishman SL, Cohen M, Hopkins B.Medical versus surgical treatment of pedi-

atric acute mastoiditis: a systemic review. Laryngoscope. 2018;129:754–60.

Goderis J, De Leenheer E, Smets K, etal. Hearing loss and congenital CMV infection: a systemic

review. Pediatrics. 2014;134(5):972–82.

Papsin BC, Gordon KA.Cochlear implants for children with severe-to-profound hearing loss. N

Engl J Med. 2007;357(23):2380–7.

Yellon RF.Atresiaplasty versus BAHA for congenital aural atresia. Laryngoscope. 2011;121(1):2–3. Yiin RS, Tang PH, Tan TY.Review of congenital inner ear abnormalities on CT temporal bone. Br

J Radiol. 2011;84(1005):859–63.

Part II

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Rhinology/Allergy

Chapter 6

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Rhinology

KatiePhillips, KatherineFedder, andZaraM.Patel

Pearls

• Osteomas are the most common benign sinonasal lesion, with the frontal sinus the most common location.

• On sinus MRI, dried secretions show as hyperintense on T1 and hypointense on T2, and polyps show hypointense on T1 and hyperintense on T2.

• Rhinoscleroma is caused by Klebsiella rhinoscleromatis with histopathology showing Mikulicz cells (macrophages containing pathogen) and Russell bodies (plasma cells).

Anatomy

• Nasal framework

– Cartilages: Upper lateral, lower lateral, accessory sesamoid, quadrilat-

eral septal

– Bones: Nasal bones, vomer, perpendicular plate of the ethmoid, maxillary

crest, palatine bone, anterior nasal spine of maxilla

K. Phillips Otolaryngology Head and Neck Surgery, University of Cincinnati College of Medicine, Cincinnati, OH, USA e-mail: katie.phillips@uc.edu

K. Fedder Otolaryngology - Head and Neck Surgery, University of Virginia, Charlottesville, VA, USA e-mail: klf2e@virginia.edu

Z. M. Patel (*) Otolaryngology - Head and Neck Surgery, Stanford University School of Medicine, Palo Alto, CA, USA e-mail: zmpatel@stanford.edu

https://doi.org/10.1007/978-3-031-26048-3_6

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K. Phillips et al.

– Lateral nasal wall: inferior, middle, superior (sometimes supreme) turbinates

Inferior meatus (inferior to inferior turbinate): nasolacrimal duct opening (valve of Hasner). Middle meatus (lateral to middle turbinate): semilunar hiatus (2D structure) opens to ethmoid infundibulum (3D structure), which receives drainage from maxillary, anterior ethmoid, and frontal sinuses. Superior meatus (anteroinferior to superior turbinate): opening to posterior ethmoid sinuses. Sphenoethmoidal recess (posterosuperior to superior turbinate): opening to sphenoid sinuses.

• Blood supply

– External carotid system

Facial artery

• Angular artery (located in alar-facial groove): nasal sidewall, tip, and dorsum

• Superior labial artery: columella, lateral wall

Internal maxillary artery (divides into terminal branches in pterygopalatine fossa)

• Sphenopalatine artery (enters sphenopalatine foramen on lateral wall at junction of middle turbinate basal lamella and orbital wall)

• Lateral nasal artery: anterior portion of lateral nasal wall

• Posterior septal artery: courses over sphenoid face and supplies nasal septum

• Descending palatine artery (found in greater palatine canal and then enters the nasal cavity via incisive foramen): anterior nasal septum and nasal oor

– Internal carotid system

Ophthalmic artery terminates into anterior and posterior ethmoid arteries.

• Anterior ethmoid: Anterior and superior septum, lateral wall, and roof of nasal cavity

• Posterior ethmoid: Superior turbinate, posterior septum

– Nasal plexuses

Kiesselbach’s plexus (Little’s area): anteroinferior 1/3 of nasal septum; junction of sphenopalatine, greater palatine, anterior ethmoid, and superior labial arteries Woodruff’s plexus: posterior portion of inferior meatus and nasopharynx; junction of posterior nasal, sphenopalatine, and ascending pharyngeal veins

6 Rhinology

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– Venous drainage

Corresponds with the arterial supply. “Danger triangle” = area of skin from the corners of the mouth to the bridge of the nose. Veins draining this region are valveless, so skin infection can easily spread retrograde intracranially via angular vein → inferior ophthalmic vein → cavernous sinus.

• Lymphatics

– Anterior → facial nodes or upper cervical nodes – Posterior → retropharyngeal nodes

• Innervation

– Muscles of facial expression: CN VII – Sensory: branches of V1 and V2 for pain, temperature, and touch; CN I at roof

of nasal cavity for olfaction

– Parasympathetic (acetylcholine and VIP): superior salivatory nucleus of CN

VII → greater supercial petrosal nerve → vidian nerve → sphenopalatine ganglion (synapse) → terminates on blood vessels and glands of the nasal mucosa (induces vasodilation and secretion)

– Sympathetic (NE): superior cervical ganglion (synapse) → deep petrosal

nerve → vidian nerve → terminates on blood vessels and glands of the nasal mucosa (induces vasoconstriction)

• Paranasal sinuses

– Maxillary sinus

Two periods of growth: age 3 and ages 7–12, coincides with dental growth periods. Volume 15cm3, triangular space completely bound within bone of maxilla. Ostium drains into middle meatus; accessory ostia present up to 30% of the time. Separated from rst and second molars by thin layer of bone, can be dehiscent; dental infections can spread to the sinus via this route, and chronic infection or removal of these teeth can cause an oroantral stula.

– Ethmoid sinuses

Reach adult size by age 12, separated into anterior (2–8 cells)/posterior (1–5 cells) by basal lamella of middle turbinate, volume 15cm Bound by sphenoid face posteriorly, lamina papyracea laterally, middle and superior turbinates medially, and skull base superiorly Keros classication: can assist in determining risk of violating skull base during FESS

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K. Phillips et al.

• I: Cribriform plate 1–3mm inferior to fovea ethmoidalis

• II: 4–7mm inferior

• III: 8–16mm inferior

• Asymmetry at cribriform often most dangerous conguration

Lamellae of ethmoid sinus:

• Uncinate process (forms medial wall of ethmoid infundibulum)

• Ethmoid bulla (largest anterior ethmoid air cell)

• Basal lamella of middle turbinate (separates anterior from posterior ethmoid)

• Lamella of superior turbinate

Retrobullar recess=space posterior to ethmoid bulla if bulla not fused to basal lamella Suprabullar recess = space superior to ethmoid bulla if not fused to skull base Agger nasi= most anterior ethmoid air cell, pneumatization of lacrimal bone, can block frontal recess Supraorbital ethmoid cell = always posterolateral to true frontal sinus ostium, can be confused for frontal sinus septation Haller cell = infraorbital ethmoid cell pneumatizing into the maxillary sinus, can block maxillary sinus ostium and predispose to recurrent acute sinusitis Onodi cell=posterior ethmoid cell located superolateral to sphenoid sinus, may interface with or contain the internal carotid and optic nerve Osteomeatal complex vs. ethmoid infundibulum vs. semilunar hiatus

• Semilunar hiatus=2D gap between uncinate and ethmoid bulla

Infundibulum=3D space bounded by uncinate medially, lamina papyracea laterally, and frontal process of maxilla anterosuperiorly=route of drainage for maxillary, anterior ethmoid, and frontal sinuses

• Osteomeatal complex = includes middle turbinate, uncinate process, semilunar hiatus, ethmoid bulla, and infundibulum=functional drainage pathway for maxillary, anterior ethmoid, and frontal sinuses

– Frontal sinus

Pneumatized portion of frontal bone Drains through ostium into frontal recess (bounded by agger nasi anteriorly, ethmoid bulla posteriorly, lamina papyracea laterally, middle turbinate medially, skull base superiorly) Drainage pattern determined by attachment of uncinate process (UP)

• Attached to lamina papyracea (most common 60–70%) → drains medial to UP

• Attached to skull base (5–15%) or middle turbinate (10–20%) → drains lateral to UP

6 Rhinology

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Visible on X-rays by ages 2–6, continues growth into adolescence Types of frontal cells (Older Classication): Kuhn classication

• I: Single cell above the agger nasi

• II: Two or more cells above the agger nasi

• III: Single cell extending from the agger nasi superiorly into fron-

• IV: Cell isolated within frontal sinus

Types of frontal cells (newer classication): International Frontal Sinus Anatomy Classication (IFAC)

• Anterior cells (push the drainage pathway of frontal sinus medial, pos-

• Posterior cells (push the drainage pathway anteriorly): supra bulla cell,

• Medial cells (push the drainage pathway laterally): frontal septal cell

– Sphenoid sinus

Pneumatization from age 3 to 18 Landmarks: 30° angle relative to nasal oor, 1/3 distance superiorly from choana to skull base, 7cm from nasal sill, at the same latitude as the roof of the maxillary sinus Closely related to internal carotid, optic nerve, vidian canal, foramen rotundum, cavernous sinus; extremely variable intersinus septum (Fig.6.1)

tal sinus

teriorly or posteromedially): agger nasi cell, supra agger cell, and supraagger frontal cell

supra bulla frontal cell, supraorbital ethmoid cell

Fig. 6.1 Sphenoid sinus surrounded by critical structures (seen bilaterally, named from superior to inferior): optic nerve, carotid artery, V2, vidian nerve

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K. Phillips et al.

Physiology

• Histology

– Pseudostratied ciliated columnar epithelium covers majority of nasal cavity

except nasal vestibule (covered by stratied squamous epithelium)

Ciliated columnar cells (9+2 microtubules w/ dynein arms, beat 10–20×/ s), non-ciliated columnar cells (microvilli covering surface increase surface area for humidication and warming), basal cells, and goblet cells (produce mucin, which traps irritants)

• Mucin physiology

– Sol layer=deep lubricating layer, produced by microvilli – Gel layer=supercial viscous layer, produced by goblet cells, traps particles – Mucus ows → nasopharynx → secretions swallowed

• Olfactory epithelium

– Located along upper 1/3 of septum, medial superior/supreme turbinates, roof

of nasal cavity – Gets roughly 15% of nasal airow – Neural sensory contributions from CN I and small contribution from CN V – Pseudostratied columnar epithelium with multiple different cell types:

Bipolar olfactory neurons (develop from neuroblasts; have cilia that do not beat) Sustentacular cells (support cells, have microvilli, protective function) Bowman’s glands (produce secretions that bathe olfactory epithelium, required to dissolve odorants prior to nerve stimulation) Basal cells (differentiate into neurons or sustentacular cells)

• Hyposmia/anosmia: Can be caused by damage to nerve/bulb/tract/cortex itself, inammation of support cells and surrounding epithelium, or obstruction of airow, preventing odorants from reaching the nerve

– Most common causes are sinonasal disease with or without polyps or URI

with suspected viral attack on nerve or supporting cells (COVID-19 or others) causing inammation and dysfunction.

– Also consider trauma, tumors, iatrogenic surgical damage, chemical irritant

or medication-induced damage, endocrine or metabolic disorders (e.g., hypothyroidism), age-related loss of smell (presbyosmia), or early signs of neurologic disease (Alzheimer’s or Parkinson’s disease).

– Foster Kennedy Syndrome= unilateral anosmia, optic atrophy, and papill-

edema due to frontal lobe masses.

– Kallman’s syndrome=hypogonadotropic hypogonadism and anosmia (fail-

ure of hypothalamus to secrete GnRH, several types of inheritance including X-linked and autosomal dominant).

– Evaluation and management of hyposmia/anosmia:

6 Rhinology

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Full history and physical examination including neurologic exam and rigid nasal endoscopy to identify any obvious possible underlying causes. Treat patients medically with course of oral steroids, nasal steroid spray, and nasal saline irrigations, and then reevaluate in clinic to assess symptoms. High volume steroid irrigations and olfactory training are mainstays of therapy, with high dose omega-3 used for post-endoscopic skull base surgery patients and platelet-rich plasma (PRP) a new option for treating COVID-19 related loss Consider MRI for persistent symptoms to rule out masses/tumors. UPSIT (University of Pennsylvania Smell Identication Test) or Snifn’ Sticks can be used as objective measures to identify malingering (score <10/40), for workman’s compensation documentation, and for research purposes.

• Evaluation of the nasal airway

– Main functions: humidication, warming, ltration, olfaction, alteration of

airway resistance

– Nasal air ow=accounts for 50% of total airway resistance

Internal nasal valve=most narrow part of nasal airway; bounded by nasal septum, upper lateral cartilage, head of inferior turbinate, and nasal oor Evaluated by Cottle maneuver (subjective improvement in nasal breathing with lateral distraction of the ipsilateral cheek indicates internal valve collapse) Nasal cycle=physiologic variation in vascular ow and sympathetic tone of nasal airway, engorgement of nasal tissue which alternates from one side to the other every 2–6h

– Objective measures of nasal airway resistance (commonly used only in

research)

Rhinomanometry = placement of sensors in the nose or nasopharynx, which calculate pressure generated by nasal airow through the nose before and after nasal decongestant is administered; cannot localize site of obstruction, used in research only

• 35% decrease in airway resistance=mucosal congestion

• <35% decrease in airway resistance=structural abnormality

Acoustic rhinometry=uses sound waves to measure the cross-sectional area at points along the nasal airway; can identify narrow points in airway but unable to determine whether these narrow areas have any effect on nasal airow

Imaging

• Air-uid level=purulent secretions or blood after trauma or surgery (Fig.6.2).

• Dried secretions=hyperintense on T1, hypointense on T2.

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Fig. 6.2 Air-uid level seen in left maxillary sinus, indicating purulent secretion (and not blood) in this case, as there is no history or sign of trauma

Fig. 6.3 Typical AFS imaging showing heterogeneous opacication of the sinuses and hypertelorism (sh eye effect) as the sinus cavity expands outward, displacing the orbits laterally, to accommodate accumulating polyps and fungal mucin

K. Phillips et al.

• Polyps=hypointense on T1, hyperintense on T2.

• Mycetoma (fungal ball) shows bony thickening of sinus walls and heterogeneous opacication with calcications on CT; iso- or hypointense on T1, while T2 shows marked central hypointensity with surrounding inamed mucosa, which is hyperintense.

• Allergic fungal sinusitis CT ndings include a rim of low density within sinus with central mucin, calcications, and bony expansion/erosion (Fig.6.3).

• Odontogenic sinusitis CT ndings include unilateral opacication of maxillary sinus+/−ethmoids and frontal sinus with dental ndings, classically a periapical abscess (Fig.6.4).

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