EAR , NOSE AND THROAT :

The frontal sinuses are absent at birth and progressively pneumatize from age 2 through puberty.

Tonsil stones (tonsilloliths)—commonly occurring concretions of food, cellular, and bacterial

debris—are not known to be risk factors for oropharyngeal SCC and can be managed with gentle
removal (eg, gargling with salt water). However, frequent patient manipulation (eg, with
toothpicks) can cause mucosal trauma, which may be mistaken as an ulcerated neoplasm.

A tonsil ulcer in a smoker is likely due to squamous cell carcinoma.

Loop diuretics can cause hearing loss that may be either temporary or permanent. Ototoxicity is
more common in patients taking high doses of loop diuretics, those with coexistent renal failure,
or those also being treated with other known ototoxic medications (eg, aminoglycosides). In
addition to hearing loss, patients can also have tinnitus or balance difficulties
 Retropharyngeal abscess presents with neck pain, odynophagia, and fever following penetrating
trauma to the posterior pharynx. Infection within the retropharyngeal space drains inferiorly to
the superior mediastinum. Spread to the carotid sheath can cause thrombosis of the internal
jugular vein and deficits in cranial nerves IX, X, XI, and XII. Extension through the alar fascia
into the "danger space" (between the alar and prevertebral fasciae) can rapidly transmit infection
into the posterior mediastinum to the level of the diaphragm. Acute necrotizing mediastinitis
is a life-threatening complication characterized by fever, chest pain, dyspnea, and odynophagia,
and requires urgent surgical intervention.

Cholesteatoma, a benign growth of the squamous epithelium with accumulation of keratin

debris within the middle ear. In children, cholesteatomas can either be congenital or acquired,
with congenital lesions typically found in patients around age 5. Acquired cholesteatomas
(which are more common) usually occur due to chronic middle ear disease. The diagnosis
should be suspected in any patient with continued ear drainage for several weeks despite
appropriate antibiotic therapy.

Chronic middle ear disease leads to the formation of a retraction pocket in the tympanic
membrane, which can fill with granulation tissue and skin debris, leading to chronic otorrhea.
Complications of cholesteatomas include hearing loss, cranial nerve palsies, vertigo, and
potentially life-threatening infections (eg, brain abscesses, meningitis). This patient should be
referred to an otolaryngologist for a dedicated otologic examination, possibly accompanied by a
CT and/or surgical visualization to confirm the diagnosis.

Relapsing polychondritis is an inflammatory condition that can affect any cartilage in the body
but most commonly affects the cartilaginous portions of the ear (the ear lobule is unaffected
because it has no cartilaginous structure). The ear canal is less often affected than the pinna;
drainage and itching would be uncommon.

Although the paranasal sinuses are not fully developed in children, the ethmoid and maxillary
sinuses are present at birth and rapidly expand in the first few years of life.

After evaluation to ensure there are no concurrent life-threatening injuries, avulsed permanent
teeth should be reimplanted. Ideally, this should be done within 15 minutes to 1 hour to increase
the likelihood of tooth survival. Until reimplantation takes place, the avulsed tooth can be stored
in cold milk, saliva, or tooth culture media (eg, Hank's balanced salt solution).
Prior to reimplantation, dental block can be performed to minimize pain. The tooth and socket
should be rinsed gently with normal saline or tap water. Sterilizing agents (eg, hydrogen
peroxide) or forceful scrubbing should be avoided to prevent damage to the tooth and/or socket.
The tooth should be handled by the crown, placed in the socket, and splinted to the adjacent
teeth. Patients are discharged with prophylactic antibiotics (eg, doxycycline) and advised to
follow-up with a dentist as soon as possible for definitive care.
NORMAL STRUCTURE AND
FUNCTION :
Choanal atresia
Clinical  Unilateral (most common)
findings o Chronic nasal discharge
o Symptomatic during childhood
 Bilateral
o Cyanosis that worsens with feeding & improves with crying
o Noisy breathing (stertor)
o Symptomatic shortly after birth
 May be associated with CHARGE syndrome

Diagnosis  Inability to pass catheter past nasopharynx

 Confirmation with CT scan or nasal endoscopy

Treatment  The first step in management consists of placing an oral airway and
orogastric tube feeding. Definitive treatment is surgical repair.

CHARGE = Coloboma, Heart defects, Atresia choanae, growth Retardation, Genital and
Ear abnormalities.
 Epiglottitis
Microbiology  Haemophilus influenzae type b (Hib)

Clinical  Distress (tripod position, sniffing position, stridor)

features  Dysphagia, dysphonia
 Drooling
 High fever

X-ray  "Thumb sign" (enlarged epiglottis)

Management  Endotracheal intubation

 Antibiotics

Prevention  Immunization against Hib

Signs of impending airway obstruction include anxiety and tripod positioning (ie,
upright/forward positioning with neck hyperextension)

Infectious epiglottitis
Epidemiology  Streptococcus pneumoniae, Haemophilus influenzae
 Risk reduced with H influenzae vaccination

Clinical  Rapidly progressive & life-threatening

 Fever, sore throat, drooling, muffled voice
 Airway obstruction (stridor, dyspnea)
 Pooled oropharynx secretions
 Laryngotracheal tenderness

Diagnosis  Direct visualization

 Imaging (lateral neck x-ray)

Treatment  Early artificial airway (if needed)

 Intravenous antibiotics (ceftriaxone plus vancomycin)
X-ray is not required for diagnosis if clinical suspicion is high, but lateral view shows an
enlarged epiglottis, suggestive of edema. Diagnosis is confirmed via direct visualization of an
edematous epiglottis. However, detailed oropharyngeal examination is often deferred in children
due to risk of laryngospasm from provoked aggravation. Direct laryngoscopy during intubation
(a controlled setting to secure the airway) is often preferred for diagnosis and management.

H influenzae, Streptococcus species (S pneumoniae, S pyogenes), and Staphylococcus aureus,

has increased.

Symptoms include the rapid onset of respiratory distress (eg, stridor, retractions), dysphagia, and
drooling due to impending airway occlusion from the swelling epiglottis. Therefore, the first
step in management of epiglottitis is to secure the airway, usually via endotracheal intubation.
Once the airway is secured, broad-spectrum antibiotic therapy with ceftriaxone (targeting H
influenzae and Streptococcus species) and vancomycin (targeting S aureus, including
methicillin-resistant strains) should be initiated promptly.

Patients with epiglottitis who develop rapid-onset respiratory failure (eg, tripod position,
hypoxia, drooling, tachypnea) require urgent airway management. This includes bag-valve-mask
ventilation with 100% oxygen followed by endotracheal intubation with advanced equipment
(eg, video laryngoscope). A single failed attempt at video-assisted endotracheal intubation
should prompt surgical cricothyrotomy, which bypasses the epiglottal swelling and potential
obstruction. If intubation without a video laryngoscope fails, intubation with a video
laryngoscope could be attempted.

Retropharyngeal abscess presents with fever, dysphagia, drooling, stridor, and a stiff neck in
young children. Examination reveals swelling of the posterior pharyngeal wall and x-ray shows
widening of the retropharyngeal space.
 Auricular hematoma
Risk  Contact sports injury (eg, wrestling, martial arts)

factors
Clinical  Accumulation between pericordium and cartilage.
features  Tender, fluctuant blood collection on anterior pinna

Treatment  Immediate incision & drainage

 Pressure dressing to compress the perichondrium
to the auricular cartilage to restore nutrient
diffusion to the cartilage.
 And oral antibiotics covering P. aurgeinosa then
follow up up to 3-5 days.

Complication  Cauliflower ear (fibrocartilage overgrowth)

s  Bacterial superinfection
 Reaccumulation of hematoma
 Avascular necrosis of the outer ear cartilage
 CNS INFECTIONS :
Herpes simplex virus (HSV) encephalitis mainly affects the temporal lobe of the brain and may
present acutely (<1 week duration) with focal neurological findings. The characteristic
cerebrospinal fluid findings are lymphocytic pleocytosis, an increased number of erythrocytes,
and elevated protein. HSV polymerase chain reaction analysis of CSF is the gold standard for
diagnosis. IV acyclovir. Fever and behavioral chainges, focal neurological findings (altered
mentation, focal cranial nerve deficits, ataxia, hyperreflexia, or focal seizures).
 Mastoiditis
Pathophysiology  Infection of the mastoid air cells
 Complication of acute otitis media
 Most commonly due to Streptococcus pneumoniae

Clinical findings  Fever & otalgia

 Inflammation of mastoid
 Protrusion of the auricle
 Opacification of mastoid air cells on CT scan with contrast or MRI

Management  Intravenous antibiotics

 Drainage of purulent material (eg, tympanostomy, mastoidectomy)

Complications  Extracranial extension (subperiosteal abscess, facial nerve palsy,

hearing loss, labyrinthitis)
 Intracranial extension (brain abscess, meningitis)

Protein is elevated in menengitits due to damage to BBB and RBCs is only in viral encephalitis
not menengitis due to temporal lobe hemorrhage.
BRAIN ABCESS :
 Brain abscess
Microbiology  Staphylococcus aureus
 Viridans streptococci
 Anaerobes

Pathogenesis  Direct spread (eg, otitis media, mastoiditis, sinusitis)

 Hematogenous spread (eg, endocarditis)

Clinical findings  Headache, vomiting

 Fever
 Focal neurologic deficits, seizure
 Ring-enhancing lesion on neuroimaging (CT, MRI)
 Treatment  Aspiration/surgical drainage
 Prolonged antibiotic therapy

Brain imaging (CT scan, MRI) typically reveals cerebritis initially, but within 1-2 weeks the
infection consolidates to a ring-enhancing lesion with central necrosis. Diagnosis requires CT-
guided aspiration or surgical biopsy to obtain tissue for Gram stain and culture (bacterial, fungal,
mycobacterial). Most patients are treated with empiric, intravenous antibiotics (eg,
metronidazole, ceftriaxone, and vancomycin) and aspiration of the lesion.

INFECTIONS :
Fusobacterium necrophorum causes Lemierre syndrome, a life-threatening, deep neck space
infection that progresses to suppurative thrombophlebitis of the internal jugular vein. Although
it presents with painful pharyngitis and odynophagia, it also has a more acute (<1 week) and
toxic presentation with high fevers (>39 C [102 F]), rigors, and respiratory distress from
associated septic pulmonary emboli.

Chronic suppurative otitis media

Microbiology  Often polymicrobial
 Staphylococcus aureus & Pseudomonas aeruginosa
 Fungi (eg, Aspergillus)
 Risk factors: AOM, Cholestotoma

Symptoms  Chronic (>6 wk), purulent otorrhea

 Hearing loss
 Absence of ear pain

Examination  Tympanic membrane perforation

 Otorrhea within normal-appearing external auditory canal

Treatment  Ototopical fluoroquinolone drops (eg, ofloxacin)

Complication  Infectious spread (eg, mastoiditis, meningitis, intracranial abscess)

s  Permanent hearing loss
CSOM does not typically respond to oral antibiotics, as seen in this patient, because the middle
ear is poorly vascularized due to chronic inflammation and scarring. Of note, cholesteatoma can
also cause chronic ear drainage, as seen in this patient's history, and should be considered when
the condition does not respond to topical therapy for presumed CSOM.
 PAROTIDS :
Suppurative parotitis
Risk factors  Elderly, dehydrated, postsurgical
 Decreased oral intake (eg, NPO perioperatively)
 Medications (eg, anticholinergics)
 Obstruction (eg, calculi, neoplasm)

Clinical  Firm, erythematous pre/postauricular swelling

presentation  Exquisite tenderness exacerbated by chewing and palpation
 Trismus, systemic findings (eg, fever, chills)
 Elevated serum amylase without pancreatitis

Management  Ultrasound or CT scan (eg, ductal obstruction, abscess)

 Hydration, oral hygiene
 Antibiotics
 Massage (ie, milking pus out of gland)
 Sialagogues

Retrograde seeding of bacteria from the oral cavity (eg, Staphylococcus aureus, oral flora)
through Stenson's duct to the parotid gland.

Nontender, bilateral enlargement of the parotid glands, which is consistent with sialadenosis.
Sialadenosis is a benign, noninflammatory swelling of the salivary glands. It can result from
overaccumulation of secretory granules in acinar cells (possibly due to abnormal autonomic
innervation) in patients with chronic alcohol use, bulimia, or malnutrition. It can also result
from fatty infiltration of the glands in patients with diabetes mellitus or liver disease.
Can incade facial nerve(drop) or trigeminal(numbness). CT or MRI and U/S for FNA
 CONGENITAL :
Pediatric neck masses
Thyroglossal duct cyst Midline  Tract between foramen cecum & base of
anterior neck
 Cystic, moves with swallowing or tongue
protrusion
 Often presents after upper respiratory tract
infection

Dermoid cyst Midline  Cystic mass with trapped epithelial debris

 Occurs along embryologic fusion planes
 No displacement with tongue protrusion

Branchial cleft cyst Lateral  Tract may extend to the tonsillar fossa (2nd
branchial arch) or pyriform recess (3rd branchial
arch)
 Anterior to the sternocleidomastoid muscle

Reactive adenopathy Lateral  Firm, often tender

 Multiple nodules

Mycobacterium avium Lateral  Necrotic lymph node

lymphadenitis  Violaceous discoloration of skin
 Frequent fistula formation

Cystic hygroma Posterio  Dilated lymphatic vessels

r

Abnormalities most often arise from the second branchial arch, which forms structures in the
face and upper neck. Therefore, BCCs are most often located between the internal and external
carotid arteries, anterior to the sternocleidomastoid muscle and inferior to the mandible.
Surgical resection of the entire cyst and any associated fibrous tract remnants is curative.
 Thyroglossal duct cyst
 Forms along path of thyroid descent
Embryology  Foramen cecum (base of tongue) to base of anterior neck

 Midline cystic neck mass

 Moves superiorly with swallowing or tongue protrusion
Clinical  Often present after upper respiratory tract infection (secondary
presentation infection)
 Associated with ectopic thyroid tissue

 Confirm presence of normal thyroid tissue

 Surgical resection of cyst, associated tract & central portion of
Management
hyoid bone

Due to the risk of recurrent infection, a TDC should be surgically removed. Because a TDC is
associated with ectopic thyroid tissue and may be the only source of functioning thyroid tissue,
thyroid imaging is required preoperatively.
Infected BCC
A laryngocele is an outpouching of the laryngeal mucosa that can be congenital or acquired. If it
protrudes through the thyrohyoid membrane, it can present as a lateral neck mass. It
characteristically enlarges with Valsalva maneuver due to inflation with air. Acquired
laryngoceles are classically seen in glassblowers or trumpet players due to repeated, intense
oropharyngeal pressure.
 Laryngomalacia
 Collapse of supraglottic tissues on inspiration
Pathophysiology
 Inspiratory stridor that worsens when supine
Clinical
 Peak at age 4-8 months
presentation
 Flexible fiberoptic Laryngoscopy (eg, omega-shaped [Ω] epiglottis)
Diagnosis
 Reassurance with close follow-up (± concurrent GER
treatment) for most cases
Management  Supraglottoplasty for severe symptoms, to remove redundant
supraglottic tissues.

GER = gastroesophageal reflux.

Stridor from laryngomalacia usually begins in the neonatal period and is loudest at age 4-8
months. Most patients also have symptomatic gastroesophageal reflux (eg, vomiting, arching of
the back with feeds). Antireflux treatment often improves breathing symptoms (for unclear
reasons). Infants who are feeding and growing well may be watched expectantly as
laryngomalacia typically resolves spontaneously by age 18 months. Surgery may be needed for
moderate to severe cases with respiratory distress, cyanosis, or failure to thrive.Most common
cause of stridors in infants. Although the etiology of this congenital condition is not precisely
understood, Proposed pathophysiologic etiologies include laryngeal hypotonia (due to delayed
maturation or neuromuscular disorder), redundant supraglottic soft tissue, and inflammation (due
to reflux).Patients typically have an omega-shaped (Ω) epiglottis, short aryepiglottic folds, and
characteristic inspiratory collapse of the supraglottic tissues (eg, epiglottis, arytenoids),
leading to partial obstruction of the airway and thus inspiratory stridor. subglottic narrowing (eg,
subglottic stenosis) often lead to biphasic stridor.
Rarely, obstruction of the sublingual salivary gland duct can lead to pseudocyst (ranula). If it is

This patient has a chronic mass on his hard palate consistent with torus palatinus (TP), a benign
bony growth (ie, exostosis) located at the midline suture of the hard palate. It is thought to be
caused by both genetic and environmental factors and is more common in women and Asian
individuals. TP can be congenital or develop later in life. Similar lesions at the lingual surface
of the mandible are termed "tori mandibulari."

TPs are usually <2 cm in size but can gradually enlarge over time. They are typically
asymptomatic and are frequently ignored by the patient but noted by clinicians (or family
members) when examining the mouth for unrelated reasons. However, the thin epithelium
overlying the bony growth may ulcerate with minor trauma of the oral cavity and heal slowly due
to poor vascular supply. The diagnosis is usually obvious on clinical grounds. Surgery is
indicated for patients in whom the mass becomes symptomatic, interferes with speech or eating,
or causes problems with the fitting of dentures later in life.
 WEBER AND RINNE :
Interpretation of Rinne & Weber tests
Rinne result Weber result
Normal AC > BC in both ears Midline
Conductive hearing BC > AC in affected ear, AC > Lateralizes to affected ear
loss BC in unaffected ear
Sensorineural AC > BC in both ears Lateralizes to unaffected ear,
hearing loss away from affected ear
Mixed hearing loss BC > AC in affected ear, AC > Lateralizes to unaffected ear,
BC in unaffected ear away from affected ear
AC = air conduction; BC = bone conduction.
 Otosclerosis
Epidemiology  Younger (early to mid-30s) Caucasian patients
 More common in women
 Autosomal dominant with incomplete penetrance

Pathophysiology  Imbalance of bone resorption & deposition → stiffening of stapes

Clinical  Progressive conductive hearing loss

manifestations  Paradoxical improvement in speech (paracusis of Willis), possibly
because CHL dampens the competing background noise, thereby
allowing speech to be heard more clearly. discrimination in noisy
environments
 ± Reddish hue behind tympanic membrane; excessive bony
resorption can expose underlying blood vessels.

Management  Amplification (eg, hearing aids)

 Surgery (eg, stapes reconstruction)

Tympanosclerosis (scarring of the tympanic membrane) can cause stiffening that may lead to
conductive hearing loss in severe cases. However, patients typically have a history of otitis
media (typically chronic) or previous tympanostomy tubes. Chalky, white patches are often seen
on the tympanic membrane.

Presbyucusis: High frequency SNHL (eg. Women, children), Tinnuitus, Speech

discimination(may be due to cortical atrophy), so they better hear in quite rooms, cochlear hair
cell loss.

Barotrauma to the ear occurs most commonly after flying and can result in injury (eg, ear pain,
hearing loss) to the tympanic membrane (TM). Most barotraumatic TM injuries heal
spontaneously within a few weeks.

THE NOSE :
 Nasal foreign body
 Inorganic substance: asymptomatic, mild pain/discomfort
Clinical  Organic substance: unilateral, foul-smelling, purulent discharge
manifestations  Button battery: epistaxis, purulent discharge

 Positive pressure (eg, patient exhalation with unaffected nares

occluded)
Treatment
 Mechanical extraction

 Infection (eg, sinusitis)

 Local irritation
 Aspiration into airway
Complications
 Nasal septal perforation (with button battery or multiple magnet
insertion)
Although the incidence is rare, the complications of an untreated septal hematoma are
significant. Infection can develop rapidly (2-3 days) and lead to a septal abscess. In addition,
because the septal cartilage has no direct blood supply and receives all nutrients via diffusion
from the perichondrium, a septal hematoma can cause avascular necrosis of the septal cartilage.
Destruction of the nasal septal cartilage can result in septal perforations, external nasal
deformities (eg, saddle nose), or internal nasal valve collapse (ie, nasal obstruction).

Therefore, all patients who sustain nasal trauma undergo examination of the nasal septum.
Palpation can differentiate between a deviated nasal septum (firm) and a septal hematoma (soft,
fluctuant). Patients with a septal hematoma require prompt incision and drainage. After
incision and drainage, anterior nasal packing should be placed to compress the perichondrium to
the nasal septum; ice packs and NSAIDs can reduce edema due to inflammation. Patients are
treated with antibiotics and require otolaryngology evaluation after a few days for packing
removal and assessment.

Nasopharyngeal carcinoma
 Endemic to Asia
 Linked with Epstein-Barr virus reactivation
Epidemiology
 Risk factors: Diet (salty fish), smoking, genetics

 Obstruction: Nasal congestion, epistaxis, headache

 Facial numbness (para-cavernous sinus tumor invasion)
 Mass effect: Cranial nerve palsy, serous otitis media due to (eustachian
Manifestations
tube obstruction)
 Spread: Neck mass (cervical lymphadenopathy)

 Endoscope-guided biopsy
Diagnosis
 Radiation therapy
 Chemotherapy
Treatment  Survival is excellent if the neoplasm is discovered early, but most
patients present with advanced disease.

Cerebrospinal fluid rhinorrhea

 Accidental trauma (most common)
 Surgical trauma (eg, sinus surgery)
Etiology
 Nontraumatic (eg, elevated intracranial pressure)

 Unilateral watery rhinorrhea with salty or metallic taste

Clinical
 Possible complication: meningitis
presentation
 Test for CSF-specific proteins (β-2 transferrin, β-trace
protein)
Evaluation  Imaging (with intrathecal contrast)
 Endoscopy (± intrathecal fluorescein dye)

 Bed rest, head of bed elevation, avoidance of straining

 Lumbar drain placement
Management
 Surgical repair

CSF = cerebral spinal fluid.

Testing the nasal discharge for CSF-specific proteins (eg, beta-2 transferrin, beta-trace protein) is
diagnostic. Imaging or endoscopic nasal examination can be used to localize the precise site of
the defect. Patients typically require inpatient management for bed rest, head-of-bed
elevation, and frequent neurologic evaluation because they are at risk for meningitis due to nasal
flora contamination of the CSF. If the CSF rhinorrhea does not resolve with these measures,
further interventions (eg, lumbar drain, operative repair) are necessary.

Complications are common following rhinoplasty, and up to one in four rhinoplasties may
need revision. Common complications include patient dissatisfaction, nasal obstruction and
epistaxis. Also, septal perforation. The typical postoperative presentation is a whistling noise
heard during respiration. Following nasal surgery, septal perforation is typically the result of a
septal hematoma though a septal abscess may also be the cause. Additional conditions that can
cause septal perforation are self-inflicted trauma (nose picking), syphilis, tuberculosis, intranasal
cocaine use, sarcoidosis and granulomatosis with polyangiitis (Wegener's).

Nasal furunculosis results from staphylococcal folliculitis following nose picking or nasal hair
plucking. It is potentially life threatening as it can spread to the cavernous sinus. Patients
complain of pain, tenderness and erythema in the nasal vestibule.

VOCAL CORDS :
Constant or progressive hoarseness is often related to a vocal cord lesion and should be evaluated
by laryngoscopy. Laryngeal papillomas are caused by human papillomavirus (HPV) subtypes
6 and 11, which are also the subtypes most likely to cause genital warts (condyloma
acuminatum), and therefore most likely acquired via vertical transmission prior to delivery
(because neither vaginal nor cesarean delivery prevent transmission) in toddlers.

OTITIS EXTERNA :
Otitis externa
Risk factors  Water exposure
  Trauma (eg, cotton swabs, ear candling)
 Foreign material (eg, hearing aid, headphones)
 Dermatologic conditions (eg, eczema, contact dermatitis)

Microbiology  Pseudomonas aeruginosa

 Staphylococcus aureus(covered by antipseudomonal
antibiotics.)

Clinical  Otalgia, pruritis, discharge, hearing loss

manifestations  Pain with auricle manipulation
 Ear canal erythema, edema, debris
 Tympanic membrane spared (clear, not inflamed, no middle ear
fluid)

Treatment  Topical antibiotic (eg, fluoroquinolone) ± topical glucocorticoid

 Consider wick placement to facilitate medication delivery

More common in children and adolescents.

Otitis externa occurs frequently after swimming in outdoor water sources due to alteration of
the ear canal pH, maceration of the skin, and introduction of bacteria into the ear canal, loss of
cerumen. Cerumen is acidic and has antibacterial properties; loss of cerumen due to swimming
or excessive ear cleaning increases the risk of otitis externa.
 Necrotizing (malignant) otitis externa
Risk factors  Age >60
 Diabetes mellitus
 Aural irrigation (cerumen removal)

Microbiology  Pseudomonas aeruginosa

Clinical  Severe, unremitting ear pain (worse at night &

manifestation with chewing)
s  Deficits of lower cranial nerves (eg, facial
[CN VII], vagus [CN X], accessory [CN XI])
 Granulation tissue in the external auditory canal
 Elevated erythrocyte sedimentation rate

Treatment  Intravenous antipseudomonal antibiotics (eg,

ciprofloxacin)
 ± Surgical debridement

Spread of the infection from the EAC can affect surrounding structures, including cranial
nerves. This patient's facial drooping and resultant drooling reflects damage to cranial nerve
VII (CN VII). Progression can also lead to temporomandibular joint involvement, meningitis,
brain abscess, and death. NOE is most often caused by Pseudomonas aeruginosa, which has
pro-inflammatory adhesins (leading to granulation tissue formation) and secretes tissue-
degrading proteases (leading to infection spread). Mortality rate was >50% prior to the
introduction of antipseudomonal antibiotics (eg, ciprofloxacin). As with other cases of
osteomyelitis, a prolonged antibiotic course (eg, 6-8 weeks) is required.Intravenous
ciprofloxacin is the drug of choice, even with the increased risk of tendon rupture in elderly
patients. Surgical debridement (of necrotic bone) is reserved for patients not responding to
medical therapy. Surgical excision, common before the advent of antipseudomonal antibiotics,
is no longer used.

Fungal otitis (otomycosis) occurs most commonly after treatment for acute otitis externa. It is
more common in individuals with chronically moist ear canals (eg, those with hearing aids,
especially in warm, humid climates). Examination of the EAC shows whitish fungal debris with
fruiting bodies or spores. Management is debridement and topical (eg, clotrimazole), rather than
oral (eg, fluconazole), antifungal therapy. Nystatin is not typically used for fungal otitis.
 OTITIS MEDIA :

Acute otitis media

Microbiolog  Streptococcus pneumoniae
y  Nontypeable Haemophilus influenzae
 Moraxella catarrhalis

Risk factors  Age (6-18 months), because the

eustachian tubes are straight and narrow
and drain poorly in young children
 Lack of breastfeeding
 Day care attendance
 Smoke exposure
 Previous URI

Clinical  Bulging TM
features  Middle ear effusion plus TM inflammation
(eg, fever, otalgia, erythema)

Treatment  Initial: amoxicillin

 2nd-line: amoxicillin-clavulanate
 Penicillin-allergic: clindamycin or
azithromycin

TM = tympanic membrane.

Acute otitis media

Microbiology  Streptococcus pneumoniae
 Nontypeable Haemophilus influenzae
 Moraxella catarrhalis

Clinical  Bulging TM
features  Middle ear effusion plus TM
inflammation (eg, fever, otalgia,
erythema)

Treatment  Initial: amoxicillin

 2nd-line: amoxicillin-clavulanate
 Penicillin-allergic: clindamycin or
azithromycin

Complication  TM perforation
 s  Conductive hearing loss
 Mastoiditis
 Meningitis
 Bullous myrigitis

TM = tympanic membrane.

First-line therapy with amoxicillin is indicated for infants age <6 months and for children age ≥6
months with high fever (>39 C [102.2 F]), severe pain, or bilateral disease.
Second-line therapy with amoxicillin-clavulanate is indicated for refractory symptoms after 2-3
days of antibiotic therapy or recurrent AOM (within 30 days) after antibiotic therapy.

Perforation can lead to temporary conductive hearing loss, but the TM typically heals
spontaneously within days; surgical correction may be required for perforation lasting several
months.

Group A Streptococcus is less commonly implicated in AOM alone but is often associated with
AOM with perforation. Additional risk factors apart from previous UTI include day care/school
attendance, positive family history, and cigarette smoke exposure. AOM often follows an upper
respiratory infection, which causes inflammation and edema of the already narrow eustachian
tube. Fluid accumulation in the distal tube allows for growth of colonized bacteria, most
commonly Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella
catarrhalis.

Common presenting symptoms include otalgia, fever, and irritability. In addition, patients may
have conductive hearing loss, as seen in this child, because fluid in the middle ear inhibits sound
transmission.

The most specific finding in AOM is a bulging tympanic membrane (TM) due to middle ear
inflammation. Other classic findings include decreased TM mobility on pneumatic
insufflation or visible air-fluid levels, both indicating middle ear effusion. A pale yellow,
opaque TM with bulging is suggestive of purulent effusion. TM erythema is also common but is
not required for the diagnosis; as an isolated finding (ie, no bulging or effusion), it is insufficient
for diagnosis.
Young children, particularly age 6-24 months, are predisposed to fluid accumulation within the
middle ear due to narrow, straight eustachian tubes that drain poorly. Most effusions develop in
the setting of a viral infection or following an episode of acute otitis media.

OME is typically asymptomatic but may cause mild discomfort (eg, ear tugging and pulling, as
seen in this patient) due to pressure on the TM. Because the effusion limits TM vibration,
conductive hearing loss is also common. OME does not cause fever or severe ear pain. Physical
examination reveals air-fluid levels posterior to the TM and poor TM mobility on pneumatic
insufflation. In contrast to acute otitis media, the effusion in OME is nonpurulent, and the TM is
not bulging or erythematous.

OME usually resolves within weeks and does not require treatment. However, patients should
be observed with follow-up for resolution because chronic OME (>3 months) can cause
speech delay and long-term hearing loss. Tympanostomy tube placement is warranted for
chronic OME with associated hearing loss.

Bullous myringitis is an uncommon complication of AOM and presents with TM bullae, which
are not seen in this patient

Chronic suppurative otitis media is characterized by otorrhea and hearing loss for >6 weeks and
TM perforation on examination.
Tympanocentesis and culture during tympanostomy tube placement should be considered for
multiple episodes of AOM (eg, ≥3 episodes in 6 months) or persistent (>3 months) middle ear
effusion with hearing loss.
As with AOM, mastoiditis (mcc of AOM) is most commonly seen in children age ≤2 and is
commonly caused by Streptococcus pneumoniae, Streptococcus pyogenes, and Staphylococcus
aureus. Pseudomonas aeruginosa has occasionally been implicated, especially in patients with
recurrent infections or recent antibiotic use.

Acute mastoiditis can often be diagnosed clinically. Imaging (eg, CT scan, MRI) is indicated if
the diagnosis is unclear, if there is suspicion for further complications (eg, meningitis, neurologic
deficits), if the child appears toxic, or if the condition does not respond to initial treatment.
Treatment of mastoiditis requires intravenous antibiotic therapy. Drainage of the purulent
material is also required. This can be achieved by tympanostomy (± ear tube placement) or
mastoidectomy.

Vancomycin treats mastoiditis, which classically presents with otalgia, fever, and postauricular
erythema and tenderness with outward displacement of the outer ear. ? initial therapy of
intravenous vancomycin and ceftriaxone is most appropriate until results of the culture and
sensitivity studies are available

AOM fever ear pain, erythematous bulging TM.

OME painless effusion
CSOM purulent, fever and chronic drainage from the perforated membrane
 RHINITIS & RHINOSINUSITIS:
Physical examination often shows beefy-red nasal mucosa as opposed to the edematous, pale
mucosa often seen in allergic rhinitis. The most important step in management is cessation of
the nasal decongestant spray, which is typically very uncomfortable for patients because of
rebound nasal congestion; significant counseling is required. Nasal glucocorticoids are often
prescribed to aid cessation. A short course of oral glucocorticoids can be added in severe cases.

Allergic rhinitis
Symptoms  Rhinorrhea, nasal congestion, sneezing, nasal itching
 Cough secondary to postnasal drip
 Ocular itching & tearing

Physical  "Allergic shiners" (infraorbital edema & darkening)

examination  "Allergic salute" (transverse nasal crease)
 Pale, bluish, enlarged turbinates
 Pharyngeal cobblestoning
 "Allergic facies" (high-arched palate, open-mouth breathing)
 Thick, green nasal discharge.

Treatment  Allergen avoidance

 Glucocorticoid nasal sprays (eg, fluticasone, mometasone) are
the most effective single agents.
 Acute rhinosinusitis in children
Clinical  Nasal congestion &/or purulent drainage
features  Facial pressure/pain
 ± Fever, cough, headache, loss of smell, ear pain

Etiology  Viral
o No fever or early resolution of fever
o Mild symptoms (eg, well-appearing, mild facial pain)
o Improvement & resolution by day 5-10
 Bacterial
o Fever ≥3 days OR
o Biphasic: New/recurrent fever after initial improvement OR
o Persistent symptoms ≥10 days

Treatment  Intranasal saline, saline irrigation, NSAIDs

 Antibiotics if bacterial (eg, amoxicillin, amoxicillin-clavulanate)

NSAIDs = nonsteroidal anti-inflammatory drugs.

Nontypeable Haemophilus influenzae (~40%-50%), Streptococcus pneumoniae (~20%-25%),

and Moraxella catarrhalis (~25%) are the most commonly implicated bacteria. Since the advent
of the 13-valent pneumococcal vaccine, S pneumoniae infection has become less prevalent.

Acute bacterial rhinosinusitis

Clinical  Cough, nasal discharge
features  Fever
 Face pain/headache

Diagnostic  Persistent symptoms ≥10 days without improvement

criteria  Severe onset (fever ≥39 C [102.2 F] + drainage) ≥3 days
 Worsening symptoms following initial improvement (ie, biphasic
(1 of 3) illness). Fever may be absent.

Treatment  Amoxicillin ± clavulanate

 Most cases are due to nontypeable Haemophilus influenzae or
Streptococcus pneumoniae. Worsening symptoms (eg, progressive cough
± fever), as seen in this patient, are treated with oral antibiotics (eg,
amoxicillin ± clavulanate) at the time of diagnosis. In contrast, in patients
with persistent but not worsening symptoms and a milder course, oral
antibiotics or a 3-day period of observation for clinical improvement are
both acceptable treatment options

The most common risk factor for ABRS is viral upper respiratory infection (URI); up to 10%
 of children with a viral URI develop ABRS. Thickened secretions and mucosal inflammation
from the viral infection prevent sinus drainage and impair mucociliary clearance of
contaminating bacteria, which can lead to secondary bacterial infection. Although less common
than viral URI, mucosal inflammation due to allergic rhinitis can also predispose to ABRS.
Diagnosis is usually clinical, and the first-line treatment is amoxicillin with or without
clavulanate.

Nonallergic rhinitis Allergic rhinitis

Clinical  Nasal congestion, rhinorrhea,  Watery rhinorrhea, sneezing, eye
features sneezing, postnasal drainage symptoms
 Later onset (age >20) common  Earlier age of onset
 No obvious allergic trigger  Identifiable allergen or seasonal
 Perennial symptoms (may pattern
worsen with season changes)  Pale/bluish nasal mucosa
 Erythematous nasal mucosa  Associated with other allergic
disorders (eg, eczema, asthma,
eustachian tube dysfunction)

Treatment  Mild: intranasal antihistamine  Intranasal glucocorticoids

(eg, azelastine, olopatadine) or  Antihistamines
glucocorticoids
  Intranasal ipratropium bromide
can also be used.
 Moderate to severe: combination
therapy

Staphylococcus aureus may be seen in chronic sinusitis (sinus inflammation for >12 weeks)

VERTIGO:
Common causes of vertigo
Ménière disease  Recurrent episodes lasting 20 minutes to several hours
 Sensorineural hearing loss
 Tinnitus &/or feeling of fullness in the ear

BPPV  Brief episodes triggered by head movement

 Dix-Hallpike maneuver causes nystagmus

Vestibular  Acute, single episode that can last days

neuritis  Often follows viral syndrome
 Abnormal head thrust test

Migraine  Vertigo associated with headache or other migrainous phenomenon

(eg, visual aura)
 Symptoms resolve completely between episodes

Brainstem/  Sudden-onset, persistent vertigo

cerebellar  Usually other neurologic symptoms
stroke
BPPV = benign paroxysmal positional vertigo.

Perilymphatic fistulas are a rare, but debilitating, complication of head injury or barotrauma.
They cause leakage of endolymph from the semicircular canals and cochlea into surrounding
tissues, resulting in characteristic clinical features:

 Progressive sensorineural hearing loss caused by damage to cochlear hair cells from
loss of endolymph.
 Episodic vertigo with nystagmus triggered by pressure changes in the inner ear (eg,
Valsalva maneuver, elevation changes [eg, riding in elevator]) due to acutely increased
endolymph leakage. This can be demonstrated clinically by performing a loud clap (ie,
pressure change due to sound conduction through the ossicles) near the patient's ear and
observing for nystagmus (Tullio phenomenon).
Patients are advised to limit activities that increase inner ear pressure; they also require ENT
referral for further management.

Ménière disease, a disorder of the inner ear characterized by increased

volume and/or pressure of endolymph (endolymphatic hydrops). The resulting distension of
the endolymphatic system causes damage to both the vestibular and cochlear components of the
inner ear. Ménière disease is characterized by the following triad:

 Episodic vertigo (20 min to 24 hr), commonly associated with nausea and vomiting
 Sensorineural hearing loss, fluctuating and varying in severity and usually worsening
over time (primarily affecting low frequencies at first and progressing to permanent loss
over all frequencies)
 Low-frequency tinnitus in the affected ear, often accompanied by a feeling of fullness

The diagnosis of Ménière disease is based primarily on clinical findings; however, audiometry
should be performed to fully characterize the hearing loss and follow its course over time, and
MRI should be obtained to rule out central nervous system lesions.

Initial management includes restriction of sodium, caffeine, nicotine, and alcohol.

Benzodiazepines, antihistamines, and antiemetics can relieve acute symptoms. Diuretics can be
considered. A minority of patients may require interventional techniques (eg, endolymphatic
shunt placement) for severe, intractable vertigo.

VN can be associated with significant nausea and vomiting as well as impaired gait, with the
patient falling toward the affected side. VN associated with unilateral hearing loss is termed
labyrinthitis.

The diagnosis of VN is based on clinical findings. Patients exhibit nystagmus that is suppressed
when they direct their vision toward a stationary target (consistent with peripheral rather than
central vertigo). Head thrust test is usually abnormal. In this test, the patient is asked to look at
a fixed target while the head is rapidly rotated. Patients with normal vestibular function maintain
visual fixation; however, in patients with VN, the eyes move away and then return to the target
with a horizontal saccade.

Because VN is usually self-limited, patients can be managed expectantly. Management may also
include vestibular suppressants (eg, meclizine), corticosteroids, and vestibular rehabilitation.
 DISORDERS OF (ENT) :
Perilymphatic fistula, a rare complication of head trauma, is characterized by fluid leakage from
the cochlea and semicircular canals. Unlike in this patient, the presentation involves hearing loss
and vertigo triggered by the Valsalva maneuver; riding in an elevator; or sudden, loud sounds.

Tympanometry can assess for eustachian tube dysfunction, which can cause ear pain but would
also cause hearing loss, feeling of fullness, and tympanic membrane retraction or middle ear
effusion; tympanostomy tube placement can be considered in patients who do not respond to
medical management (eg, decongestants). Tube placement is also indicated in some children
with recurrent otitis media. Eustachian tube dysfunction may present with ear pain accompanied
by popping sounds. However, it typically results in hearing loss and changes to the tympanic
membrane (eg, retraction, middle ear effusion).

For the treatment of acute epistaxis, nostril pinching is the first step in management.
Oxymetazoline (a topical vasoconstrictor) can be applied if direct compression alone is not
effective. However, oxymetazoline is not useful for prevention and should not be used for more
than 3 days due to the risk of rebound congestion (ie, rhinitis medicamentosa).
A muffled voice should make one consider a diagnosis other than uncomplicated pharyngitis or
tonsillitis. A peritonsillar abscess is a potential complication of tonsillitis and requires both
intravenous antibiotic therapy and urgent drainage of the abscess. Deviation of the uvula and
unilateral lymphadenopathy can be helpful in distinguishing a peritonsillar abscess from
epiglottitis.
 Cholesteatomas result from the accumulation of keratin debris and squamous epithelial cells
within a tympanic membrane retraction pocket. Symptoms include persistent otorrhea and
conductive hearing loss, and examination often reveals a pearly white mass behind an intact
tympanic membrane. Treatment is surgical removal, risk factors include recurrent AOM, chronic
middle ear effusion, and tympanosyomy tube.

Eustachian tube dysfunction

Physiology  Eustachian tubes normally open and close to:
o Equalize middle ear pressure
o Drain middle ear
o Prevent reflux of nasopharyngeal secretions

Pathophysiology  Inflammation (eg, infection, allergies, environmental

irritation) → tube obstruction

Signs & symptoms  Ear fullness/discomfort

 Tinnitus
 Conductive hearing loss
 "Popping" sensation

Management  Treat underlying cause (eg, antibiotics for acute bacterial

 rhinosinusitis)/Antihistamines

Otoscopic examination reveals a retracted TM due to negative pressure within the middle ear.
Dilated blood vessels surrounding the TM reflect inflammation.

CANCERS :

Evolving leukoplakia in the oral cavity requires biopsy (even if previously biopsied). Tobacco
use is the most important risk factor for oral cavity squamous cell carcinoma.
Leukoplakia

Erythroplekia
This increase is due to human papillomavirus (HPV)–positive HNSCC, often seen in younger
patients with no tobacco exposure and multiple sexual partners (as in this patient). HPV-
positive HNSCC primarily affects the oropharynx (possibly due to the higher concentration of
lymphatic tissue facilitating viral processing) and often presents with neck lymphadenopathy.
However, it is more responsive to therapy than HPV-negative HNSCC. The most common
causative subtype is HPV-16, which is covered by the HPV vaccine.

This patient should undergo biopsy of the tonsil lesion with evaluation of HPV status, neck
imaging (eg, CT scan) to characterize the lesion and associated nodal metastasis, and endoscopic
evaluation of the upper aerodigestive tract.

Topical glucocorticoids are sometimes used to treat aphthous ulcers, which tend to be multiple,
painful, and short-lasting (<2 weeks). Topical glucocorticoids and topical tacrolimus can be
used to treat oral lichen planus, which often occurs on the buccal mucosal surfaces and can
appear as reticular, white plaques; erythematous, atrophic patches; or ulcerations.

Nasopharyngeal carcinoma is associated with the reactivation of Epstein-Barr virus and occurs
most commonly in those from Asia (particularly southern China) and parts of Africa and the
Middle East. Manifestations include nasal congestion with epistaxis, headaches, cranial nerve
palsies, and otitis media. Early spread to the cervical lymph nodes is common. Tumors typically
express EBV DNA, and EBV assays are often used to monitor treatment response and disease
relapse.