ears, nose, throat Flashcards
congenital ear malformations
-External ear and EAC develops at 3 weeks gestation
-Atresia: Failure of EAC to form
-Microtia: EAC is small, collapsed, or only has an earlobe present
-Anotia: Absence of EAC -> Reconstruction of auricle usually occurs around ages 6-8 years
-Prominotia: Ears lack proper folds and protrude from skull
-Taping of ears into anatomic position is very effective if performed within first 72-96 hours of life x 2 weeks (tape applied over a molding)
-Preauricular tags, ectopic cartilage, fistulas, and cysts require surgical intervention
-Pts should have hearing tested, renal US (external anomalies associated with renal anomalies – develop during same period of embryogenesis)
-THINK RENAL
hearing screening
-Goal is identification and confirmation of hearing loss by 3 months, and intervention by 6 months
-Signs of hearing loss -> inconsistent response to sounds, not following directions, speech and language delays, and turning sound up on televisions/radios
-AUDIOMETRY:
-Birth – 6 months: Behavioral observational audiometry
-Sounds are presented at various intensity levels > watched for reaction
-6 months – 2.5 years: Visual reinforcement audiometry
-Auditory stimulus paired with positive reinforcement
-Child reacts to a sound (turning head) > behavior rewarded by activation of a toy that lights up > localizes tone in anticipation of lighted toy
-2.5 years – 5 years: Conditioned play audiometry
-Child responds to sound stimulus by performing an activity (putting peg in a board)
-5 years and older: Conventional audiometry
-Child indicates when sound is heard
hearing loss: conductive vs sensorineural
-Conductive Hearing Loss
-MCC of childhood CHL is OM and related conditions (MEE, ETD)
-Other causes: EAC atresia/stenosis, TM perforation, cerumen impaction, cholesteatoma, and middle ear abnormalities
-Sensorineural Hearing Loss
-Arises due to defect in the cochlear receptor cells or auditory nerve (CN VIII)
-Loss may be congenital or acquired (hereditary or nonhereditary)
-50% of congenital is nonhereditary: Infection, teratogens, perinatal injuries; other 50% from genetic factors
-Acquired: Delayed onset
-Nongenetic etiologies: Ototoxic medications, meningitis, autoimmune/neoplastic conditions, noise exposure, and trauma
-Infections: Syphilis, Lyme disease, CMV
-PPHTN, ECMO
-TORCH!
-Risk factors: Positive family history, BW < 1500 grams, low Apgar scores, craniofacial abnormalities, hypoxia, in utero infections (TORCH syndrome!!!), hyperbilirubinemia (requiring exchange transfusion), and mechanical ventilation for > 5 days
hearing loss tx
-Significantly impairs child’s ability to communicate; hinders academic, social, and emotional development
-Treatment entails early intervention and a multidisciplinary approach (ENT)
-Conductive hearing loss focuses on reversing cause
-SNHL is not reversible
-Cochlear implants: 9 months and older, directly stimulates cochlea with electrical impulses (hearing aids just amplify sound)
acute otitis externa (AOE)
-Cellulitis of the soft tissues of the EAC, which can extend to surrounding structures, such as the pinna, tragus, and lymph nodes
-Humidity, moisture, heat known to contribute
-Trauma to ear canal, which breaks skin-cerumen barrier (inhibiting bacterial/fungal growth) is first step in infection -> Cotton swab use, earbuds, scratching, ear plugs
-MC organisms: S. aureus, S. epidermidis, P. aeruginosa; fungal infections in 2-10% of patients
-Acute onset of pain, aural fullness, decreased hearing, and pruritis (peak within 3 days)
-Manipulation of tragus/pinna causes considerable pain
-Discharge may be clear/purulent
-EAC narrowed/swollen (may be difficult to visualize entire TM)
-Complications:
-Cellulitis of neck and face
-Malignant OE: Spread of infection to skull base with resultant osteomyelitis
-Treatment:
-Pain control, removal of debris from canal, topical antimicrobial therapy, avoidance of causative factors
-Fluoroquinolone ear drops first line; combination with a steroid may be necessary (ciprofloxacin/dexamethasone) -> Ensure no TM perforation before steroids!
-PO antibiotics for any invasive infection signs (fever, cellulitis, cervical lymphadenopathy)
acute otitis media
-MC reason antibiotics are prescribed for children in US
-Microbiology: S. pneumoniae > H. influenzae > M. catarrhalis > S. pyogenes
-Two critical findings: Bulging TM AND a MEE
-Otoscopic findings specific to AOM: Bulging TM, impaired visibility of ossicular landmarks, yellow or white effusion, opacified/inflamed TM, squamous exudate/bullae on TM
acute otitis media: risk factors
-Season (winter > summer)
-Ages 1-3
-Eustachian tube dysfunction
-Infants and young children more prone due to shorter, more compliant, horizontal ET
-Trisomy 21, cleft palate risk factors
-Bacterial colonization of nasopharynx: S. pneumoniae, H. influenzae, M. catarrhalis
-Smoke exposure: Increases risk of persistent MEE, prolonging inflammatory response, impeding drainage of fluid through ET
-Impaired host immune defenses
-Bottle feeding: Bottle propping in the crib or car seat > aspiration of contaminated secretions into the middle ear
-Daycare attendance (exposure to viral infections/URIs)
-Genetic susceptibility
acute otitis media tx
-Pain control (may take 1-3 days before antibiotic relieves pain)
-Wait and see approach:
-Observe episode without treatment
-Option for healthy children (typically > 2 years) with mild-moderate OM and without underlying conditions
-Decision made in conjunction with parents to begin antibiotics therapy if worsening of symptoms or lack of improvement within 48-72 hours
-Antibiotic therapy: (know this)
-First-line: High dose amoxicillin (80-90 mg/kg divided BID)
-Augmentin if child has had amoxicillin within last 30 days or clinically failing x 48-72 hours on amoxicillin
-Cephalosporins (cefuroxime, cefpodoxime, cefdinir) for those with rash to PCN – risk of cross-sensitivity is less than 0.1%
-Macrolide (azithromycin) only if history of type 1 hypersensitivity to PCN -> Resistance of S. pneumoniae and H. influenzae (macrolide efflux pump)
-Second-line antibiotics indicated when child experiences symptomatic infection within 1 month of finishing amoxicillin
acute otitis media tx: drug failure
-Failure to eradicate: Drug noncompliance, poor drug absorption, vomiting of drug
-Child remains symptomatic for > 3 days with second line antibiotics
-Tympanocentesis or IM ceftriaxone at 50 mg/kg/dose x 3 consecutive days
-Patients with tympanostomy tubes
-First-line: Ototopical antibiotics (fluoroquinolones)
-Treat infection and rinse drainage from tube
-Tympanostomy tubes considered (AAP):
-Three episodes in 6 months, 4 episodes in 1 year, last episode within past 6 months (not on test)
middle ear effusions
-Presence of fluid within middle ear without signs or symptoms of acute inflammation
-TM may be opacified/thickened, fluid can be clear/amber/or opaque, typically in neutral/retracted position
-Pneumatic otoscopy and/or tympanometry for confirmation
-Management:
-Abx, anti-histamines, and steroids have not been shown to be useful in treatment
-Audiology evaluation after 3 months of continuous B/L effusion
-Hearing loss/speech delay > referral to ENT for possible T-tube placement
-Uncomplicated cases, observed for 3 months with follow-up every 3-6 months to evaluate for effusion clearance
-T-tube indications:
-Hearing loss > 40 dB, TM retraction pockets, ossicular erosion, adhesive atelectasis, and cholesteatoma
tympanic membrane perforation
-Episode of AOM may result in rupture of TM
-Discharge from ear seen with rapid relief of pain
-Treatment: Ototopical antibiotics x 10-14 days with ENT follow-up for examination/hearing evaluation
-Failure to heal may require surgery (typically deferred until age 7, when ET has reached adult orientation)
mastoiditis
-Infection from middle ear space spreads to mastoid portion of temporal bone
-Inflammation of periosteum to bony destruction of mastoid air cells with abscess development
-Occurs at any age, most < 2 years old
-Clinical diagnosis
-Postauricular pain, fever, and outwardly displaced pinna
-Examination: Mastoid area appears indurated, red, swollen, fluctuant with severe tenderness (earliest symptom)
-AOM is almost always present
-Imaging Studies:
-CT scan to determine extent of disease
-Progressed disease: Coalescence of mastoid air cells with bone destruction
-Complications:
-Meningitis (high fever, stiff neck, severe headache)
-Brain abscess (fever, headache, changes in sensorium)
-Facial palsy, sigmoid sinus thrombosis, epidural abscess, cavernous sinus thrombosis, thrombophlebitis
ear canal foreign bodes/cerumen impaction
-Intentional or accidental, very common in childhood
-Can be removed if easily visualized and with appropriate instrumentation
-ENT referral for large FBs, rounded/globular objects, deep objects
-Vegetable matter should never be irrigated (may swell)
-Button-battery > emergent referral
-Cerumen impactions removed if symptomatic and obstructing visualization of TM
acute viral rhinitis
-common cold is the MC pediatric infectious disease
-Children younger than 5 years typically have 6-12 colds per year
-Approximately 30-40% caused by rhinoviruses
-Sudden onset sore throat followed by clear or mucoid rhinorrhea, nasal congestion, and sneezing, with or without cough/fever
-Nose, throat, TMs may be erythematous
-Nasal secretions tend to become thicker and more purulent x 2 days (shedding of epithelial cells/neutrophils)
-Discoloration does not mean sinus infection! – Unless 10-14 days persistent
-Treatment: Symptomatic (time, education, reassurance)
-Antipyretics, anti-histamines, humidification, nasal saline drops/bulb suctioning
-OTC cold and cough medications are not effective in children and may have serious adverse effects -> we want them to cough out the mucus -> can lead to pneumonia if not
acute bacterial rhinosinusitis
-Bacterial infection of the paranasal sinuses, lasts < 30 days with complete symptom resolution
-Almost always preceded by a cold; other predisposing factors include allergies and trauma
-Cold does not improve by 10-14 days or worsens after 5-7 days
-a lot of facial pressure
-Sinus formation:
-Maxillary and ethmoid sinuses present at birth
-Sphenoid sinuses developed by 7-8 years of age
-Frontal sinuses by puberty
-Viral URI causes mucosal injury/swelling > sinus outflow obstruction, loss of ciliary activity, mucous hypersecretion > bacterial overgrowth: S. pneumoniae, H. influenzae, M. catarrhalis, B-hemolytic strep
-Nasal drainage/congestion, facial pressure/pain, hyposmia/anosmia, fever, cough, maxillary dental pain, and ear fullness/pressure
Complications:
-Spread to adjacent structures (eye/brain)
-Pre-septal cellulitis > orbital cellulitis > subperiosteal/orbital abscess > cavernous sinus thrombosis
-Pott’s puffy tumor: Osteitis of frontal bone > intracranial extension
acute bacterial rhinosinusitis tx
-Observation versus antibiotic therapy
-First-line antibiotic: High-dose amoxicillin or amoxicillin-clavulanate x 10-14 days (7 days after symptoms have resolved)
-Cephalosporins for non-type 1 hypersensitivity
-Other agents: Clindamycin, linezolid, quinolones
-Second-lines for those who fail to improve x 2-3 of first-line; consider referral for imaging/sinus aspiration as well
-Patients who are toxic/evidence of invasive spread – Hospitalization for IV antibiotics (nafcillin) + ceftriaxone
-Adjuvant treatments: Decongestants, anti-histamines, nasal saline irrigations
-Topical decongestants (oxymetazoline, phenylephrine) should not be used > 3 days due to risk of rebound edema
allergic rhinitis
-Recurrent rhinitis, “one cold after another,” “constant colds,” or “always being sick”
-Chronic disorder of upper airway, induced by IgE-mediated inflammation secondary to allergen exposure
-Affects 40% of children in US: Quality of life, interferes with physical/social activities, concentration, school performance, and sleep
-Congestion/rhinorrhea, sneezing, pruritis of nose/palate/throat/eyes
-Swollen turbinates, red/pale pink-purple
-Treatment:
-Intranasal corticosteroids (as young as 2 years of age), PO/IN antihistamines, leukotriene antagonists, and decongestants
epistaxis
-MC from anterior (Kesselbach area) nasal septum due to dryness, nose rubbing, nose blowing, or nose picking
-Exam reveals red, raw surface with fresh clots/old crusts
-Treatment:
-Sit up, lean forward
-Soft part of nose below nasal bones is pinched and held firmly enough to prevent arterial blood flow x 5 minutes
-Persistent bleeding – oxymetazoline > gelatin sponge (Gelfoam)/collagen sponge (Surgicel) inserted over visualized vessel
-ENT cautery for treatment failures
-Prevention: Increase nasal moisture
-Daily application of water-based ointment to nose
-BID nasal saline irrigation and humidifier
-Avoiding aspirin and ibuprofen, nose picking, and vigorous nose blowing
nasal foreign bodies
-If delayed identification > unilateral, foul-smelling rhinorrhea, halitosis, bleeding, or nasal obstruction often result
-Removal methods:
-Vigorous nose blowing
-mom blows into the pts mouth (if infant)
-Nasal decongestant, good lighting, correct instrumentation, and physical restraint
-Alligator forceps, right-angle instrument, balloon extractor
-Failed attempt: Referral to ENT
-Batteries: Emergent referral
acute stomatitis: recurrent aphthous stomatitis (canker sores)
-Painful ulcers (3-10 mm) usually found on the inner aspect of the lips, gingiva, or tongue
-Last 1-2 weeks; may recur in conjunction with infectious/autoimmune disease
-Treatment: Symptomatic (analgesics) and bland diet
-Local corticosteroid, swish/spit dexamethasone
acute stomatitis: herpes simplex (type 1)
-Type-1 (HSV-1) causes most cases of oral, perioral, skin, and cerebral disease in children
-Latent infection is routinely established in sensory ganglia during primary infection > reactivation/recurrence is spontaneous or induced by external events (fever, menstruation, sunlight, immunosuppression)
-Transmission is via direct contact (asymptomatic excreter)
-Gingivostomatitis
-High fever, irritability, and drooling in infants
-Oral ulcers on tongue, buccal, and gingival mucosae, occasionally extending into pharynx
-Diffusely swollen, red gums that are friable and bleed easily
-Cervical nodes swollen/tender
-Symptoms 1-2 weeks
-Mucocutaneous Infection
-Perioral lesions with prodrome of tingling or burning limited to the vermillion border > followed by vesiculation, scabbing, and crusting around the lips over 3-5 days
herpes simplex (type 1): tx
-Gingivostomatitis
-Pain relief and fever control
-Maintaining hydration
-Magic mouthwash (viscous lidocaine + diphenhydramine + Kaopectate/Maalox) – Only for children who will not swallow solution!
-Severe (primary infection): PO nucleoside analogue (acyclovir)
-Mucocutaneous Infection
-PO nucleoside analogues (acyclovir, valacyclovir, famciclovir)
acute stomatitis: oral candidiasis (thrush)
-Adherent, creamy white plaques on the buccal, gingival, or lingual mucosa
-Risk factors: Common in immune-normal infants (first weeks of life), corticosteroid inhalation (asthma), immunodeficiency
-May resemble milk/formula (easily wiped away revealing normal mucosa)
-Treatment:
-Oral nystatin (100,000U) 4-6 x daily for 2-3 days following resolution
-Washing all pacifiers, bottle nipples, toys, mother’s breasts
-Older children with refractory cases: Oral azoles (fluconazole)
-D/C antibiotics and corticosteroids (if/when possible
acute pharyngotonsillitis: viral pharyngitis: Infectious Mononucleosis (Epstein-Barr Virus)
-Infectious Mononucleosis (Epstein-Barr Virus)
-Usually, patients > 5 years of age
-Exudative tonsillitis!, generalized cervical adenitis, fever; palpable spleen or axillary lymphadenopathy increases likelihood of diagnosis
-Presence of > 10% atypical lymphocytes on peripheral blood smear or positive Monospot supports diagnosis (though falsely negative in children < 5 years)
-Epstein-Barr virus serology showing elevated IgM antibody is definitive
-Treatment: Supportive, avoiding contact sports, 4-6-week follow-up (LFTs)
Amoxicillin is contraindicated – precipitates rash
acute pharyngotonsillitis: bacterial pharyngitis
-Approx 20-30% of children with pharyngitis have a group A streptococcal (GAS) infection
-Other causes: Mycoplasma pneumoniae, Chlamydia pneumoniae, groups C/G streptococci, and Arcanobacterium hemolyticum
-MC in children 5-15 years, winter/early spring
-Sudden onset sore throat, fever, tender cervical adenopathy, palatal petechiae!, beefy-red uvula, and a tonsillar exudate
-Headache, stomachache, nausea/vomiting
-Scarlet fever!: 1-2 days into symptoms > sandpapery rash (diffuse, finely papular, erythematous, blanchable) with strawberry tongue appearance
-Modified Centor Score
-Definitive diagnosis with throat culture or rapid antigen test -> RAT specific but only 85%-95% sensitive
-KNOW THE CHART
bacterial pharyngitis: complications (untreated)
-Acute rheumatic fever
-Glomerulonephritis
-Suppurative complications: Cervical adenitis, peritonsillar abscess, AOM, cellulitis, septicemia
-Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS)
-Sudden onset of OCD and/or tics (or worsening of such symptoms) following a strep infection
bacterial pharyngitis: tx
-First-line: PCN/Amoxicillin (50 mg/kg divided BID x 10 days)
-Alternatives: Cephalosporin (cephalexin), macrolide (azithromycin), clindamycin
-Avoid tetracyclines, sulfonamides, and quinolones
-Repeat culture following treatment is not recommended; indicated only for patients who remain symptomatic, have recurrence of symptoms, or have had rheumatic fever
-RF patients may require long-term antibiotic prophylaxis (sometimes life-long)
-Carrier state may last 2-6 months and is not contagious
-Treated with clindamycin (x 10 days) or rifampin (x 5 days) only if patient or another family member has frequent strep infections or if family member/patient has history of RF or glomerulonephritis
-Recurrent infections: Tonsillectomy is now preferred for those with recurrent strep tonsillitis (Paradise criteria):
-7 tonsillitis episodes/year, 5 episodes/year for 2 consecutive years, 3 episodes/year for at least 3 years (dont memorize)
acute pharyngotonsillitis: diptheria
-Acute infection of URT or skin caused by exotoxin-producing Corynebacterium diphtheriae (3 cases reported between 2010 and 2019)
-Gram-positive, club-shaped rods on gram stain
-Toxin absorbed into mucous membranes > destruction of epithelium > inflammatory response > embedded in fibrin with WBCs/RBCs > grayish pseudomembrane forms over tonsil, pharynx, larynx
-Pharyngeal diphtheria:
-Mild sore throat, moderate fever, and malaise > rapid decompensation
-Pharyngeal membrane forms (tenacious, gray, border of erythema/edema) and may spread to nasopharynx or trachea > obstruction
-Cervical lymph node swelling > “bull neck”
-Diagnosis: Culture of C. diphtheriae from infected tissue(s)
-Treatment:
-Reported to CDC to acquire anti-toxin (administered within 48 hours of symptom onset)
-Antibiotics (erythromycin IM/PO or procaine PCN G IM, q12hrs) x 14 days
-Vaccination during convalescence, observation in hospital setting 10-14 days (isolated for at least 1-7 days, until respiratory secretions are noncontagious)
peritonsillar cellulitis/abscess (quinsy)
-Cellulitis (tonsillar infection extending to the surrounding tissues) > cellulitis untreated > necrosis occurs > peritonsillar abscess forms
-Usually unilateral with fever and severe sore throat
-Affected tonsil bulges medially, anterior tonsillar pillar is prominent, uvula deviates to unaffected side
-Progression: Trismus (limited mouth opening/muffled voice), ear pain, dysphagia, and drooling
-Jugular vein thrombosis, septic thrombi into lungs
-Treatment:
-Cellulitis responds to parenteral antibiotics (PCN, cephalosporin, or clindamycin)
-Abscess typically requires drainage (needle aspiration or I&D)
retropharyngeal abscess
-Infection of lymph nodes draining oropharynx, nasopharynx, and paranasal sinuses
-Fever, respiratory symptoms, restriction in neck ROM (extension) -> Dysphagia, drooling, dyspnea, and gurgling respirations
-hot potato voice
-may not be able to see it
-Prominent swelling on one side of posterior pharynx (stops at midline)
-Imaging: Lateral neck x-ray (tissues wider than C4)
-CT scan w/ contrast distinguishes between soft tissue swelling versus abscess
-Treatment:
-Immediate hospitalization and IV antibiotics (PCN or clindamycin)
-If only adenitis > improvement within 12-24 hours; if not, more likely abscess
-Surgical emergency! I&D under general anesthesia
ludwigs angina
-Rapidly progressive cellulitis of both submandibular spaces that pushes the tongue posteriorly against the pharyngeal wall > life-threatening airway obstruction
-Fever and tender swelling of the tongue and floor of mouth
-Treatment:
-High-dose IV clindamycin or ampicillin + nafcillin until C&S available
-Airway obstruction: Tracheotomy versus ICU admission with intubation
tonsillectomy/adenoidectomy
-Tonsillectomy
-MC indication is hypertrophy or recurrent infections
-Second MC cause is recurrent tonsillitis (Paradise criteria)
-Adenotonsillectomy
-MC indication is hypertrophy associated with an obstructive breathing pattern during sleep (may also cause dysphagia or dental malocclusion)
-Adenoidectomy
-Indications: Upper airway obstruction, orofacial conditions (mandibular growth abnormalities, dental malocclusion), speech abnormalities, persistent MEE, and recurrent OM/sinusitis
mumps
-Caused by paramyxovirus, spread by respiratory route
-Incubation period 14-21 days, infectious 2 days prior to and 5 days after parotitis
-Salivary glands
-Prodrome of fever, headache, arthralgia, and anorexia > swelling of parotid glands (70-80% B/L)
-Ear displaced upward and outward, mandibular angle is obliterated
-Parotid stimulation with sour foods may be painful
-Stensen duct orifice may be red, swollen, secretory (yellow)
-Lasts 1 week
-Other manifestations: Aseptic meningitis, pancreatitis, orchitis/oophoritis
-Diagnosis: CSF analysis, PCR, serology
-Treatment: Supportive (fluids, pain control, scrotal support)
ankyloglossia (tongue tied)
-Short lingual frenulum > hindered protrusion and elevation of tongue
-Can cause feeding difficulties, speech problems, and dental problems
-Treatment: Referral to ENT > frenulectomy in neonatal period
cleft lip and cleft palate
-Submucous Cleft Palate
-Translucent zone in middle of soft palate; palpation of hard palate reveals absence of posterior bony protrusion
-Risks: 40% risk of MEE; velopharyngeal incompetence (inability to close palate against posterior pharyngeal wall > hypernasal speech and nasal regurgitation of food)
-Surgical repair
-High-Arched Palate
-Genetic trait, chronic mouth breathers, premature infants who undergo prolonged oral intubation; Marfan, Ehler-Danlos syndromes
-Orthodontic treatment for childhood OSA
-Pierre Robin Syndrome: Micrognathia, glossoptosis (posterior tongue displacement), and airway obstruction, usually associated with cleft palate
-Positioning strategies: Side-lying, prone positioning
-Nasal trumpet, tongue-lip adhesion, mandibular distraction osteogenesis, tracheotomy with gastric tube
-Palate repair deferred until 10-12 months
dental caries
-Microorganisms metabolize sugars > acid production > demineralization of enamel and dentin
-MC chronic disease of childhood and most prevalent overlooked health need of U.S. children
-Visualization: Chalky white > dark, brown cavitations
-Tooth sensitivity (temperature change, sweetness)
-Treatment: Filling versus root canal (if invasion of pulp/deeper structures)
-Prevention: Fluoride (topical (varnish)/systemic sources); food, drinking water, sugar substitutes (xylitol), and frequency of brushing
-Fluoride interferes with bacterial metabolism (interferes with enzyme activity) > inhibits demineralization > enhances remineralization
-Dietary Guidelines:
-Water in bottles at bedtime, weaning from bottle between 12 and 18 months, encouraging drinking from a cup
-Avoiding sugar-containing carbonated beverages, 100% juice, and powdered beverages
-Protective foods: High fat, protein, and minerals, such as milk and cheese (calcium and phosphate)
-Oral Hygiene:
-After birth, caregivers should clean intra-oral surfaces on daily basis with moist, soft cloth
-Once teeth erupting, brushing/flossing by caregivers up to age 8 (manual dexterity still developing) with fluoridated toothpaste
