Eyes, Ears, Nose, Oral Cavity & Throat (EENOT)

What is barotrauma?

Tissue injury caused by failure to equalize pressure between an air-filled body cavity and the surrounding environment, most commonly affecting the middle ear during diving or flying.

What is the most common form of barotrauma seen in the ED?

Middle ear barotrauma (barotitis media), typically during descent in diving or aircraft landing when the eustachian tube fails to equalize.

What otoscopic findings suggest middle ear barotrauma?

Erythema and retraction of the TM, hemotympanum, serous middle ear effusion, or TM perforation in severe cases.

What symptoms distinguish inner ear barotrauma from middle ear barotrauma?

Inner ear barotrauma causes vertigo, sensorineural hearing loss, and tinnitus (suggests round or oval window rupture) and requires urgent ENT consultation and avoidance of Valsalva.

What is the treatment for uncomplicated middle ear barotrauma?

Decongestants (oral pseudoephedrine and/or topical oxymetazoline), analgesics, autoinflation maneuvers, and avoidance of flying or diving until resolved; antibiotics only if perforation with contaminated water exposure.

What life-threatening condition results from pulmonary barotrauma during rapid ascent?

Arterial gas embolism, presenting with sudden loss of consciousness or stroke-like symptoms within minutes of surfacing; treat with high-flow oxygen, supine positioning, and emergent hyperbaric recompression.

What emergency department finding suggests barodontalgia?

Tooth pain triggered by altitude or depth change due to trapped gas under a defective restoration or in a carious tooth; refer to dentistry.

What is eustachian tube dysfunction?

Impaired ventilation and pressure equalization of the middle ear due to a blocked or poorly functioning eustachian tube, most often following viral URI or allergic rhinitis.

What are the classic symptoms of eustachian tube dysfunction?

Ear fullness or pressure, muffled hearing, popping or crackling, autophony, and mild intermittent pain without significant fever.

What otoscopic findings are seen in eustachian tube dysfunction?

Retracted TM with prominent lateral process of the malleus, decreased mobility on pneumatic otoscopy, and possible serous effusion with air-fluid levels or bubbles.

How is eustachian tube dysfunction differentiated from acute otitis media?

ETD lacks a bulging erythematous TM, purulent effusion, and systemic fever; ETD shows retraction rather than bulging.

What is the ED treatment for eustachian tube dysfunction?

Intranasal steroids, oral or topical decongestants, antihistamines if allergic, autoinflation (Valsalva or Toynbee), and analgesics; antibiotics are not indicated.

What red flag in an adult with unilateral persistent ETD requires referral?

Unilateral serous effusion in an adult raises concern for nasopharyngeal carcinoma obstructing the eustachian tube and requires ENT evaluation with nasopharyngoscopy.

What is external ear trauma and auricular hematoma?

Blunt or shearing injury to the pinna causing blood to collect between the perichondrium and cartilage, threatening cartilage necrosis if not evacuated.

Why must an auricular hematoma be drained emergently?

The cartilage is avascular and depends on the perichondrium for nutrition; an undrained hematoma causes avascular necrosis and fibrocartilage overgrowth, producing cauliflower ear.

What is the correct ED management of an auricular hematoma?

Local anesthesia, incision and drainage or needle aspiration for small acute collections, followed by a compressive bolster or through-and-through mattress sutures, and recheck in 24 hours.

Within what time frame should an auricular hematoma be drained?

Ideally within 7 days of injury, but as soon as possible; hematomas older than 7 days often require ENT management for organized clot.

How are auricular lacerations involving cartilage managed?

Irrigate, close the perichondrium and skin with the cartilage covered (avoid suturing through cartilage when possible), give antibiotic coverage against Pseudomonas and Staph, and never leave cartilage exposed.

What antibiotic prophylaxis is recommended for auricular cartilage injury or human bite of the ear?

Fluoroquinolone (ciprofloxacin) for Pseudomonas coverage, or amoxicillin-clavulanate for bites.

What is an ear foreign body?

An object lodged in the external auditory canal, most common in children, that may cause pain, decreased hearing, discharge, or canal trauma.

What ear foreign body is a true emergency requiring immediate removal?

A button (disc) battery, which causes liquefactive necrosis and TM perforation within hours; also removal is urgent for penetrating objects.

How should a live insect in the ear canal be managed?

Kill or immobilize it first with mineral oil, lidocaine, or viscous lidocaine before removal to prevent further canal trauma and pain.

What removal techniques are used for ear foreign bodies?

Irrigation (only if the TM is intact and the object is not organic or a battery), alligator forceps for graspable objects, right-angle hook behind smooth objects, suction, or cyanoacrylate on a swab tip.

Why should organic material like beans or peas not be irrigated?

Water causes swelling of organic material, making removal more difficult and increasing canal trauma.

When should an ear foreign body be referred to ENT?

Failed attempts, uncooperative patient requiring sedation, TM perforation, penetrating objects, significant canal trauma or bleeding, or objects lodged medial to the isthmus.

What is mastoiditis?

Suppurative infection of the mastoid air cells, most often a complication of untreated or inadequately treated acute otitis media.

What are the classic physical exam findings of acute mastoiditis?

Postauricular erythema, swelling, and tenderness with protrusion of the auricle anteriorly and inferiorly, plus findings of acute otitis media.

What imaging study confirms mastoiditis?

CT of the temporal bone with contrast, showing coalescence of mastoid air cells and bony septal destruction.

What organisms most commonly cause acute mastoiditis?

Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, and Pseudomonas aeruginosa in chronic cases.

What is the ED management of mastoiditis?

Admission, IV antibiotics (vancomycin plus ceftriaxone or an antipseudomonal agent), emergent ENT consultation, and possible myringotomy or mastoidectomy.

What intracranial complications must be considered in mastoiditis?

Meningitis, epidural or brain abscess, lateral (sigmoid) sinus thrombosis, subperiosteal abscess, and facial nerve palsy.

What is Gradenigo syndrome?

Petrous apicitis triad of otorrhea, retro-orbital pain (CN V), and lateral rectus palsy (CN VI) complicating middle ear or mastoid infection.

What is otitis externa?

Infection and inflammation of the external auditory canal, commonly called swimmer's ear, usually bacterial and precipitated by moisture or canal trauma.

What physical exam finding strongly suggests otitis externa rather than otitis media?

Pain with traction of the pinna or pressure on the tragus, along with canal edema, erythema, and debris.

What are the most common pathogens in otitis externa?

Pseudomonas aeruginosa and Staphylococcus aureus.

What is the first-line treatment for uncomplicated otitis externa?

Topical antibiotic drops such as ciprofloxacin-dexamethasone or ofloxacin, canal cleaning, and a wick if the canal is too edematous for drops to penetrate.

Which topical agents must be avoided if the TM is perforated?

Aminoglycoside-containing drops (neomycin, gentamicin) due to ototoxicity; use fluoroquinolone drops instead.

What is necrotizing (malignant) otitis externa and who gets it?

Osteomyelitis of the skull base caused by Pseudomonas, seen in elderly diabetics and immunocompromised patients, presenting with severe pain, granulation tissue at the bony cartilaginous junction, and possible cranial nerve palsies.

What is the management of necrotizing otitis externa?

Admission, IV antipseudomonal antibiotics (piperacillin-tazobactam or ciprofloxacin), CT or MRI of the temporal bone, ENT consultation, and glycemic control.

What is otitis media?

Infection or inflammation of the middle ear space, most often following eustachian tube dysfunction from a viral URI, peaking in children 6 to 24 months old.

What otoscopic findings confirm acute otitis media?

Bulging, erythematous, opaque TM with decreased or absent mobility on pneumatic otoscopy and possible air-fluid level or otorrhea from perforation.

What are the most common bacterial pathogens in acute otitis media?

Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis.

What is the first-line antibiotic for acute otitis media?

High-dose amoxicillin 80 to 90 mg/kg/day divided BID; use amoxicillin-clavulanate if antibiotics were used within 30 days, with concurrent purulent conjunctivitis, or treatment failure.

What antibiotic is used for acute otitis media in a penicillin-allergic patient?

Cefdinir, cefuroxime, or ceftriaxone for non-anaphylactic allergy; azithromycin or clindamycin for severe type I hypersensitivity.

When is observation without antibiotics appropriate in acute otitis media?

Children 6 months to 2 years with unilateral non-severe disease, or children 2 years and older with non-severe unilateral or bilateral disease, when reliable follow-up in 48 to 72 hours is assured.

What is the classic presentation of otitis media with effusion versus acute otitis media?

Otitis media with effusion has a retracted or neutral TM with serous fluid, decreased mobility, and hearing loss without pain or fever, and does not require antibiotics.

What complication should be suspected in a child with otitis media and facial droop?

Facial nerve palsy from middle ear infection, requiring urgent ENT consultation, IV antibiotics, and myringotomy.

What is tympanic membrane perforation?

A hole in the tympanic membrane caused by infection, barotrauma, penetrating injury, or blast injury, resulting in sudden pain relief, hearing loss, and possible otorrhea.

What is the classic presentation of traumatic TM perforation?

Sudden severe ear pain followed by immediate relief, conductive hearing loss, tinnitus, and possible bloody otorrhea after Q-tip insertion, slap to the ear, or blast.

What findings suggest an associated inner ear injury with TM perforation?

Vertigo, nystagmus, or sensorineural hearing loss, which suggest ossicular disruption or perilymph fistula and require emergent ENT consultation.

What is the ED management of an uncomplicated traumatic TM perforation?

Keep the ear dry, avoid irrigation and ototoxic drops, provide analgesia, and arrange ENT follow-up; most perforations heal spontaneously within weeks to months.

When are antibiotics indicated for TM perforation?

Contaminated water exposure, associated otitis media, or penetrating trauma; use fluoroquinolone otic drops, never aminoglycosides.

What percentage of traumatic TM perforations heal spontaneously?

Approximately 80 to 90 percent heal without intervention; larger or non-healing perforations may require tympanoplasty.

What is vertigo?

The false sensation of movement or spinning caused by dysfunction of the vestibular system, classified as peripheral (inner ear or vestibular nerve) or central (brainstem or cerebellum).

What features distinguish peripheral from central vertigo?

Peripheral: sudden onset, severe symptoms, horizontal or rotary fatigable nystagmus suppressed by fixation, hearing loss or tinnitus, no neuro deficits. Central: gradual onset, milder vertigo, vertical or direction-changing non-fatigable nystagmus, ataxia, and neurologic deficits.

What is the HINTS exam and how is it interpreted?

Head Impulse, Nystagmus, Test of Skew in acute continuous vertigo; a central cause is suggested by a NORMAL head impulse test, direction-changing nystagmus, or the presence of skew deviation.

What maneuver diagnoses and what maneuver treats BPPV?

Dix-Hallpike maneuver diagnoses (delayed fatigable upbeat-torsional nystagmus); Epley canalith repositioning maneuver treats it.

What is the classic presentation of Meniere disease?

Episodic vertigo lasting minutes to hours with fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness, caused by endolymphatic hydrops.

How does vestibular neuritis differ from labyrinthitis?

Vestibular neuritis causes vertigo without hearing loss; labyrinthitis causes vertigo WITH sensorineural hearing loss.

What is the ED treatment of acute peripheral vertigo?

Vestibular suppressants for short-term symptom relief (meclizine, benzodiazepines), antiemetics, IV fluids for dehydration, and steroids for vestibular neuritis; avoid prolonged suppressant use, which delays compensation.

What must be excluded in an older patient with new vertigo and vascular risk factors?

Posterior circulation stroke, particularly cerebellar or lateral medullary (Wallenberg) infarct; MRI with diffusion-weighted imaging is preferred since CT misses most posterior fossa strokes.

What is angioedema?

Nonpitting subcutaneous or submucosal swelling of the face, lips, tongue, larynx, or bowel caused by histamine-mediated or bradykinin-mediated increases in vascular permeability.

How do histaminergic and bradykinin-mediated angioedema differ?

Histaminergic angioedema has urticaria, pruritus, and responds to epinephrine, antihistamines, and steroids; bradykinin-mediated (ACE inhibitor and hereditary) has no urticaria or itching and does NOT respond to these agents.

What is the priority in any patient with angioedema in the ED?

Airway assessment; signs of stridor, voice change, drooling, or tongue or floor of mouth swelling mandate early definitive airway management, ideally awake fiberoptic nasotracheal intubation with double setup for surgical airway.

When can ACE inhibitor angioedema occur relative to starting the drug?

Any time from hours to years after initiation, most commonly in the first week but frequently after months of use; the drug must be discontinued permanently.

What is the underlying defect in hereditary angioedema?

C1 esterase inhibitor deficiency or dysfunction leading to unopposed bradykinin production; screen with low C4 level.

What targeted therapies treat hereditary angioedema attacks?

C1 esterase inhibitor concentrate, icatibant (bradykinin B2 receptor antagonist), ecallantide (kallikrein inhibitor), or fresh frozen plasma when these are unavailable.

What is the treatment of allergic angioedema with airway involvement?

IM epinephrine 0.3 to 0.5 mg (0.01 mg/kg in children) in the anterolateral thigh, plus H1 and H2 blockers and corticosteroids, with airway monitoring.

What is dacryoadenitis?

Inflammation or infection of the lacrimal gland producing pain and swelling of the superolateral upper eyelid.

What is the classic physical exam finding in dacryoadenitis?

S-shaped curve deformity of the upper eyelid with tenderness and swelling over the lateral third of the lid, and possible lateral conjunctival injection.

What organisms cause acute bacterial dacryoadenitis?

Staphylococcus aureus and Streptococcus species; viral causes include Epstein-Barr virus, mumps, and adenovirus.

How is dacryoadenitis distinguished from dacryocystitis?

Dacryoadenitis affects the lacrimal gland in the superolateral upper lid; dacryocystitis affects the lacrimal sac in the inferomedial canthus and produces purulent discharge from the punctum with pressure.

What is the ED management of bacterial dacryoadenitis?

Warm compresses, oral antibiotics such as amoxicillin-clavulanate or first-generation cephalosporin, analgesia, and ophthalmology follow-up; IV antibiotics and CT if orbital extension is suspected.

What findings in dacryoadenitis warrant urgent CT imaging?

Proptosis, restricted extraocular movements, decreased visual acuity, or fever, which suggest orbital cellulitis or abscess.

What is a dental abscess?

A localized collection of pus from a bacterial infection of the tooth pulp (periapical) or supporting periodontal structures that can spread into deep neck spaces.

How is a periapical abscess distinguished from a periodontal abscess?

Periapical abscess originates in a necrotic pulp with pain on percussion and a nonvital tooth; periodontal abscess arises in the gingival sulcus alongside a vital tooth.

What is Ludwig angina and why is it a true emergency?

Rapidly spreading bilateral cellulitis of the submandibular, sublingual, and submental spaces, usually from a mandibular molar infection, that elevates the tongue and causes airway obstruction and death.

What are the classic findings of Ludwig angina?

Woody, brawny induration of the submandibular area, elevated tongue, trismus, drooling, muffled voice, fever, and inability to handle secretions.

What is the management of Ludwig angina?

Immediate airway assessment with preparation for awake fiberoptic intubation or cricothyrotomy, IV ampicillin-sulbactam or clindamycin, CT neck with contrast, and emergent ENT or oral surgery consultation.

What is the ED treatment of a simple localized dental abscess?

Incision and drainage if fluctuant, analgesia including dental block with bupivacaine, oral antibiotics (amoxicillin, penicillin VK, or clindamycin), and urgent dental follow-up for definitive treatment.

What deep space infections can result from spread of dental abscesses?

Ludwig angina, retropharyngeal abscess, parapharyngeal abscess, mediastinitis, and cavernous sinus thrombosis via the pterygoid plexus.

What are dental caries?

Progressive demineralization and destruction of tooth enamel and dentin caused by acid-producing bacteria, primarily Streptococcus mutans, in dental plaque.

Why do dental caries matter in the emergency department?

They are the most common cause of atraumatic dental pain and can progress to pulpitis, periapical abscess, and life-threatening deep space infections.

How is reversible pulpitis distinguished from irreversible pulpitis?

Reversible pulpitis causes brief pain with hot, cold, or sweet stimuli that stops when the stimulus is removed; irreversible pulpitis causes prolonged, spontaneous, often nocturnal pain lasting minutes to hours.

What is the ED management of dental caries with pain but no abscess?

Analgesia with NSAIDs plus acetaminophen, dental nerve block for severe pain, temporary filling material if a cavity is exposed, and urgent dental referral; antibiotics are NOT indicated without infection.

Which nerve blocks are useful for dental pain in the ED?

Inferior alveolar nerve block for lower teeth, supraperiosteal infiltration or infraorbital block for upper anterior teeth, and posterior superior alveolar block for upper molars.

What is epiglottitis?

Acute inflammation and edema of the epiglottis and supraglottic structures that can rapidly progress to complete airway obstruction.

Why has the epidemiology of epiglottitis shifted, and who gets it now?

Widespread Haemophilus influenzae type b vaccination shifted the disease predominantly to adults, now most often caused by Streptococcus, Staphylococcus aureus, and H. influenzae.

What is the classic presentation of epiglottitis?

The three Ds of Drooling, Dysphagia, and Distress, plus rapid-onset fever, muffled hot potato voice, stridor, and the tripod or sniffing position.

What lateral neck radiograph finding suggests epiglottitis?

The thumbprint sign, an enlarged, rounded epiglottis; radiographs are only appropriate in stable patients and should never delay airway management.

What is the gold standard for diagnosing epiglottitis?

Direct visualization by laryngoscopy or fiberoptic nasopharyngoscopy, performed in a controlled setting such as the operating room in children.

What is the critical management principle in pediatric epiglottitis?

Do not agitate the child, do not examine the pharynx with a tongue blade, keep the child with the caregiver in a position of comfort, and take the child to the OR for controlled intubation with ENT and anesthesia present.

What antibiotics are used for epiglottitis?

Third-generation cephalosporin (ceftriaxone or cefotaxime) plus vancomycin for MRSA coverage; add dexamethasone for airway edema.

What is laryngitis?

Inflammation of the larynx and vocal cords, most often from viral upper respiratory infection or vocal strain, causing hoarseness or aphonia.

What is the most common cause of acute laryngitis?

Viral infection, particularly rhinovirus, parainfluenza, influenza, and adenovirus; bacterial causes are uncommon.

What is the ED treatment of acute viral laryngitis?

Supportive care with voice rest, hydration, humidified air, and analgesics; antibiotics and steroids are generally not indicated.

What red flags in a hoarse patient warrant further evaluation?

Hoarseness lasting more than 2 to 3 weeks, stridor, dyspnea, dysphagia, hemoptysis, neck mass, or tobacco and alcohol use, raising concern for malignancy or airway compromise.

What causes of hoarseness must be excluded in the ED before diagnosing simple laryngitis?

Epiglottitis, angioedema, retropharyngeal abscess, inhalation or caustic injury, laryngeal trauma, and vocal cord paralysis.

What is laryngotracheobronchitis (croup)?

Viral infection causing subglottic airway inflammation and edema in children 6 months to 3 years, producing a barking cough and inspiratory stridor.

What is the most common causative organism of croup?

Parainfluenza virus type 1, followed by parainfluenza types 2 and 3, RSV, influenza, and adenovirus.