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OTOLOGY TABLE OF CONTENTS:
Otology On-call Consult Podcast Episodes:
EAR FOREIGN BODIES
Overview
Ear canal foreign bodies are most commonly seen in pediatric patients, although occasionally in adults. Patients can present with self-admission/sibling story, witnessed placement, unilateral foul-smelling otorrhea, and ear pain. In most adults and older cooperative children, ear canal foreign bodies can be removed at bedside with the use of an otic speculum, headlight, loupes, and otologic instruments. If an ear microscope is available, this should be used preferentially over loupes and a headlight as this may reduce the risk of inadvertent trauma to the ear canal and tympanic membrane. If the patient is not tolerant of bedside instrumentation, sedation in the Emergency Department or evaluation in the OR may be necessary, especially if several failed attempts have been made. Rocks, popcorn kernels, and other small smooth round objects may be difficult to retrieve without inadvertently pushing the object medially. In these cases, it is often best to carefully advance a small microhook just beyond the object to pull it out. In some cases, having a second set of hands to help retract the tragus and gently apply posterior pinna traction can allow for improved visualization and bimanual removal of the foreign body. After removal, if ear canal skin or tympanic membrane are irritated, antibiotic/steroid drops or steroid drops alone can be helpful. In patients who exhibit tympanic membrane trauma such as perforation, a follow-up with audiogram is pertinent to assess for hearing loss.
Key Supplies for Ear Foreign Body Consultation
Otoscope, loupes, and headlight
Ear microscope if available
Right angle hook
Loop curette
Alligator or microcups forceps
5 or 7 French Frazier tip suction
Management
Imaging is not generally indicated unless middle ear trauma suspected.
Visualize item with otoscope, develop plan for which tool would best remove it.
Right angle useful for objects with sharp edges, soft objects that you can hook, or smooth round objects.
Alligator forceps or microcups are useful for flatter objects that can be grasped.
If live insect is seen in canal, consider killing the insect prior to removal by filling ear canal with mineral oil.
Review plan thoroughly with patient and family prior to procedure.
Visualize well with speculum, headlight, and loupes, or preferably ear microscope if available.
Locate gap where instrument (loop/right angle) can be passed just distal to object without ear canal trauma, or where object can be grasped.
Remove atraumatically and efficiently because children will not always permit multiple attempts at bedside; have a low threshold for removal in the OR for challenging cases.
After removal, complete an otologic exam to assess for injury to the tympanic membrane and ear canal.
If tympanic membrane injury present:
Consider otic antibiotic drops.
Audiogram.
Otolaryngology follow-up.
Consider otic antibiotic/steroid drops (i.e., ciprofloxacin/dexamethasone) if significant canal laceration or edema.
Follow-up with Primary Care is reasonable unless significant canal laceration or concern of other injuries.
Example Procedure Note
Procedure: Ear foreign body removal
After discussion of risks and benefits, written consent was obtained. The patient was restrained by the mother/father/family member, and visualization of the ___ ear canal was obtained with the ear microscope and ear speculum. The foreign body was visualized in the mid canal. A right angle hook was carefully inserted just deep to the object and was used to remove the foreign body atraumatically. Following removal, the ear was inspected and seen to be mildly edematous without any lacerations or tympanic membrane injury. The patient tolerated the procedure well.
References
1. Friedman EM. VIDEOS IN CLINICAL MEDICINE. Removal of Foreign Bodies from the Ear and Nose. N Engl J Med. 2016;374(7):e7. doi:10.1056/NEJMvcm1207469
2. Lotterman S, Sohal M. Ear Foreign Body Removal. In: StatPearls. Treasure Island (FL): StatPearls Publishing; March 25, 2020.
3. Olson MD, Saw J, Visscher S, Balakrishnan K. Cost comparison and safety of emergency department conscious sedation for the removal of ear foreign bodies. Int J Pediatr Otorhinolaryngol. 2018;110:140-143.
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ACUTE OTITIS EXTERNA
Overview
Acute otitis externa, colloquially known as “swimmer’s ear,” is an acute inflammation of the external auditory canal with a typically infectious etiology. Acute otitis externa is frequently seen and treated by Primary Care providers who consult our specialty when patients have recurrent, severe, or unresponsive disease. The common presenting symptoms include otalgia, otorrhea, aural fullness, pruritis, and hearing loss. On exam, traction of the pinna or pressure on the tragus typically results in significant pain. In some cases, concomitant parotid gland swelling can be seen secondary to the connection between the anterior external auditory canal and parotid space via the fissures of Santorini. The pathogenesis of acute otitis externa is thought to result from disruption of the protective cerumen barrier and naturally occurring acidic pH of the external auditory canal, epithelial injury including maceration from water exposure or moisture, and bacterial inoculation. This can be caused by mechanical trauma from cotton swabs and hearing aid use or from retained moisture from water exposure, external auditory canal masses, or dermatologic conditions such as psoriasis or eczema. Mechanical disruption and moisture cause epithelial damage allowing for growth of pathologic bacteria or fungi, most commonly Pseudomonas aeruginosa followed by Staphylococcus species. Fungal otitis externa, while less commonly the offending pathogen in acute otitis externa, is thought to play a more significant part in chronic otitis externa. Immunocompromised or diabetic patients are at higher risk for acute and chronic otitis externa.
Key Supplies for Acute Otitis Externa Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope
Cerumen curette
Consider culture swab
Ear wick with medium alligator forceps for placement
Anti-pseudomonal ototopical drops (e.g., ofloxacin or Ciprodex®), if available
If cleaning debris from the ear canal, will need operating microscope, size 3, 4, or 5 ear speculums, size 5 or 7 straight suction, and suction source
Management
Complete history with attention to otologic history including cotton swab or hearing aid use, water exposure, skin conditions such as psoriasis and eczema, and diabetes.
Complete detailed head and neck exam with tuning fork tests (may need to repeat after debridement if the ear canal is occluded); look for other concomitant dermatologic conditions affecting the scalp or extremities.
Treatment focuses on drying and debriding the ear canal, acidifying the ear canal, and eradicating infectious pathogens.
Carefully suction the ear canal, inspect the tympanic membrane for perforations if possible (avoiding ototoxic, acidic, or alcohol drops if present), and survey for signs of other diseases (Ramsay Hunt syndrome, cancer of the external auditory canal, otitis media with perforation, etc.); in some cases, the ear canal may be too edematous or painful to see the tympanic membrane.
Culture of the external auditory canal drainage is generally indicated if the infection is severe or the patient is immunosuppressed or unresponsive to prior treatment; cultures are generally not taken in routine uncomplicated acute otitis externa.
Place ear wick if canal edema is severe and prohibits ototopical medication from reaching the medial external auditory canal.
To place an ear wick, grasp the end of the ear wick with a medium sized alligator forceps; while visualizing the canal under microscopy, slowly advance the end of the wick until it is bridging the most inflamed portion of the external auditory canal, being careful not to plunge the wick into the tympanic membrane; may need to place two wicks side-by-side if the entire canal is edematous.
If case is mild and tympanic membrane intact, acetic acid may be effective.
Antibiotics drops with or without steroids are generally recommended for moderate or severe disease; see common commercially available options below.
Ciprodex® (ciprofloxacin and dexamethasone): Widely available and well-tolerated; can be expensive.
Ciprofloxacin drops: Widely available and less expensive compared to Ciprodex® but lacks steroid component that may be helpful with canal edema.
Cortisporin® (polymyxin, neomycin, and hydrocortisone): Widely available and inexpensive but has a >10% incidence of atopic reactions to neomycin.
Explain proper application technique: Contralateral ear on pillow, place drops in affected external auditory canal, press or “pump” tragus to improve medial penetration, and remain with treated ear up for at least 5 minutes.
Generally reserve systemic antibiotics for patients with extension beyond the ear canal (auricular chondritis or facial extension), immunocompromised patients or those with poorly controlled diabetes, and patients with a history of temporal bone irradiation.
Dry ear precautions for minimum of 2 weeks following symptomatic resolution.
Patients can usually be managed as an outpatient with reassessment and debridement in 2-3 days. If patient has not improved by that time, consider more advanced disease such as malignant otitis externa, antimicrobial resistance, contact dermatitis to prescribed drops, noncompliance or poor application technique, external auditory canal carcinoma, and other rare pathology. Inpatient management may be required for patients with high risk features and evidence of more severe infection.
We recommend the AAO-HNS Clinical Practice Guideline on acute otitis externa for additional reading on this topic.
Example Procedure Note
Procedure: Ear canal cleaning and placement of ear wick
After obtaining written and verbal consent, the patient’s head was turned, and an ear speculum was gently inserted. The ear canal appeared ___. Debris was gently removed the from external auditory canal using ___ (insert here if culture obtained). Care was taken to ensure the tympanic membrane was not violated. Next, an ear wick was gently inserted and inflated using ototopical drops. The patient tolerated the procedure relatively well.
References
1. Linstrom, C.J., Lucente, F.E. (2013). Diseases of the External Ear. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2333-2357). Baltimore, MD: Lippincott Williams & Wilkins.
2. Naples, J.G., Brant, J.A., Ruckenstein, M.J. (2020). Infections of the External Ear. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2093-2100). Philadelphia, PA: Elsevier.
3. Rosenfeld, R.M., Schwartz, S.R., Cannon, C.R., et al. (2014). Clinical Practice Guideline: Acute Otitis Externa. Otolaryngology–Head and Neck Surgery, 150(1_suppl), S1–S24.
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PERICHONDRITIS AND AURICULAR HEMATOMA
Overview
Auricular perichondritis most commonly occurs following trauma such as with cartilage piercings, lacerations, insect bites, or with certain sports such as wrestling. Signs of perichondritis include auricular flaking, loss of natural folds of the pinna, erythema, weeping, and tenderness. In certain cases, trauma may be associated with auricular hematoma development. Perichondritis and auricular hematoma, if left untreated, may lead to eventual abscess formation and cartilage necrosis. Early identification of hematoma and abscess formation improves outcomes if drained to prevent impending ischemia of the cartilage. Untreated auricular perichondritis, auricular hematoma, and auricular abscess can have a dramatic cosmetic impact leaving the patient with “cauliflower ear” or complete loss of recognizable structures of the auricle. Oral antibiotics with cartilage penetration are generally required. Fluroquinolones are the preferred antibiotic choice due to their cartilage penetration, although local antibiograms must be considered as Pseudomonal resistance to fluroquinolones nears 30% in some areas. If fluoroquinolones are prescribed, patients should be counseled regarding the associated risk of tendinopathy and arthropathy, although this can typically be managed by abruptly stopping the antibiotic at the first sign of pain without lasting deleterious effect. Intravenous antibiotics should be considered in patients with severe disease or an immunosuppressed state. If a fluid collection is evident (usually through fluctuant swelling) drainage with bolster placement is generally advisable. Although less common, spread of infection from acute otitis externa to the periauricular soft tissue, auricular cartilage, and skin requires prompt identification and initiation of systemic antibiotics. Lastly, recurrent perichondritis without known antecedent trauma should raise suspicion for relapsing polychondritis. This classically presents with sparing of the fatty lobule of the ear, and often presents in patients with other systemic manifestations of the underlying autoimmune disease.
Key Supplies for Perichondritis and Auricular Hematoma Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope
Cerumen curette
Consider culture swab
Ear wick with small alligator forceps for placement
If cleaning debris from the ear canal, will need operating microscope, size 3, 4, or 5 ear speculums, size 5 or 7 straight suction, and suction source
For hematoma or abscess drainage and bolster, will need iodine or alcohol swabs, 15- or 11-blade scalpel, angiocatheter and saline flushes, 3-0 Prolene® or silk suture for bolster, and Xeroform® gauze or dental rolls
Management
Complete history (including any recent trauma to the auricle) and physical exam with attention to the middle ear, mastoid (ensure no mastoid tenderness or fluctuance), and external ear, with detailed documentation of the extent of the infection (facilitates tracking response to treatment).
Drain auricular hematoma or abscess if present, usually needle aspiration or small stab incision with 15-blade scalpel, flush thoroughly with saline, apply topical antibiotic ointment, and use a suture bolster (dental rolls often work well for this purpose).
Obtain cultures from the abscess if present or if able to express any purulence from the auricle.
No imaging indicated unless concern for malignant otitis externa, mastoiditis, or other more severe underlying infection.
Labs generally not necessary unless systemic symptoms are present or in high risk patients.
Initiate systemic antibiotics.
Consider fluoroquinolones given strong cartilage penetration.
Counsel all patients, especially pediatric patients, on the risk of arthropathy and tendinopathy if fluoroquinolones prescribed.
Mild cases can be managed as outpatient, with close follow-up within 2-3 days. More severe cases may require admission for IV antibiotics and close monitoring.
References
1. Linstrom, C.J., Lucente, F.E. (2013). Diseases of the External Ear. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2333-2357). Baltimore, MD: Lippincott Williams & Wilkins.
2. Naples, J.G., Brant, J.A., Ruckenstein, M.J. (2020). Infections of the External Ear. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2093-2100). Philadelphia, PA: Elsevier.
3. Rosenfeld, R.M., Schwartz, S.R., Cannon, C.R., et al. (2014). Clinical Practice Guideline: Acute Otitis Externa. Otolaryngology–Head and Neck Surgery, 150(1_suppl), S1–S24.
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MALIGNANT OTITIS EXTERNA
Overview
Malignant otitis externa, sometimes referred to as necrotizing otitis externa or temporal bone osteomyelitis, represents an aggressive form of otitis externa that occurs almost exclusively in immunocompromised or diabetic patients. Classic findings include pain out of proportion to exam and granulation tissue at the osseocartilaginous junction. Paralleling uncomplicated acute otitis externa, the most common pathogen is Pseudomonas aeruginosa followed by Staphylococcus species. Spread of the infection along the skull base can lead to cranial nerve paresis (predominantly affecting the facial nerve), bony erosion, and intracranial spread leading to complications such as meningitis, abscess, and venous sinus thrombosis. The long-term prognosis of this disease is variable (10-20% mortality); however, patients with a reversible underlying disease state, such as diabetes, typically have an improved prognosis if managed appropriately.
Key Supplies for Malignant Otitis Externa Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope
Cerumen curette
Consider culture swab
Ear wick with alligator forceps for placement
Anti-pseudomonal ototopical drops (e.g., ofloxacin or Ciprodex®), if available
If cleaning debris from the ear canal, will need operating microscope, size 3, 4, or 5 ear speculums, size 5 or 7 straight suction, and suction source
Management
Complete history with focus on any prior otologic history, immunosuppression, diabetes (including recent hemoglobin A1C), and temporal bone radiation.
Complete detailed head and neck exam with focus on the external auditory canal and middle ear, cranial nerves, and hearing using tuning fork tests.
Carefully debride the ear canal under microscopy.
Culture of drainage and antibiotic sensitivity studies are useful to guide long-term antibiotic selection.
Lab tests should include CBC, CMP, CRP, ESR, hemoglobin A1C, and blood cultures if patient is showing systemic symptoms; additional tests may be considered based on clinical context.
Imaging is indicated when malignant otitis externa is suspected.
High-resolution temporal bone CT is excellent for initial assessment of bony erosion; however, it may underestimate soft tissue and intracranial involvement.
MRI internal auditory canal and brain with and without contrast demonstrates skull base and intracranial disease extent; at many centers contrast enhanced MRI has become the imaging modality of choice to diagnose and follow disease progression and course.
Nuclear medicine Technetium-99 scan is the traditional diagnostic imaging modality of choice due to its high sensitivity to osteoblastic activity before bony destruction would be visible on CT; however, osteoblastic activity continues after infection resolution, and thus this scan cannot be reliably used to monitor progress after diagnosis.
Gallium-67 radiolabeled leukocyte study detects active inflammation and may be useful for monitoring resolution of infection.
Start systemic antibiotics; generally requires inpatient admission.
Mild cases with early detection can be treated with extended oral antipseudomonal therapy, such as with ciprofloxacin.
Moderate or severe cases require IV antibiotic therapy with antipseudomonal coverage. Culture results may direct treatment and Infectious Disease should be consulted to guide antibiotic management.
Most patients will require a minimum of a 4-week course of antibiotics. Duration of antibiotic therapy is often guided by symptomatic improvement and imaging findings. Note that imaging findings often lag behind clinical improvement.
Medical management and reversal of underlying immunocompromising disease state may improve prognosis.
Close inpatient monitoring of otologic symptoms, cranial nerve status, and imaging based on clinical need.
Surgical treatment is infrequently required and is generally reserved for cases with abscess development and rarely for persistent disease that does not resolve with long-term antibiotic treatment.
References
1. Linstrom, C.J., Lucente, F.E. (2013). Diseases of the External Ear. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2333-2357). Baltimore, MD: Lippincott Williams & Wilkins.
2. Naples, J.G., Brant, J.A., Ruckenstein, M.J. (2020). Infections of the External Ear. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2093-2100). Philadelphia, PA: Elsevier.
3. Rosenfeld, R.M., Schwartz, S.R., Cannon, C.R., et al. (2014). Clinical Practice Guideline: Acute Otitis Externa. Otolaryngology–Head and Neck Surgery, 150(1_suppl), S1–S24.
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ACUTE OTITIS MEDIA, UNCOMPLICATED
Overview
Acute otitis media is defined as an acute infection of the middle ear for less than 3 weeks. This is distinct from the diagnosis of otitis media with effusion, which is the presence of a middle ear effusion without acute infection. Acute otitis media typically presents with a rapid onset of symptoms including otalgia, conductive hearing loss, and sometimes fever. In younger children, the symptoms may be nonspecific including irritability, fussiness, poor sleep, and ear pulling. Clinical diagnosis is made on otologic exam; signs typically include a bulging, erythematous tympanic membrane with or without purulent effusion or a perforated tympanic membrane with suppurative otorrhea. The most common pathogens associated with acute otitis media include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Differential diagnostic considerations should include otitis media with effusion (middle ear effusion, aural fullness, hearing loss, but without acute signs of acute infection), myringitis (otalgia with thickened erythematous tympanic membrane), otitis externa, ear trauma, or referred pain from pharyngitis or the temporomandibular joint.
Key Supplies for Acute Otitis Media (Uncomplicated) Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope
512-Hertz tuning fork
Consider culture swab if otorrhea present
Ototopical antibiotic drops (e.g., ofloxacin or Ciprodex®), if available
Management
Complete history with focus on any prior otologic history.
Complete detailed head and neck exam with focus on the external auditory canal and middle ear, cranial nerves, and hearing using tuning fork tests.
Carefully clean the ear canal under microscopy if necessary for visualization.
Lab tests generally not indicated unless concern for complicated disease or systemic process.
Imaging generally not indicated unless concern for complicated disease.
Antibiotic management is recommended in most cases.
In patients 6-23 months of age with non-severe unilateral disease, watchful waiting may be offered for 48-72 hours from onset of symptoms; generally antibiotic therapy should be recommended in all other cases.
Most typical cases of acute otitis media can be successfully treated with amoxicillin.
Patients who have been treated with amoxicillin within the last 30 days, have an allergy to penicillin, or have failed prior therapy with amoxicillin should receive an alternative antibiotic to start.
Acute otitis media with tympanic membrane perforation may be treated with ototopical antibiotics, most commonly ciprofloxacin/dexamethasone drops.
Treatment should improve symptoms in first 48-72 hours; if symptoms persist or recur within the first several days, consider escalating antibiotic therapy for treatment failure.
Failure with amoxicillin alone or cases of recurrent or severe acute otitis media can be treated with amoxicillin-clavulanate, typically for 10 days.
Although uncommon, failure of oral medications may necessitate intramuscular or IV antibiotic therapy for both adults and children and consideration of tympanocentesis with culture-directed therapy.
In patients with pressure equalization tubes presenting with acute otitis media, ototopical antibiotics may be used as single therapy if the tubes are patent.
We recommend the AAO-HNS Clinical Practice Guidelines on otitis media with effusion and tympanostomy tubes in children for additional reading on these topics.
References
1. Arts, H.A., Adams, M.E. (2013). Intratemporal and Intracranial Complications of Otitis Media. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2399-2409). Baltimore, MD: Lippincott Williams & Wilkins.
2. Rosenfeld, R.M., Shin, J.J., Schwartz, S.R., et al. (2016). Clinical Practice Guideline: Otitis Media with Effusion (Update). Otolaryngology–Head and Neck Surgery, 154(1_suppl), S1–S41.
3. Rosenfeld, R.M., Schwartz, S.R., Pynnonen, M.A., et al. (2013). Clinical Practice Guideline: Tympanostomy Tubes in Children. Otolaryngology–Head and Neck Surgery, 149(1_suppl), S1–S35.
4. Schilder, A.G., Rosenfeld, R.M., Venekamp, R.P. (2020). Acute Otitis Media and Otitis Media with Effusion. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2956-2969). Philadelphia, PA: Elsevier.
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ACUTE OTITIS MEDIA (COMPLICATED) INCLUDING MASTOIDITIS
Overview
Rarely, untreated acute otitis media can progress to extracranial or intracranial complications. Most commonly, the Otolaryngologist will be consulted for “possible mastoiditis” when fluid is detected within the mastoid air cells on CT. It is important to remember that the mastoid is in direct communication with the middle ear space through the antrum, and therefore fluid in the mastoid alone in the setting of acute otitis media can be expected. As such, acute mastoiditis is a diagnosis that is primarily made clinically, rather than radiographically, although imaging findings of coalescence or subperiosteal abscess are strongly indicative. Physical exam typically demonstrates erythema, postauricular edema, tenderness over the mastoid process, and possible proptosis (anterior and inferior displacement of the pinna). The contralateral mastoid can often serve as a good “normal” comparison. It is also important to note that in many cases, the Otolaryngologist will be asked to evaluate incidental (and often asymptomatic) limited mastoid “fluid” found on CT or MRI that generated the concern for mastoiditis. This finding is quite common and again, in the absence of symptoms or physical exam findings, does not usually constitute true clinical mastoiditis.
Rapid diagnosis and treatment are critical as a diagnosis of acute mastoiditis is associated with an elevated risk of temporal bone, neck, and intracranial complications. In cases of clinical mastoiditis with neurologic symptoms, head CT or MRI with and without contrast should be performed to rule out intracranial involvement. Additionally, CT or MRI angiography with venography may be useful to assess for dural sinus thrombosis more specifically. With acute mastoiditis, treatment will often consist of inpatient admission, IV antibiotics, and potentially ototopical therapy. Surgery is often warranted for treatment of subperiosteal abscess or other complications. Intratemporal and intracranial complications are described below.
Key Supplies for Acute Otitis Media (Complicated) Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope
512-Hertz tuning fork
Consider culture swab if otorrhea present
Ototopical antibiotic drops (e.g., ofloxacin or Ciprodex®), if available
If performing tympanostomy tube placement, will need operating microscope, size 4 or 5 ear speculum, myringotomy blade, size 5 or 7 straight suction, suction source, and device to push tube in place (e.g., pusher or small right angle)
Management
Complete history with focus on any prior otologic history, symptom timeline and progression, and underlying medical conditions, especially immunosuppressing conditions.
Complete detailed head and neck exam with focus on the external auditory canal and middle ear, cranial nerves, and hearing using tuning fork tests.
Carefully clean the ear canal under microscopy.
Lab tests should include CBC and CMP; can consider CRP, ESR, and blood cultures if systemic symptoms.
Imaging should be performed if concern for complicated disease.
CT Temporal Bone: May usually be performed without contrast unless concern for disease involvement of the neck or intracranial space.
MRI Brain: Consider if concern for intracranial involvement; consider angiography with venography if concern for dural sinus thrombosis.
Antibiotic management is recommended in virtually all cases of complicated acute otitis media.
Acute otitis media with tympanic membrane perforation or tube placement may be treated with ototopical antibiotics in addition to systemic antibiotics; common topical therapy includes ciprofloxacin/dexamethasone drops.
For systemic antibiotics, consider IV antibiotics for patients being admitted or with proven or suspected complicated disease.
Consider tympanocentesis or tympanostomy tube placement for culture-directed therapy.
Cortical mastoidectomy may be considered for more adequate source control depending on clinical context (see below).
Intracranial complications as listed below warrant Neurosurgery consultation.
Intratemporal Complications
Coalescent Mastoiditis
More advanced disease characterized by destruction of the mastoid bony septa, often associated with subperiosteal abscess.
Abscess evident on contrast enhanced CT.
Fluctuance over the mastoid process may be appreciated.
Broad spectrum antibiotic therapy with or without tympanostomy tube placement is generally advisable; consider contrast-enhanced head CT or MRI angiography and venography to rule out intracranial involvement if concerning temporal bone CT findings present or neurological changes develop.
In cases of subperiosteal abscess, postauricular incision and drainage, cortical mastoidectomy, and pressure equalization tube placement is commonly pursued.
May develop concomitant abscess involving the insertion of the sternocleidomastoid muscle (i.e., Bezold abscess), digastric groove (i.e., Citelli abscess) or at the root of the zygoma (i.e., Luc abscess).
Petrous Apicitis
Occurs when the infection extends medially into the air cells of the petrous apex.
Symptoms classically characterized by Gradenigo’s triad of otorrhea, retroorbital pain, and diplopia from abducens nerve palsy, although this full triad of symptoms is frequently not present.
Not all patients have a pneumatized petrous apex, so CT utility is often limited and comparison with the contralateral side along with obtaining MRI may be necessary.
CT will usually show destruction of the bony septa of the petrous apex and MRI will classically exhibit T1 hypointense, T2 hyperintense fluid with peripheral or diffuse enhancement after gadolinium administration (characteristics of abscess or severe inflammation).
Often managed with IV antibiotics with or without pressure equalization tube placement but can require surgical debridement in more severe or recalcitrant cases.
Facial Paralysis
Occurs secondary to nerve edema or compression from suppurative acute otitis media.
Generally requires prompt treatment with a pressure equalization tube, oral and ototopical antibiotics, and high-dose oral corticosteroids if not medically contraindicated; consideration of simple cortical mastoidectomy along with pressure equalization tube placement.
Serous and Suppurative Labyrinthitis
Rare complications diagnosed clinically following a rapid progression of vertigo, nystagmus, tinnitus, and sensorineural hearing loss.
Treatment geared towards preventing further complications (e.g., meningitis) and supportive care with antibiotics and pressure equalization tube placement.
Disequilibrium may persist for weeks and hearing loss may be permanent.
Intracranial Complications
Meningitis
Most common intracranial complication, especially in children.
Evaluate for classic symptoms including headache, fever, nuchal rigidity, photophobia, seizures, and altered mental status.
Diagnosis involves lumbar puncture (usually after CT obtained to rule out increased intracranial pressure and signs of herniation).
Treatment requires high-dose IV antibiotics, possible steroids, and consideration of tympanocentesis or tympanostomy tube placement for culture data; Neurosurgery consultation is recommended.
Patients should be monitored for sensorineural hearing loss and if present, serial MRI should be considered to survey for labyrinthitis ossificans as this may impact timing of cochlear implantation in cases of profound loss.
Subdural Abscess
Patients generally present with neurologic symptoms such as headache, delirium, seizures, lethargy, and focal neurologic deficits.
Diagnosis often requires MRI with gadolinium to differentiate findings from non-enhancing reactive subdural effusion.
Treatment involves high-dose IV antibiotics, possible mastoidectomy, and Neurosurgery consultation for cranial abscess drainage.
Epidural Abscess
When symptomatic, patients generally present with a temporoparietal headache and often with mental status changes.
Diagnosis often requires MRI with gadolinium, which shows biconvex disk-shaped enhancement.
Neurosurgery consultation is recommended for surgical drainage.
Treatment involves high-dose IV antibiotics and surgical drainage via a transmastoid approach or craniotomy, depending on location.
Intraparenchymal Brain Abscess
Patients may be asymptomatic in the setting of a well-organized abscess; if symptomatic, may have a temporoparietal or diffuse headache, change in mental status, fever, seizures, or focal neurological deficit.
Treatment involves IV antibiotics, Neurosurgery consultation for drainage, and possible mastoidectomy for source control.
Lateral Sinus Thrombosis and Thrombophlebitis
Often found in association with an epidural abscess, patients will commonly exhibit a headache, “picket fence” spiking fevers, and Griesinger’s sign (edema and pain over mastoid from occlusion of a mastoid emissary vein).
Primary risk surrounds the possibility of a propagating clot and resultant elevated intracranial pressure or intracranial abscess.
Diagnosis often includes MRI with gadolinium with MR angiography with venography, which will demonstrate thrombus formation; CT with and without contrast may demonstrate the empty delta sign, characterized by enhancement of the sinus wall and loss of central vein enhancement.
Treatment typically involves IV antibiotics and mastoidectomy; the benefits of sigmoid decompression, thrombus evacuation, and anticoagulation in this setting are controversial.
Otitic Hydrocephalus
Phenomena of increased intracranial pressure without associated dilation of ventricles; can be secondary to lateral sinus thrombosis.
Patients present with symptoms of increased intracranial pressure (e.g., nausea, vomiting, papilledema, diplopia secondary to abducens nerve palsy).
Symptoms are often chronic in nature and can present weeks beyond resolution of acute otitis media.
Risk of blindness secondary to elevated intracranial pressure.
Treatment aims to eradicate underlying infection and otologic complications, lower intracranial pressure, and mitigate ophthalmologic complications.
Example Procedure Note
Procedure: Myringotomy with pressure equalization tube placement
After obtaining written and verbal consent, the patient’s head was turned, an ear speculum was inserted, and obstructing cerumen was gently removed under the operating microscope. The tympanic membrane appeared ___. Topic anesthesia was obtained using ___. A posteroinferior myringotomy was fashioned with a myringotomy blade, the middle ear was suctioned (insert here if culture obtained), and a pressure equalization tube was placed. Ototopical drops were instilled and a cotton ball was placed. The patient tolerated the procedure well.
References
1. Arts, H.A., Adams, M.E. (2013). Intratemporal and Intracranial Complications of Otitis Media. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2399-2409). Baltimore, MD: Lippincott Williams & Wilkins.
2. Rosenfeld, R.M., Shin, J.J., Schwartz, S.R., et al. (2016). Clinical Practice Guideline: Otitis Media with Effusion (Update). Otolaryngology–Head and Neck Surgery, 154(1_suppl), S1–S41.
3. Rosenfeld, R.M., Schwartz, S.R., Pynnonen, M.A., et al. (2013). Clinical Practice Guideline: Tympanostomy Tubes in Children. Otolaryngology–Head and Neck Surgery, 149(1_suppl), S1–S35.
4. Schilder, A.G., Rosenfeld, R.M., Venekamp, R.P. (2020). Acute Otitis Media and Otitis Media with Effusion. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2956-2969). Philadelphia, PA: Elsevier.
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SUDDEN SENSORINEURAL HEARING LOSS
Overview
Sudden sensorineural hearing loss (SSNHL) is classically defined as sensorineural hearing loss that occurs acutely in 3 days or less and of 30 dB or greater in at least three contiguous frequencies. It is important to note that sudden hearing loss below this arbitrary threshold can still be clinically significant and therefore generally deserves treatment. Most patients do not have a previous recent hearing test for comparison, so the degree of hearing loss is usually inferred by comparing to the contralateral ear. The most common associated symptoms include tinnitus and aural fullness. When SSNHL presents with vertigo, the constellation of symptoms is commonly termed “labyrinthitis.” Sudden sensorineural hearing loss harbors a wide differential diagnosis and treatment may be time sensitive; therefore, sudden hearing loss generally requires urgent evaluation. An audiogram is a critical component of the evaluation and will differentiate between SNHL and conductive hearing loss. Otoscopy can rule out cerumen impaction, effusion, or other causes of conductive hearing loss. Tuning fork testing can provide gross information on conductive versus sensorineural hearing loss; however, early formal audiometric testing is crucial to definitively quantify the magnitude and type of hearing loss and provide a baseline to follow.
While SSNHL is most commonly idiopathic, this is a diagnosis of exclusion and other etiologies should be ruled out with appropriate work-up based on history and exam findings. Additional etiologies include but are not limited to autoimmune hearing loss, various infections, endolymphatic hydrops (i.e., Meniere’s disease), acoustic trauma, retrocochlear pathology such as vestibular schwannoma, stroke, and malingering (see table below). If the patient has no medical contraindications (e.g., uncontrolled diabetes), treatment with high-dose oral steroids should be strongly considered and administered as soon as feasible, as earlier use generally portends a better outcome. This is often given in combination with GI ulcer prophylaxis. Intratympanic steroid injections can also be initiated upfront or can be reserved for salvage treatment. Additional salvage therapy of hyperbaric oxygen therapy can be offered depending on severity of hearing loss, logistics, and patient preference. Practically speaking, hyperbaric oxygen is not commonly pursued in most practices.
Regardless of improvement in hearing loss, whether spontaneous or post-treatment, patients should undergo contrast enhanced head MRI to rule out any underlying retrocochlear pathology (e.g., vestibular schwannoma); in patients who cannot undergo MRI for various reasons, auditory brainstem responses or head CT with contrast can be used, although less sensitive and reliable. If the clinical history and imaging work-up is negative, the SSNHL is termed idiopathic, and prognosis generally follows the rule of thirds: one-third of patients will recover completely, one-third will recover to a degree, and one-third will not recover at all. Younger patients, those with less severe hearing loss, low frequency hearing loss, and patients without vertigo have a better prognosis for improvement.
Key Supplies for SSNHL Consultation
Otoscope
512-Hertz tuning fork
If performing transtympanic steroid injection, will need operating microscope, size 4 or 5 ear speculum, phenol and applicator (optional), size 3 or 5 straight suction, suction source, 27-gauge needle, and 1-2 mL syringe
Management
Detailed history
Otologic history (otalgia, otorrhea, aural fullness, tinnitus, vertigo).
Time course of hearing loss.
Previous episodes.
Recent head trauma.
Associated eye symptoms (e.g., keratitis seen in Cogan’s syndrome).
New cranial nerve weakness or hypoesthesia.
History of recent travel or tick exposure.
Medication use (e.g., narcotics, sildenafil, etc.).
Past medical history with attention to meningitis, autoimmune conditions or vasculitis, diabetes, or other possible contributing pathologies.
Perform a complete head and neck physical exam, with specific attention to the otologic, cranial nerve, and tuning fork exams.
Obtain audiogram as soon as possible, preferably same day.
Consider high dose steroids (consider 1 mg/kg prednisone to max dose of 60 mg) if no contraindications and initiate as soon as feasible. Duration is controversial and an area of ongoing research, but treatment duration typically continues for 5-10 days, and in many cases includes a taper. Providers should discuss risks and benefits of use with patients before prescribing oral steroid therapy, and all dosing is dependent on individual patient circumstances and risk factors. Steroids are often not prescribed if beyond 4-6 weeks after the episode of sudden hearing loss based on uncertain benefit.
Lab testing is not routinely ordered; consider targeted labs if suspicion of underlying conditions (e.g., ANA, ESR, RF, RPR/VDRL).
Transtympanic steroid injections can also be initiated immediately or can be delayed and used as salvage therapy if oral steroids fail; optimally should be initiated within 2 weeks of hearing loss.
Position patient in a comfortable position in exam chair.
Under binocular microscopy, can consider the application of pinpoint phenol to the posterior superior quadrant (note that phenol use is controversial and may increase patient’s risk of long-term tympanic membrane perforation).
Consider making a separate small ventilation hole with a 27-gauge needle; this is not required.
Inject approximately 1 mL of steroid solution (commonly dexamethasone, preferably warmed to body temperature) into posterior quadrant using a 27-gauge needle until middle ear is filled based on meniscus level.
Keep patient supine with their head turned to the contralateral ear for 10-30 minutes based on provider preference, while attempting to avoid swallowing.
Protocols vary but oftentimes injections are performed weekly for 3 weeks.
Consider hyperbaric oxygen treatment within up to 3 months of the hearing loss depending on severity, patient preference, logistics, response to steroid treatment, and ability to equalize pressure in ears (will need pressure equalization tubes to tolerate dive pressures if unable to equalize).·
Head MRI with gadolinium or high-resolution heavily T2-weighted sequences to rule out retrocochlear pathology in all patients regardless of hearing recovery; consider auditory brainstem responses or CT if patient is unable to undergo MRI.
Follow-up with patient following treatments and stabilization of hearing, usually around 3 months, and offer rehabilitative measures if residual hearing is not sufficiently useful (conventional or contralateral routing of signals [CROS] hearing aid, bone-anchored hearing implant, or cochlear implantation).
We recommend the AAO-HNS Clinical Practice Guideline on SSNHL for additional reading on this topic.
Example Procedure Note
Procedure: Transtympanic steroid injection
After obtaining written and verbal consent, the patient was positioned supine in the exam chair. Visualization of the tympanic membrane was obtained with binocular microscopy with removal of cerumen as necessary. A 27-gauge needle was used to create a pinpoint ventilation hole and 1 mL of ___ mg/mL dexamethasone, warmed to body temperature, was slowly injected into the middle ear with a 27-gauge needle in the posterior quadrant of the tympanic membrane and confirmed to fill the middle ear space. The patient was kept laying in the supine position for 30 minutes. The patient tolerated the procedure well.
References
1. Chandrasekhar, S.S., Tsai Do, B.S., Schwartz, S.R., et al. (2019). Clinical Practice Guideline: Sudden Hearing Loss (Update). Otolaryngology–Head and Neck Surgery, 161(1_suppl), S1–S45.
2. Le Prell, C.G. (2020). Sensorineural Hearing Loss in Adults. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2311-2327). Philadelphia, PA: Elsevier.
3. Oliver, E.R., Hashisaki, G.T. (2013). Sudden Sensory Hearing Loss. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2589-2596). Baltimore, MD: Lippincott Williams & Wilkins.
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ACUTE FACIAL NERVE PARALYSIS
Overview
Acute onset paresis or paralysis of the facial nerve, defined as an onset of less than 72 hours, has a wide differential diagnosis including idiopathic or Bell’s palsy, various viral and bacterial infections, skull base osteomyelitis, primary neoplasms (e.g., facial nerve schwannoma, geniculate hemangioma) anywhere along the course of the facial nerve, malignancy with direct or perineural invasion, autoimmune conditions, trauma, and stroke (see table below). This chapter details the appropriate work-up and early management strategies for the most common etiology of acute facial nerve paralysis: Bell’s palsy. Facial paralysis secondary to temporal bone trauma, penetrating facial lacerations, and otitis media is covered in separate respective chapters. Bell’s palsy is a diagnosis of exclusion and the primary concern in the early management of these patients is an accurate diagnosis, early initiation of high dose steroids, consideration for antiviral therapy, and prevention of corneal injury from impaired eye closure.
Bell’s palsy presents as a sudden onset unilateral facial weakness that involves weakness of the entire involved hemiface. Some patients experience prodromal otalgia. Bell’s palsy can occur in any demographic, but patients at higher risk include pregnant women and patients with diabetes, upper respiratory infection, or immunodeficiency. Most cases of Bell’s palsy show some recovery in facial function within 2-4 weeks of onset. Approximately 70% of patients with Bell’s palsy with complete paralysis (House-Brackmann grade VI) and 94% of patients with incomplete paralysis will recover normal facial function within 6 months of onset. Symptoms or signs that should raise suspicion for a cause of acute facial nerve paralysis other than Bell’s palsy include auricular vesicular eruption (Ramsay Hunt, also known as herpes zoster oticus syndrome), concomitant cranial neuropathies (skull base pathology or systemic conditions such as granulomatosis with polyangiitis or sarcoidosis), otorrhea or middle ear effusion (complicated otitis media or cholesteatoma), target skin rash (Lyme disease), indolent progression (malignancy or primary facial nerve tumors), segmental involvement (cutaneous or parotid malignancy), other concomitant neurological symptoms (stroke or other central neurological process), bilateral involvement (systemic disease or Guillain-Barre syndrome), and lack of recovery within 3 months of onset.
Key Supplies for Acute Facial Nerve Paralysis Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope
512-Hertz tuning fork
Management
History
Unilateral or bilateral.
Timing and rate of progression.
Acute: Less than 72 hours and often 24 hours to nadir.
Associated symptoms (fever, dizziness, diplopia or other sign of concomitant cranial neuropathy, any pain, otorrhea, dysgeusia, hyperacusis, dysarthria or other neurologic signs, etc.).
History of trauma.
History of similar events in the past (raises concern of Melkersson-Rosenthal Syndrome, especially if accompanied by facial edema and fissured tongue).
History of target rash (Lyme disease) or vesicular rash (Ramsay Hunt syndrome) around ear.
History of ear surgery or other notable ear history.
History of other non-melanoma skin cancer or parotid malignancy.
Complete history including past medical history, medications, allergies, past surgical history, family history, and social history.
Physical Exam
Detailed head and neck physical exam with attention to the ear, facial nerve, and other cranial nerves.
Otoscopic exam to evaluate ear canal, tympanic membrane, and middle ear.
Evaluate for otitis media, ear canal drainage, or evidence of ear canal or middle ear masses.
Evaluate for concomitant perichondritis, rash of the ear or ear canal, vesicular eruption, or parotid swelling.
Idiopathic facial nerve paralysis (Bell’s palsy) generally demonstrates a normal ear exam.
Facial nerve exam usually recorded using House-Brackmann grade (see below) with attention to sparing of upper division or any segmental involvement.
Examine skin of face, cheek, upper neck, and scalp for malignancy.
512-Hertz tuning fork exam.
Brief neurological exam (especially critical if anything in history or head and neck exam suggests central process).
Labs and Imaging
Acute onset facial nerve paralysis without other concerning history or findings is indicative of Bell’s palsy and imaging and labs are not generally necessary, unless other atypical findings develop or recovery is not seen within 3 months.
A temporal bone CT may be indicated for evaluation of trauma or facial nerve paralysis in the setting of complicated otitis media or malignant otitis externa.
In the acute setting, CT may be indicated if concern of neurologic process; however, ultimately, a head MRI will likely be required.
In most cases, an audiogram is not obtained unless hearing loss is reported.
Targeted labs may be indicated if concern of infectious or autoimmune pathology.
Treatment of Bell’s Palsy
Initiate high dose systemic steroid treatment within 72 hours of onset; patients should be counseled regarding the risks of systemic steroids, including but not limited to changes in mood, disrupted sleep, increase in blood pressure, increase in blood glucose levels, GI bleed (relatively rare), and avascular necrosis of the hip (rare). Options include prednisone 1 mg/kg to max dose of 60 mg for 10 days with taper for adults.
Strongly consider concomitant GI ulcer prophylaxis with a proton pump inhibitor.
Use of antivirals is controversial but can be considered in the setting of Bell’s palsy and particularly if suspicion for Ramsay Hunt (herpes zoster oticus) syndrome.
Dosing based on immunocompetency and renal function; can consider acyclovir or valacyclovir.
If suspicion of Ramsay Hunt syndrome, higher dosing is warranted and consider Infectious Disease consultation and Ophthalmology consultation if involvement of the orbit.
Aggressive eye care to prevent exposure keratitis.
Daytime drops (artificial tears).
Night-time eye lubricant.
Eye moisture chamber during sleep or tape eye shut.
Electrodiagnostic testing in select cases.
Not recommended if incomplete paralysis.
Can consider electroneuronography (ENoG; also known as evoked electromyogram) if the patient has a complete unilateral paralysis (House-Brackmann grade VI), it has been at least 3 days since onset of paralysis and not more than 14 days since onset of paralysis, and you are considering facial nerve decompression.
ENoG showing <90% reduction in amplitude compared to the normal side: Good prognosis for spontaneous recovery, decompressive surgery not recommended.
ENoG showing >90% reduction in amplitude compared to normal side: May still recover but worsened prognosis, decompressive surgery may be considered.
Close follow-up for all patients to assess facial nerve recovery and adequate eye care.
Counseling for Patients with Bell’s Palsy
Good prognosis for patients with incomplete paralysis: Over 90% complete recovery.
Fair prognosis for patient with complete paralysis: Over 70% complete recovery.
Maintain aggressive eye care.
Tight glucose control if diabetic, especially if starting steroids.
Should seek medical attention if other neurological symptoms develop.
Should reconsider the diagnosis of Bell’s palsy if other symptoms develop or the patient fails to show recovery within 3 months of onset.
References
1. Baugh, R.F., Basura, G.J., Ishii, L.E., et al. (2013). Clinical Practice Guideline: Bell’s Palsy. Otolaryngology–Head and Neck Surgery, 149(3_suppl), S1–S27.
2. Vrabec, J.T., Lin, J.W. (2013). Acute Facial Nerve Paralysis. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2503-2518). Baltimore, MD: Lippincott Williams & Wilkins.
3. Mattox, D.E., Vivas, E.X. (2020). Clinical Disorders of the Facial Nerve. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2587-2597). Philadelphia, PA: Elsevier.
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TEMPORAL BONE TRAUMA
Overview
The temporal bone houses several important structures including the otic capsule containing the cochlea and vestibular labyrinth, facial nerve, ossicles, and carotid canal. Furthermore, its superior and medial boundaries comprise the dura of the middle fossa and posterior fossa, respectively. Thus, temporal bone fractures may result in temporary or permanent facial nerve injury, hearing loss (conductive, sensorineural, or mixed), vertigo, CSF leak, or meningitis. Fractures of the temporal bone typically require significant force and therefore frequently occur in association with other significant maxillofacial, skull base, or cranial injuries. Diagnosis is made most often following emergent head or maxillofacial CT in the trauma bay. Typically, head CTs have thick cuts that may not adequately capture small structures in the temporal bone and additional imaging may be required.
Evaluation and management of temporal bone trauma typically ensues following general trauma stabilization. Patient evaluation should assess for injuries involving the critical structures within the temporal bone. The most important information to document upon patient arrival to the hospital is facial nerve function. If a patient has facial nerve paralysis at the time of evaluation, it would be important to attempt to determine if this occurred immediately after the injury or in a delayed fashion. This may be challenging to elicit, because many patients experience polytrauma and facial nerve function is often not prioritized during an initial in-field assessment. Symptomatically, patients will most commonly experience conductive hearing loss secondary to hemotympanum, tympanic membrane tear, or external auditory canal occlusion from soft-tissue injury or debris. However, temporal bone fractures can violate the otic capsule and thereby cause sensorineural hearing loss. Although patients with major traumatic injuries may be intubated and sedated, effectively precluding a good facial nerve and audiological assessment, a 512-Hertz tuning fork exam in an awake patient can be helpful. Concomitant vertigo and associated nystagmus should also raise concern for otic capsule involvement.
As the consulting Otolaryngologist, a careful radiologic review of available temporal bone imaging should be performed. It is often helpful to review the scans with the Neuroradiology team if any questions arise. A systematic review of structures should include evaluation of the otic capsule, internal auditory canal, facial nerve path, ossicles, external auditory canal, middle and posterior fossa bony plates, temporomandibular joint, and vascular structures (carotid and sigmoid). Prognostically, otic capsule-involving fractures are more likely to have facial nerve injury, CSF leak, and sensorineural hearing loss. Identification of fluid signal in the mastoid, air in the labyrinth (i.e., pneumolabyrinth) and intracranial air (i.e., pneumocephalus) – fluid where air should be and air where fluid should be – offer immediate and reliable clues to injury of the respective regions. The astute resident should also use the contralateral ear as a “control” to ensure that normal sutures and other structures (e.g., singular canal, cochlear aqueduct) are not misinterpreted as fracture lines.
Classification Schema
Historically, temporal bone fractures were classified based on their relationship with the long axis of the petrous ridge. Under this classification, longitudinal fractures occurred in parallel to the petrous ridge whereas transverse fractures occurred in perpendicular orientation to the petrous ridge, most commonly traversing the foramen magnum. Transverse fractures are considered less common than longitudinal fractures but portend increased risk of facial nerve injury and otic capsule involvement. Fractures are now commonly classified as otic capsule sparing or violating.
Key Supplies for Temporal Bone Trauma Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope
512-Hertz tuning fork
Cerumen curette
Suction trap if fluid collection for CSF analysis is anticipated
Ear wick
If cleaning debris from the ear canal, will need operating microscope, size 3, 4, or 5 ear speculum, size 5 or 7 straight suction, and suction source
Complications and Management
Facial Nerve Injury
Documentation of the timing and severity of facial nerve paresis is key. The House-Brackmann facial nerve scale is a convenient way to record facial nerve function.
Facial nerve paresis (partial weakness) or delayed facial nerve paralysis carry a more favorable prognosis compared to immediate onset complete facial nerve paralysis.
Facial nerve paresis or paralysis, regardless of timing, is typically treated with high-dose corticosteroids (such as oral prednisone) if not medically contraindicated.
In the setting of significant facial weakness, careful attention must be paid to the patient’s eye closure.
Patients with lagophthalmos should be given artificial tears, lubricating eye ointment, and precautions to avoid inadvertent corneal injury (e.g., moisture chamber at night while sleeping).
In the setting of immediate complete facial nerve paralysis (House-Brackmann grade VI), surgical exploration with decompression may be considered, particularly when impinging bone fragments or clear radiological involvement of the fallopian canal can be seen on imaging. Although controversial, electroneuronography (EnOG) can be obtained if one is contemplating facial nerve decompression.
Degeneration of greater than 90% on EnOG and confirmation with EMG indicates more severe injury and further supports considering facial nerve exploration and decompression.
Close follow-up to monitor facial nerve function and related complications.
Hearing Loss
External auditory canal skin laceration is very common. Bedside debridement is recommended to allow for treatment with ototopical antibiotics. In some cases, circumferential lacerations may benefit from stenting with ear wick placement.
In the acute setting, conductive hearing loss secondary to hemotympanum, tympanic membrane tear, or ossicular chain disruption is typically treated conservatively with observation.
Sensorineural hearing loss stemming from an otic capsule-involving fracture can be treated with high-dose corticosteroids, although outcomes are variable. Patients with otic capsule involvement will also commonly have associated vertigo and nystagmus on exam.
Early after the injury, a 512-Hertz tuning fork exam is important to perform. A Weber test (tuning fork placed firmly on midline, such as the forehead or central maxillary incisors) will lateralize to the size with better sensorineural function or the side with the greater conductive hearing loss. The Rinne test is used to distinguish sensorineural from conductive hearing loss for each individual ear. In a normal healthy ear, air conduction (tuning fork held 2-4cm from the external auditory canal) should be greater than bone conduction (tuning fork firmly pressed on mastoid process). A person with temporal bone trauma and isolated conductive hearing loss will usually have a Weber that lateralizes to the affected ear, and on Rinne testing bone conduction will be greater than air. A crude bedside test using the phone dial tone can also be considered. An early audiogram with bone conduction thresholds should be obtained if sensorineural hearing loss is suspected.
If only conductive hearing loss is suspected and imaging does not reveal otic capsule involvement, a formal audiogram is generally obtained about 8-12 weeks after injury to allow for resolution of middle ear fluid and inflammation. Surgical treatment may be indicated in large persistent conductive hearing loss.
CSF Leak
While CSF leaks are relatively uncommon, patients should be evaluated for CSF otorrhea or rhinorrhea, especially in cases of otic capsule or skull base violation. Draining fluid suspected to be CSF can be tested for Beta 2-transferrin, which is highly sensitive and specific for CSF. Notably, a halo or ring sign is not sensitive or specific for a CSF leak.
Because most traumatic CSF leaks self-resolve, initial management is conservative and aims to reduce intracranial pressures with head of bed elevation to 30 degrees, limited activity, stool softeners, and avoidance of straining.
Use of prophylactic antibiotics is controversial, although commonly administered.
Lumbar drains are typically avoided in the early setting.
Persistent CSF leak beyond 1-2 weeks may require surgical repair.
Others
Persistent vertigo is uncommon but may be associated with posttraumatic BPPV, otic capsule fracture, or perilymphatic fistula.
Fractures involving the carotid canal should be evaluated with CT angiogram to rule out internal carotid dissection with Neurosurgery consultation if carotid injury is found.
References
1. Wilkerson, B.J., et al (2020). Management of Temporal Bone Trauma. In P.W. Flint, et al (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2207-2219). Philadelphia, PA: Elsevier.
2. Diaz, R.C., et al. (2013). Middle Ear and Temporal Bone Trauma. In J.J. Johnson, C.A. Rosen. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2410-2432). Baltimore, MD: Lippincott Williams & Wilkins.
3. Fusetti, S. et al. “Treatment of Temporal Bone (Lateral Skull Base).” AO Foundation Surgery Reference, https://surgeryreference.aofoundation.org/cmf/trauma/skull-base-cranial-vault/temporal-bone-lateral-skull-base
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TYMPANIC MEMBRANE PERFORATION
Overview
Although definitive treatment of a non-healing tympanic membrane perforation is generally elective, it is not uncommon that Otolaryngology is consulted in the Emergency Department or inpatient setting for evaluation of tympanic membrane perforations in the context of acute trauma, acute otitis media, or chronic perforation with acute suppurative otorrhea. Depending on the underlying cause and chronicity of the tympanic membrane perforation, perforations may present with conductive hearing loss, aural fullness, otalgia, and bloody or suppurative otorrhea. In addition, penetrating or blunt temporal bone or tympanic membrane trauma may result in vertigo, mixed or sensorineural hearing loss, CSF leak, or facial nerve injury. The clinical context, patient history, and physical exam will guide recommendations regarding acute evaluation and management. While CT may be performed in some cases depending on the circumstance, the conclusive diagnosis of a tympanic membrane perforation is determined via physical exam (careful otoscopy). While a tympanic membrane perforation alone is not considered an emergency per se, acute management requires ruling out any significant associated injury, addressing any concomitant infection or underlying condition, and optimizing the likelihood of spontaneous healing of the perforation.
Key Supplies for Tympanic Membrane Perforation Consultation
Appropriate PPE including mask, eye protection, gloves, and gown
Otoscope or endoscope
512-Hertz tuning fork
Cerumen curette
Suction trap if fluid collection for CSF analysis is anticipated
Ototopical antibiotic drops (e.g., ofloxacin or Ciprodex®), if available
If cleaning debris from the ear canal, will need operating microscope, size 3, 4, or 5 ear speculum, size 5 or 7 straight suction, and suction source
Broadly, when documenting physical exam findings, it is helpful to consider any pertinent findings as described below. With the exam, it is also prudent to remove any obstructing debris, purulence, or blood to visualize the tympanic membrane, using a microscope whenever feasible. If an endoscope and a recording device are readily accessible, consider photo-documenting the exam findings.
Physical Exam Considerations
State of the skin surrounding the ear (e.g., fluctuant, erythematous, tender, edematous/doughy, lacerated, tender to palpation).
State of the pinna and ear canal (e.g., narrowed, edematous, erythematous, tender to palpation, presence of blood or purulence, laceration, exposed bone, presence of debris or foreign body).
Approximate size of the perforation (i.e., approximate percent of the tympanic membrane involved); subtotal tympanic membrane perforation implies most of the pars tensa is absent; however, the peripheral annular edge is preserved. Other descriptive terms can be used such as “pinpoint” or “pressure equalization tube sized.”
Location of the perforation (e.g., pars tensa versus pars flaccida, anterior versus posterior to the malleus).
Nature of the perforation (e.g., central, not involving the annulus, or marginal that includes the annular rim).
Concomitant tympanic membrane findings including myringosclerosis, myringitis, retraction, crusting, or aural polyp.
State of the middle ear space (e.g., hemotympanum, purulence, inflamed mucosa, granulation tissue, foreign body, keratinizing epithelium).
Hearing should be tested using a 512-Hertz tuning fork. In most cases, one should expect the Weber to lateralize to the affected ear and bone conduction to be greater than air conduction, indicating a conductive hearing loss of greater than approximately 20 dB. The primary goal is to exclude acute inner ear injury that may result from temporal bone trauma with otic capsule fracture, subluxation of the stapes with traumatic perilymphatic fistula, or suppurative labyrinthitis, for example. In the acute setting, patients with these conditions may also report vertigo and exhibit nystagmus on exam.
Cranial nerve exam, with particular attention to facial nerve function.
Mechanism, Management, and Disposition
Acute Otitis Media with Perforation
Tympanic membrane perforation in the setting of acute otitis media typically manifests with progressive otalgia with subsequent otorrhea. In some cases, the ear canal may be inflamed and narrowed secondary to the acute infection, making it difficult to fully visualize the tympanic membrane. In other cases, a purulent bleb or medial inflammatory polyp may be present. For uncomplicated cases [refer to chapter “Acute Otitis Media (Uncomplicated)”] in otherwise immunocompetent patients, conservative suctioning of purulence from the ear canal, application of ototopical antibiotic drops for approximately 10 days, and avoidance of water in the ear canal will resolve the acute infection within 10-14 days. For a more severe infection, oral antibiotics can be considered. For immunocompromised patients, or in patients presenting with a more aggressive infection, temporal bone imaging, culture of purulent material, and inpatient treatment (or at very least close outpatient follow-up) should be considered. In otherwise healthy patients, a perforation from acute otitis media is expected to spontaneously heal within 3 months in most cases. The patient should avoid water exposure in the ear canal until the perforation is healed.
Barotrauma, Blast Injury, or Direct Tympanic Membrane Injury
Tympanic membrane perforations that develop as a result of barotrauma (e.g., scuba diving, open hand slap on ear, water skiing), blast injury (e.g., combat), or direct penetrating tympanic membrane injury (e.g., cotton swab, water irrigation) deserve special consideration. Perhaps more important than managing the acute perforation is promptly identifying and treating any potential concomitant inner ear injury. The potential mechanism(s) of inner ear injury include an acute large pressure differential or an acute mechanical injury to the tympanic membrane/ossicles that may lead to stapes footplate subluxation/dislocation, inner ear trauma, or tearing of the round window membrane. Patients developing tympanic membrane perforation from these mechanisms will usually report otalgia, hearing loss, and otorrhea. Symptoms that raise suspicion for concomitant inner ear injury include vertigo with or without straining, tinnitus, and hearing loss. On exam, the patient may exhibit nystagmus (generally spontaneous that may be provoked by Valsalva). A 512-Hertz tuning fork test should be performed to evaluate for sensorineural hearing loss. Generally, a person with a significant acute sensorineural hearing loss will lateralize a tuning fork to the unaffected side on the Weber test. The result of Rinne testing is more variable and largely depends on the magnitude of a conductive hearing loss or sensorineural hearing loss in the affected ear. In cases where there is a high suspicion for inner ear injury based on history, exam, or mechanism of injury, CT and an audiogram may be valuable to obtain in the acute setting. A CT may visualize a dislocated stapes footplate and possible pneumolabyrinth (i.e., air bubbles within the labyrinth). The audiogram may help confirm the type and magnitude of hearing loss.
If the patient is diagnosed with an uncomplicated tympanic membrane perforation without evidence of concomitant inner ear injury, then conservative measures including a short course of topical ear drops and maintaining dry ear precautions is generally sufficient. In such cases, the patient should follow-up routinely as an outpatient to ensure the tympanic membrane has healed, and generally an audiogram should be obtained thereafter to ensure there is no persistent conductive hearing loss, which may indicate ossicular discontinuity from trauma. While somewhat controversial, in some cases it may be advisable to orient or reposition any torn tympanic membrane leaflets outward to mitigate the risk of medial skin growth causing cholesteatoma. This should only be performed under microscope visualization by an experienced physician.
The management of cases with concomitant inner ear injury is nuanced and decision-making should be thoroughly discussed with the chief resident and attending physician. Broadly, if an acute perilymph fistula is suspected, options may include bedrest with stool softeners for a short time, steroid therapy, or early middle ear exploration for “patching” of the oval or round windows.
Chronic Otitis Media with Acute Exacerbation
Patients with a history of a chronic tympanic membrane perforation may develop an acute infection following water exposure or spontaneously. In most cases, the primary presenting symptoms include purulent otorrhea, hearing loss, and otalgia. Similar to patients presenting with acute otitis media and perforation, initial treatment for uncomplicated cases includes careful suctioning of purulence from the ear canal, application of ototopical antibiotic drops typically for 10-14 days, and avoidance of water exposure. Outpatient follow-up is generally recommended within the month to ensure the infection has fully resolved, and to ensure there is no evidence of underlying cholesteatoma or other potential causes.
Higher risk patients (e.g., immunocompromised, diabetic, etc.) and those presenting with features concerning for a more advanced infection may require imaging and inpatient treatment [refer to chapter “Acute Otitis Media (Complicated) Including Mastoiditis”].
Temporal Bone Trauma
Tympanic membrane perforations associated with temporal bone fracture are common. In many cases, a longitudinal or mixed fracture may be associated with ear canal skin laceration and tympanic membrane tear or perforation. The full algorithm for approaching temporal bone fractures can be viewed in the chapter “Temporal Bone Trauma.”
References
1. Diaz, R.C., Kamal, S.M., Brodie, H.A. (2013). Middle Ear and Temporal Bone Trauma. In Johnson, J.J., Rosen, C.A. (Eds.), Bailey’s Head and Neck Surgery-Otolaryngology 5e (pp. 2410-2432). Baltimore, MD: Lippincott Williams & Wilkins.
2. Prueter, J.C., Teasley, R.A., Backous, D.B. (2020). Clinical Assessment and Surgical Treatment of Conductive Hearing Loss. In Flint, P.W., et al. (Eds.), Cummings Otolaryngology Head and Neck Surgery 7e (pp. 2186-2196).Philadelphia, PA: Elsevier.
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