3.1 Otologic Emergencies
3.1.1 Sudden Hearing Loss
Key Features
Sudden hearing loss can be sensorineural or conductive in nature.
Audiogram is performed to differentiate between sensorineural and conductive hearing loss.
Idiopathic sudden sensorineural hearing loss is diagnosed when other causes have been excluded.
Early treatment of idiopathic sudden sensorineural hearing loss with oral and/or intratympanic steroids is commonly recommended.
Sudden hearing loss is the rapid onset of subjective hearing impairment over 72 hours or less. Sudden sensorineural hearing loss (SSNHL) is one type of sudden hearing loss. The potential causes of SSNHL are broad: infection, vascular insult, trauma, autoimmune, neoplasm, acoustic trauma, drug-related, iatrogenic, and idiopathic. One common criterion used to define SSNHL is at least a 30-decibel (dB) reduction in sensorineural thresholds in at least three consecutive frequencies compared to baseline. Early implementation of high-dose systemic and/or intratympanic steroids is commonly recommended.
Epidemiology
SSNHL affects 5 to 20 per 100,000 people in the United States. Men and women are affected equally. Most commonly it affects middle-aged people.
Clinical
Signs and Symptoms
Patients may report sudden subjective hearing loss, ear fullness, and/or tinnitus in one or both ears. Dysequilibrium or vertigo can also occur. A history of upper respiratory tract infection, head trauma, cardiac surgery, ototoxic drug intake, otologic surgery, barotrauma, and loud noise exposure may precede onset of symptoms. Preexisting history or family history of autoimmune disorder may be ascertained.
Differential Diagnosis
Idiopathic SSNHL is diagnosed when other causes have been excluded. The potential causes of SSNHL are broad and include viral infections, syphilis, vascular insult, trauma, autoimmune disease, internal auditory canal or cerebellopontine angle neoplasm, acoustic trauma, ototoxic drugs, barotrauma, perilymphatic fistula, endolymphatic hydrops, Menière′s disease, and iatrogenic injury. Middle ear or external auditory causes such as middle ear effusion and cerumen impaction are causes of conductive hearing loss and should be excluded.
Evaluation
Physical Exam
A complete head and neck examination, including cranial nerve assessment, should be performed. External and middle ear disorders should be assessed on otoscopy. Neurologic exam can identify signs of central or systemic disorders. Vestibular exam can demonstrate any associated vestibular weakness. A tuning fork and fistula test are important as well.
Audiometry
Pure tone and speech audiometry and tympanogram are required. Causes of conductive hearing loss can be excluded on these examinations. A poor word recognition score out of proportion to pure tone thresholds and rollover should raise suspicion for a retrocochlear lesion. A low-frequency sensorineural hearing loss is suspicious for endolymphatic hydrops or Menière′s disease. A notch at 3 to 4 kHz suggests acoustic trauma. A commonly accepted definition for SSNHL is a reduction in sensorineural hearing of at least 30 dB in at least three contiguous frequencies compared to baseline; however, in clinical practice, SSNHL includes hearing loss of lesser degrees.
Imaging
Magnetic resonance imaging (MRI) of the brain with and without gadolinium enhancement is obtained to rule out retrocochlear or cerebellopontine angle tumor.
Intracranial disorders can also be excluded on MRI. Auditory brainstem response (ABR) testing and follow-up audiometry are acceptable alternatives to MRI if appropriate counseling regarding limitations is performed. In patients with a presenting history of head trauma, computed tomography (CT) of the temporal bone without contrast is considered to assess for temporal bone fractures and pneumolabyrinth causing SSNHL.
Labs
Routine ordering of laboratory tests in patients with unilateral idiopathic SSNHL is not recommended. In patients with fluctuating and bilateral SSNHL, additional testing is suggested: (1) rapid plasma reagin (RPR) test or a fluorescent treponemal antibody absorption (FTA-ABS) test to rule out syphilis, (2) erythrocyte sedimentation rate (ESR) to screen for inflammatory disorder, (3) rheumatoid factor, antinuclear antibody, and antineutrophil cytoplasmic antibodies to assess for autoimmune etiology, (4) Lyme serology if risk factors are present, (5) thyroid function tests, (6) and (7) glucose testing for diabetes.
Treatment Options
Treatment is tailored to the etiology of SSNHL. However, approximately 85% of cases are considered idiopathic. SSNHL may resolve spontaneously in up to 65% of patients. Early treatment with oral and/or intratympanic steroids is commonly recommended as initial therapy for SSNHL, as prolonged delay in treatment may result in permanent hearing loss. Most clinicians prescribe oral prednisone (1 mg/kg daily) for 1 week with 1 week additional taper. Intratympanic dexamethasone has been used in various concentrations but usually requires at least three injections. Routine use of antivirals, thrombolytics, vasodilators, vasoactive substance, and antioxidants is not recommended. Hyperbaric oxygen therapy may be offered within three months of onset of idiopathic SSNHL.
Outcome and Follow-Up
Although approximately two-thirds of patients with idiopathic SSNHL experience some recovery without treatment, early treatment is associated with better hearing outcomes. Follow-up audiograms to assess for recovery or progression are performed within 6 months of diagnosis and treatment of idiopathic SNHL. Hearing rehabilitation is offered to patients with incomplete recovery. Tinnitus associated with hearing impairment should also be addressed and treated appropriately.
3.1.2 Ear and Temporal Bone Trauma
Key Features
Auricular injuries include lacerations, avulsions, blunt injury with hematoma, thermal injury, and frostbite. Treatment depends on etiology.
Penetrating and blunt trauma to the temporal bone can cause hearing loss, dizziness, facial paralysis, cerebrospinal fluid leak, and life-threatening hemorrhage. Early recognition and treatment of complications can reduce morbidity and mortality.
Penetrating and blunt trauma can affect all aspects of the ear and temporal bone, including the auricle, external auditory canal (EAC), tympanic membrane, ossicles, inner ear, carotid artery, venous sinuses, tegmen, and facial nerve. High suspicion and prompt recognition and treatment of associated temporal bone injuries is important in reducing trauma-related complications.
Epidemiology
The most common cause of temporal bone fractures is motor vehicle accidents. Assault is the second most common cause; males are more commonly affected. Approximately 20% of skull fractures involve the temporal bone. Soft tissue injuries to the auricle are common.
Clinical
Signs and Symptoms
Presentation depends upon the type of trauma and the location and extent of injury. Trauma to the auricle can be due to laceration, avulsion, blunt injury, thermal injury, or frostbite. Trauma to the temporal bone can be from acoustic trauma, barotrauma (e.g., diving), penetrating trauma (e.g., cotton tip applicator, gunshot wound), or blunt trauma (e.g., motor vehicle accident, assault). Thermal injury can also injure the tympanic membrane; for example, hot slag from a blast.
Auricular Injury
Blunt injury to the auricle may result in auricular pain, edema, erythema, and hematoma. Localized pain and bleeding are common after lacerations and avulsions of the auricle. Burn injuries can cause blistering, skin de-epithelialization, and cartilage exposure. The auricle is a common site of frostbite injury, which may present as a spectrum of findings over several weeks, from clear blistering, hemorrhagic blisters, or a dry insensate wound to blackened tissue demarcation and necrosis.
External, Middle, and Inner Ear Injuries
EAC trauma and traumatic tympanic membrane perforations can present with pain, bloody otorrhea, and conductive hearing loss. Injuries affecting the middle ear present as hemotympanum (blood in the middle ear) and/or conductive hearing loss and can involve ossicular fracture or discontinuity. Trauma involving the inner ear can cause sensorineural hearing loss (e.g., cochlear concussion, otic capsule violating fracture) and vertigo (e.g., benign paroxysmal positional vertigo, labyrinthine concussion, perilymphatic fistula, vestibular loss).
Other Injuries
Penetrating trauma and temporal bone fractures can involve the facial (fallopian) canal and cause immediate and delayed facial palsies. The perigeniculate area is the most common site of facial nerve injury in temporal bone fractures. Blunt trauma to the extratemporal facial nerve can also cause facial paralysis. Penetrating trauma and temporal bone fractures involving the middle cranial fossa plate, posterior cranial fossa plate, or otic capsule can cause leakage of cerebrospinal fluid (CSF) into the temporal bone, which can manifest as clear middle ear effusion, otorrhea, or rhinorrhea. Injuries to the horizontal and vertical petrous internal carotid artery, sigmoid sinus, or jugular bulb can cause life-threatening hemorrhage and hemodynamic instability.
Temporal Bone Fractures
Temporal bone fractures are most often seen in patients with severe head trauma. Additional injuries requiring resuscitation and multi-team care are common. ENT findings may include otorrhea, hearing loss, nystagmus, and facial paralysis. A bruise over the mastoid (Battle sign) is an indication of fracture of the middle cranial fossa and injury of the posterior auricular artery. Periorbital ecchymosis (raccoon eyes) suggests a basal skull fracture.
Temporal bone fractures are classified as either otic-sparing or otic-violating fractures. Otic-violating fractures are more commonly associated with sensorineural hearing loss. Older classifications divide temporal bone fractures with respect to the long axis of the petrous pyramid ( Fig. 3.5 ): (1) longitudinal fracture (oriented along the petrous axis, parallel to the petrotympanic fissure), (2) transverse fracture (oriented perpendicular to the petrous axis), (3) oblique (oriented along the petrous axis, crossing the petrotympanic fissure), or (4) mixed fractures.
Oblique/longitudinal fractures represent 80% of all temporal bone fractures (~25% associated with facial nerve injury). Transverse fractures are less common; however, 40 to 50% are associated with facial palsy. Transverse fractures more commonly affect the otic capsule and cause sensorineural hearing loss.
Differential Diagnosis
There is a broad range of causes of trauma and associated injuries, some of which have been listed in preceding paragraphs.
Evaluation
Physical Exam
Soft tissue injuries isolated to the auricle are evaluated with a focused otologic exam. Exposed cartilage, auricular hematoma, and auricular viability should be noted.
Patients with severe head or multisystem injury should receive standard trauma and resuscitation. Life-threatening injuries (e.g., cervical spine trauma, intracranial bleeding) must be treated emergently, and the patient should be stabilized. Complete head and neck, otologic, neurologic, and cranial nerve examinations are recommended.
When feasible, immediate or delayed facial paralysis should be assessed early and prior to intubation. The ear canal should be cleaned, and injuries to the EAC and tympanic membrane should be assessed. Presence of CSF leak should be ascertained. Hearing can be evaluated with a 512-Hz tuning fork, and the presence and type of nystagmus should be noted.
In patients with less severe injury, a more focused exam is feasible. Foreign body or penetrating injuries should be evaluated with an oto-microscope. In uncooperative children, there should be a low threshold for exam under anesthesia.
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