ED Management of Acute Hearing Loss: Pearls and Pitfalls
- Sep 10th, 2018
- Rachel Ely
Author: Rachel Ely, DO, MHA, NRP (EM Attending Physician, San Antonio, TX) // Editors: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)
A 34-year-old male presents with left-sided hearing loss, ear ringing, and a sensation of room spinning that he first noticed upon waking this morning. He denies any recent trauma or illness, and this has never happened before. He denies pain in the ear. He has mild nausea that accompanies his intermittent vertigo, but his primary concern is the noticeable hearing loss. He is otherwise healthy, takes no daily medications, and has never had any surgeries. His vitals are normal, as are his otoscopic and neurologic exams. You are reassured by his exam, but you are unsure how to proceed. What are the emergent conditions for which the patient needs evaluated? Is a normal head CT and some basic labs sufficient for work-up? Are there any treatments you can implement from the ED to improve his chances of recovery?
Sudden non-traumatic hearing loss is rare but can be a fear-provoking and functionally limiting experience for patients. Specifically, sudden hearing loss refers to a rapid decline in hearing over a 72-hour period of greaterthan 30dB in at least three contiguous frequencies in one or both ears.1 Hearing loss can be categorized as conductive, sensorineural, or mixed.2 Conductive hearing loss is a disorder of any of the structures that carry sound waves to the cochlea, such as the external ear, tympanic membrane, ossicles, etc.2,3 Sensorineural hearing loss results from damage to the sensory and neural transmission structures of the ear, such as the cochlea or auditory nerve, or higher aspects of central auditory perception or processing.2,3 There are approximately 4000 new cases per year in the United States.2,4 More than 80% of cases of sudden hearing loss are categorized as sensorineural.5 This review will focus on sudden sensorineural hearing loss (SSNHL).
Most cases of SSNHL are unilateral, and up to 90% are thought to be idiopathic.6 Up to 65% of patients with unilateral SSNHL will have complete spontaneous recovery within two weeks.6 However, it is important to recognize that while most cases have an unclear and relatively benign etiology, a minority of patients will have an underlying condition that is important to recognize to preserve the patient’s hearing. This is especially true in the case of bilateral SSNHL, which often suggests underlying systemic disease.6 Bilateral sudden hearing loss occurs inapproximately 2-8% of sudden SNHL patients andis associated with more severe hearing loss and has a poorer prognosis than unilateral deficits.6–8
Sudden SNHL is more likely to occur in men, and the incidence increases dramatically with increasing age.1 Patients may present with mild subjective decrease in unilateral hearing, the sensation of ear fullness, or with profound bilateral hearing loss. Often, the change in hearing is first noted upon waking for the day, and the initial complaint is the sensation of a full or blocked ear.2,6 Approximately 30-40% of patients will have vertigo, and the majority will have tinnitus; these symptoms seem to be independent of a conductive or sensorineural etiology.2 The average time to ENT presentation is 55 days, suggesting that patients do not often present at the time of symptom onset.9
The majority of cases of SSNHL are considered idiopathic.2 A theory of cochlear microvascular thrombosis is discussed as a possible explanation for many of these cases, though confirmatory testing is lacking.4 Approximately 1% of cases are related to retro-cochlear pathology, such as schwannoma, CVA, or demyelinating disease.4 Between 10-15% of patients will be found to have systemic infectious, inflammatory, or primary middle ear disease.4 The following section will review those etiologies that present the most urgent need for identification or that may be urgently intervened upon to improve patient prognosis.
Certain classes of medications are known to cause damage to either to the cochlear or vestibular division of the eighth cranial nerve, or to the structures of the inner ear itself, such as the cochlea or semicircular canals.10 Common offenders are aminoglycoside antibiotics (gentamycin, tobramycin), loop diuretics (furosemide), platinum-based chemotherapeutic drugs (carboplatin, cisplatin), macrolide antibiotics (clarithromycin, erythromycin), NSAIDS (aspirin), and anti-malarial drugs (quinine, chloroquine).10 Some of these deficits are reversible, such as in the case of loop diuretics, macrolides, and anti-malarials.10 Unfortunately, the damage caused by aminoglycosides and platinum-based drugs are irreversible.10 Chronic lead toxicity is also a known cause of sensorineural hearing loss, though the loss is typically gradual and unlikely to present with acute deficit.11 One review of bilateral SSNHL found that medication toxicity was one of the most prevalent causes of bilateral hearing loss.6
It is theorized that viral invasion of the cochlea or cochlear nerve, or direct damage to the cochlear hair cells, can lead to SSNHL.2,12 This may result from acute infection or reactivation of latent virus within the spiral ganglion.2 At least one study has found an association between young patients with chronic rhinosinusitis and incidence of SSNHL.13 A case series demonstrated found that some patients with SSNHL have been found at autopsy to have evidence of viral destruction of the temporal bone.14 Specifically, herpes zoster oticus can infiltrate and destroy the cochlea as well as the auditory nerve.12
Meningitis is a known etiology of sensorineural hearing loss but is unlikely to present with isolated hearing loss. However, meningitis from other than infectious causes (such as malignant or inflammatory) has been reported to present as acute hearing loss in rare circumstances.2 Lyme disease is a well-known cause of cranial nerve VII palsy but can also present with acute hearing loss, as it affects cranial nerve VIII.15 Syphilis is another infectious cause of sensorineural hearing loss and can present with either unilateral or bilateral symptoms with or without accompanying symptoms of vertigo or tinnitus.16
Endocarditis can lead to septic emboli, and in theory SSNHL could result from either cochlear artery occlusion or infection of the inner ear.7 A case report documents a patient ultimately diagnosed with endocarditis who initially presented with only unilateral hearing loss and fever.7
Vascular occlusion is suspected to play a significant role in idiopathic SSNHL but is difficult to demonstrate via histopathology in the microvasculature of the ear. Studies demonstrating an association of hypercoagulable states and cardiovascular risk factors with SSNHL support the theory of microvascular disease as a contributor to idiopathic SSNHL.4,17,18 However, certain vascular events can be specifically identified as contributing to sudden hearing loss. The cochlea has a tenuous blood supply without collateral circulation; therefore, any decrease in flow can lead to cochlear dysfunction.3 The internal auditory artery, also referred to as the labyrinthine artery, is a branch of the anterior inferior cerebellar artery (AICA), which arises from the basilar artery.2 The internal auditory artery supplies both the cochlea and the semicircular canals, and a vascular insult at this level often produces both hearing deficit and vertigo.2 Symptoms of a more proximal insult, such as in the AICA, may produce diplopia, nystagmus, ataxia, dysarthria, and Horner syndrome, in addition to hearing deficit and vertigo.2,5 Bilateral, simultaneous hearing loss accompanied by these symptoms may suggest a vertebral or basilar artery occlusion.2 A stroke affecting the primary auditory cortex is not commonly associated with symptomatic hearing loss.2
Cerebral venous thrombosis is sited as a rare care of SSNHL and is more typically accompanied by other symptoms such as headache, seizure, or other focal neurologic deficit, rather than in isolation.19 A theory of the mechanism of this hearing deficit is that the increased intracranial pressure in the subarachnoid space is conveyed to the perilymph and endolymphatic system. This may lead to increased inner ear pressure and cause cochlear damage, or the global increased intracranial pressure may directly cause dysfunction of the eighth cranial nerve.19 Another theorized mechanism is venous congestion and impaired drainage of the inner ear structures causing anoxia.19
Autoimmune inner ear disease is responsible for approximate 1% of acute sensorineural hearing loss.20 Unlike many other etiologies, presentation due to an auto-immune process is more likely to present with bilateral hearing deficit.2 Inflammatory conditions that can lead to SSNHL are systemic lupus erythematosus, rheumatoid arthritis, systemic vasculitis, sarcoidosis, myasthenia gravis, and multiple sclerosis, among others.20 Cogan’s syndrome is an auto-immune process that causes a symptom complex of corneal irritation, vertigo, and hearing loss.21
Approximately 3-10% of patients with presentations that prompt MRI will be found to have a tumor of the cerebellopontine angle.2 Such tumors, to include vestibular schwannoma, typically present with tinnitus, otalgia, ataxia, cranial nerve deficit, or limb weakness or clumsiness, but in some situations may present with unilateral sensorineural hearing loss.2 Typically the hearing loss is slowly progressive, but between 10-20% will report a more acute change in unilateral hearing.2
One theory of SSNHL is a mechanical defect of the intracochlear membrane, especially those patients with a truly acute hearing deficit.22 Barotrauma can also result in mixing of the endolymph and perilymphatic fluid, known as a perilymphatic fistula.23 This mixing results in a disruption of the fine electrolyte balance that exists between the two fluids within the cochlea.23 Trauma causing rupture or dislocation of the delicate structures that separate the endolymph and perilymph is challenging to demonstrate without histopathologic evidence.22 Despite this, it is not unreasonable to avoid additional trauma such as performing Valsalva maneuver in attempt to allow healing of the intracochlear structures.22
Intralabyrinthine hemorrhage (ILH) often presents with sudden unilateral partial or complete hearing loss and is almost universally accompanied by vertigo (incidence of 92%).24 Intralabyrinthine hemorrhage can be detected on MRI.24 Unfortunately, ILH has a worse prognosis than other causes of SSNHL, and hearing is often not completely recovered.24
In 2012, the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) published a clinical practice guideline for the evaluation and management of the patient presenting with acute sensorineural hearing loss.2 While the impetus in the ED may be to widely explore the broad differential potentially responsible for SSNHL, the diagnostic tests commonly available in the ED are often inadequate to detect the etiology, and for this reason a broad diagnostic net is discouraged.
The first priority is to distinguish sensorineural hearing loss from conductive hearing loss.2 The external and otoscopic exam is an important, but often unremarkable part of the evaluation, though removing a large cerumen impaction may both identify a conductive etiology and provide symptom resolution.2 The definitive diagnosis of sensorineural hearing loss requires audiometry, which is typically not available in the emergency department.25 One approach to differentiating conductive from sensorineural hearing loss is to perform Weber and Rinne testing.2 These tests are not well-supported by literature, but they can provide a preliminary diagnosis to guide work-up and management until specialty consultation is obtained.2
- Weber: Used to identify whether a lateralizing hearing deficit exists. A tuning fork is struck and placed on the midline of the top of the head. In a normal test, no lateralization occurs. In conductive hearing loss, the tone is perceived as louder in the affected ear. In sensorineural hearing loss, the tone is perceived as louder in the unaffected ear.
- Rinne: Used to differentiate conductive versus sensorineural deficit. Strike a tuning fork and place it on the patient’s mastoid. Ask the patient to indicate when they can no longer hear to tone; at that point, move the device in front of the ear. In an ear with normal conduction, the patient should still be able to hear the tone, since air conduction is perceived for longer than bone conduction. In conductive hearing loss, bone conduction is greater than air conduction, and the patient will not be able to hear the tone after it is removed from the mastoid.
Patients at highest risk of a significant systemic cause of SSNHL are those that have bilateral sudden hearing loss, recurrent episodes or unilateral hearing loss, or those with a concurrent neurologic deficit on exam.2,25 It is estimated that between 10-31% of patients with SSNHL will have an identifiable etiology on contrast-enhanced MR.2,26 The 2012 clinical practice guidelines set forth by the AAO-HNS recommend appropriate imaging of all patients with SSNHL, though patients without high-risk features may be able to defer imaging to an outpatient setting.2 When considering work-up for these patients, it is important to be aware that commonly available diagnostic modalities, such as CT imaging of the brain, are of low yield and are not recommended.2 In their guideline, the AAO-HNS specifically recommends against CT of the head in patients with suspected SSNHL, unless they present with a focal neurologic finding or recent history of trauma, and based on this clinical practice guideline the Choosing Wisely campaign has also recommended against non-contrast CT of the head in isolated acute hearing loss.2,27 Gadolinium-enhanced thin sectioned MR detects tumors of the internal auditory canal with a sensitivity of greater than 98%, and even certain non-contrast enhanced MR protocols have excellent sensitivity, though are less sensitive in detection of etiologies beyond tumors of the IAC.26,28 A systematic review of CT imaging of the brain and temporal bones in children demonstrated a diagnostic yield of ranging from 7% to 74%.29 The imaging modality of choice to evaluate for retrocochlear pathology is MRI brain, brainstem, and internal auditory canals (IACs) with gadolinium enhancment.26 MRI can identify retro-cochlear lesions such as vestibular schwannoma and can also visualize cochlear inflammation, evidence of cerebral ischemia, or pathology such as multiple sclerosis.2 In the likelihood that MRI is not available in the ED or when MRI is contraindicated, a fine-cut CT of the temporal bones with contrast is a reasonable alternative in combination with referral for outpatient auditory brainstem response evaluation.2,25
Routine lab evaluation is also discouraged in the patient with isolated SSNHL.2 While other symptoms might prompt specific laboratory testing, in general routing laboratory testing rarely contributes to the ability to diagnose or treat patients with SSNHL.5,30 Examples of specific testing might include Lyme titers in endemic regions, or ESR and CRP if evidence of systemic inflammation are present.2
In most circumstances, emergency physicians will not be able to identify a clear etiology when evaluating a patient for isolated SSNHL, and these patients will commonly go on to have an unremarkable outpatient work-up resulting in a diagnosis of idiopathic SSNHL. While prescribing medications without a clear etiology might give some pause, there is evidence that a course of steroids in patients with idiopathic SSNHL can improve hearing recovery, especially if initiated within 7 days of symptom onset.2,9,25,31 Steroids have benefit in multiple etiologies of hearing loss, including viral, vascular, inflammatory, and Meniere disease, and have been observed to improve prognosis in some studies, even when the hearing loss etiology is unclear.2,6,25 A meta-analysis yielded inconclusive results on the benefit of steroids due to small sample size; however, the American Academy of Otolaryngology-Head and Neck Surgery recommends a 7-14 day course in those patients with suspected idiopathic SSNHL.2,14,32 The recommended dose is prednisone 1 mg/kg/d (maximum 60 mg/day), methylprednisolone 48 mg/day, or dexamethasone 10 mg/day in a single daily dose.2 In addition, many sources cite benefit from a combination of systemic and intratympanic steroids, and this is another reason for prompt outpatient specialist evaluation.25,31,33–35 For those patients in which systemic steroids are contraindicated or who are refractory to a course of oral steroids, intratympanic steroids are recommended and in a single study were found to be non-inferior to oral prednisone.2,36
There is a small amount of literature that suggests that hyperbaric oxygen therapy (HBOT) can hasten hearing recovery and may achieve more hearing recovery than those treated with steroids alone.2,37,38 The AAO-H&S clinical practice guidelines state that clinicians ‘may’ offer this therapy within 3 months. HBOT increases oxygen deliver to the perilymphatic fluid of the inner ear, which supports the theory that a proportion of those with SSNHL have a component of microvascular ischemia.37 One study found a 22% improvement in hearing for those treated with HBOT, with a NNT of 5.38 Those that seem to benefit most from HBOT are patients under age 60 with moderate to severe hearing loss who receive treatment between 2 weeks to 3 months after symptom onset, though a Cochrane review suggests that most benefit is observed when initiated within 2 weeks of symptom onset.2,38 While hyperbaric therapy does not need to occur on an emergent basis, referral to a hyperbaric center is a reasonable way to optimize chance of recovery while awaiting ENT evaluation.
While the prevailing theories of SSNHL include viral infection and vascular events, the routine use of antivirals and vasoactive medications are not recommended.2 There is no evidence to support the use of such medications, and vasodilators and thrombolytics are at high risk of adverse events.2,25
Between 32% to 65% of patients will have some level of spontaneous recovery after SSNHL, with the greatest improvement in spontaneous recovery occurring within the first 2 weeks after symptom onset.2,14,39 Treatment with steroids improves this early recovery but does not seem to offer benefit when initiated beyond a month from symptom onset.2 Characteristics that portend a more favorable prognosis are low tone loss, absence of vertigo, and early treatment with corticosteroids.40 Poor recovery is predicted by factors such as severe initial hearing loss; advanced age; concomitant vertigo; and a history of cardiovascular risk factors such as diabetes, hypertension, smoking, and dyslipidemia.25,41 After an episode of unilateral SSNHL, approximately 3.5% of patients will have a second episode.8
After a brief literature search, you realize that your previous plan for non-contrast head CT and shotgun lab approach are unlikely to contribute to this patient’s diagnosis. After some searching, you find a tuning fork in the ED and believe that the testing suggests a sensorineural hearing loss. You consider testing for Lyme and syphilis, but feel this patient is at low risk for either of these infections. MRI is not available in your ED, so you obtain a CT of the temporal bones with contrast, which is unremarkable. You discuss with the patient the most likely causes of acute sensorineural hearing loss and the likelihood that a cause may not be isolated. You start the patient on prednisone 60 mg/day and refer the patient to audiology and ENT for follow up.
- Most cases of acute hearing loss are sensorineural, unilateral, and in most circumstances have no clear etiology.
- Though the differential for SSNHL is broad, most do not require an in-depth evaluation in the emergency department. Most patients do not require any laboratory studies. If concern for a retrocochlear lesion exists, the imaging modality of choice is MRI brain, brainstem, and internal auditory canals or a fine-cut CT of the temporal bones.
- A trial course of corticosteroids is recommended in patient with suspected SSNHL. If prompt ENT follow up cannot be assured, consider referral for hyperbaric oxygen therapy while awaiting specialty evaluation.
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3 Chung S-D, Chen P-Y, Lin H-C, Hung S-H. Sudden Sensorineural Hearing Loss Associated With Iron-Deficiency Anemia. JAMA Otolaryngol Neck Surg 2014;140:417. doi:10.1001/jamaoto.2014.75.
4 Passamonti SM, Di Berardino F, Bucciarelli P, Berto V, Artoni A, Gianniello F, et al. Risk factors for idiopathic sudden sensorineural hearing loss and their association with clinical outcome. Thromb Res 2015;135:508–12. doi:10.1016/j.thromres.2015.01.001.
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41 Kang WS, Yang CJ, Shim M, Song C Il, Kim TS, Lim HW, et al. Prognostic Factors for Recovery from Sudden Sensorineural Hearing Loss: A Retrospective Study. J Audiol Otol 2017;21:9–15. doi:10.7874/jao.2017.21.1.9.