HD: 10

Traumatic Injuries of the Ear, SSNHL and Tinnitus

Outline of Topics Covered

• Auricular injuries
• Barotrauma
• Perilymphatic fistula
• Temporal bone fractures

Auricular Injury

• Hematomas can separate the perichondrium from the cartilage, disrupting blood supply and causing cartilage deformities.
• Severe trauma may result in avulsion.

Barotrauma

• Barotrauma is any trauma induced by pressure.
• "Baro" is defined as pressure.
• Diving, sneezing, valsalva maneuvers, and elevation changes may result in barotrauma.
• Injuries resulting from barotrauma can be implosive or explosive.
• Caisson disease, also known as "the bends" or decompression sickness, can occur with deep sea diving.
• Caisson's disease arises from dissolved gasses forming bubbles inside the body on depressurization
• Compressed nitrogen is soluble, but decompressed nitrogen forms gas emboli/bubbles that can affect the back, joints, and muscles.
• Hyperbaric oxygen is a treatment for this condition

Perilymphatic Fistula

• A fistula is an abnormal connection
• A perilymphatic fistula specifically, is an abnormal connection between the inner and middle ear.
• May occur at the round window, oval window, or other locations.
• Inciting events include blows to the head, sneezing, lifting heavy objects, and sudden pressure changes.
• A perilymphatic fistula may sometimes be spontaneous.
• A high-risk population to get a perilymphatic fistula includes post-stapedotomy patients as well as inner ear anomalies (Mondini malformation and large vestibular aqueduct)
• Difficult to diagnose.
• Diagnosis requires considering the patient history.
• Hennebert's sign and Tullio's phenomenon may be examined for diagnosis.
• Sudden or rapid progressive hearing loss can be revealed in an audiogram.
• Definitive diagnosis can be obtained by looking in the operating room.
• Hennebert's sign is a fistula test where Nystagmus/dizziness is produced when pressure is applied to the EAC, and is positive in PLF, syphilis.
• Tullio's phenomenon is dizziness induced by loud sound and is positive in PLF, SSCDS, and Meniere's disease.
• Treatment includes a referral to ENT specialists as well as strict bed rest.
• Elevating the HOB to 30 degrees, avoiding lifting, straining, or hard nose blowing, and using stool softeners is recommended.
• Surgery, involving middle ear exploration and patching of the fistula, may be necessary if there's no improvement.

Temporal Bone Fracture

• Causes include motor vehicle accidents (MVA), physical assaults, falls, motorcycle accidents, pedestrian injuries, and bicycle accidents.
• Hearing loss is one effect due to hemotympanum, ossicular chain disruption, inner ear fracture, concussion, nerve injury, and/or TM rupture.
• Fracture types can be longitudinal vs. transverse or otic capsule sparing vs. otic capsule violating.
• Fracture types are defined with respect to the long axis of the temporal bone
• They are diagnosed with CT scans.
• Longitudinal temporal bone fractures often result from lateral blows, causing blood in the external auditory canal (EAC), TM perforation, conductive hearing loss (CHL), and facial nerve weakness in 20% of cases.
• Transverse fractures result from front/back blows, often presenting with hemotympanum, an intact TM, sensorineural hearing loss (SNHL), 50% facial nerve weakness, and vertigo.
• Hemotympanum is blood in the middle ear.
• Skull base fractures can result in retroauricular ecchymosis (Battle's sign) and bilateral periorbital ecchymosis (raccoon eyes).

Temporal Bone Fractures - Acute Complications

• Acute complications include hearing loss (CHL, SNHL, mixed), vertigo, tinnitus, facial paralysis, CSF leak/perilymphatic fistula, and vascular injury.

Temporal Bone Fractures - Ossicular Injuries

• Ossicular injuries include separation of the incudostapedial joint, dislocation of the incus, fracture of stapedial arches, fracture of malleus handle, and footplate fracture-dislocation.

Temporal Bone Fractures - Delayed Complications

• Delayed complications include BPPV (most common), Meniere's disease, tinnitus, central vestibular disorders, meningitis, cholesteatoma, pneumocranium, and psychogenic malingering.

SSNHL - Sudden Sensorineural Hearing Loss

• Sudden Sensorineural Hearing Loss is the sudden onset of SNHL greater than or equal to 30 dB.
• The hearing loss should occur over 3 contiguous frequencies, within 3 days or less.
• SSNHL can be devastating to patients and frustrating for healthcare providers.
• The definitive etiology and treatment are still unknown.
• There are 15,000 cases reported worldwide per year and 4,000 in the US.
• The affliction rate is 1/10,000.
• The highest incidence is in 50-60 year olds.
• Females and males are equally affected.
• Bilateral involvement is present one percent of the time
• Ninety percent of cases are idiopathic (cause unknown)

SSNHL - History

• The time course of the symptoms to be investigated.
• Associated symptoms include vertigo/dizziness, aural (ear) fullness, and tinnitus.
• Other factors include neurological symptoms, ototoxic medication use, recent viral infections, head trauma, straining, sneezing, nose blowing, intense noise exposure, and recent flying or scuba diving.
• Important information include past medical history for autoimmune diseases, vascular diseases, malignancies, neurologic conditions, and hypercoagulable states such as sickle cell disease.
• Past surgical history should be taken including stapedectomy and mastoidectomy.

SSNHL - Examination and Investigations

• Ears should be examined (otoscopy) for effusion, cholesteatoma, and cerumen impaction.
• A tuning fork exam should also be performed
• The patient should undergo a neurologic exam.
• The patient should also have laboratory tests such as the following:
  • Complete blood count CBC - checks for infections
  • Erythrocyte sedimentation rate ESR - inflammation
  • VDRL FTA-Abs to test for syphillis
  • Coagulation studies
• MRI (magnetic resonance imaging) can assess for brainstem (CPA) tumors.
• An MRI can also check for multiple sclerosis and ischemic (stroke) changes.
• MRI must be done in patients who have unilateral tinnitus
• 10% of patients with vestibular schwannomas (acoustic neuromas) present with SSNHL.

SSNHL - Etiology/Treatment/Prognosis

• Etiologies include idiopathic causes, infectious (viral) causes, autoimmune, traumatic, vascular, and neoplastic causes.
• Viral infections cause 30% of reported cases where patients have a recent viral illness.
• Autopsy studies demonstrates viral particles in the inner ear
• Cogan's syndrome, Wegener's granulomatosis, polyarteritis nodosa, temporal arteritis, and systemic lupus erythematosus are autoimmune causes.
• Vasculitis of blood vessels of the inner ear and autoantibodies that attack the inner ear (cross-reacting antibodies) are autoimmune's pathophysiology.
• Heat shock protein 70, discovered by Harris in 1990, can be a marker for SSNHL.
• 22%-58% will have a positive test result, with 94% specificity. Vascular etiologies can disrupt blood supply to the cochlea.
• The cochlea is intolerant to ischemia because there is no collateral blood supply.
• Strokes (vasospasms, embolism) and blood clotting tendencies (Sickle-cell disease) are causes.
• Treatment depends on the cause of SSNHL.
• General treatment for idiopathic SSNHL: Steroids, antivirals (controversial), vasodilators (controversial), or anticoagulants (controversial).
• Wilson et al. (1980) preformed double blind studies, showing that Decadron (steroid) given over 10-12 days resulted in better patient outcomes
• Moskowitz (1984) confirmed above findings
• Prognosis = long-term outcomes
• 1/3 of patients with SSNHL return to normal hearing in the long term
• 1/3 of patients with SSNHL continue to have hearing loss in the long term
• A worse prognosis is associated with vertigo, total deafness, advanced age, downsloping audiogram, and associated vascular risk factors.
• A better prognosis is associated with minimal/mild hearing loss and low-frequency loss.

Tinnitus

• "Tinnere" translated from Latin means ringing
• Definition: perception of sound in the absence of external stimuli.
• Tinnitus is described as originating in the ears or around the head.
• It can be extremely annoying and cause reduced quality of life.
• It may be the first or only symptom of a serious disease, such as a vestibular schwannoma.
• Ludwig von Beethoven - 1801: "...only my ears whistle and buzz continuously day and night. I can say I am living a wretched life."
• Tinnitus can be ringing, buzzing, hissing, roaring, clicking, or pulsatile sounds.
• It can be high or low pitched, and unilateral or bilateral.

Epidemiology of Tinnitus

• Over 40 million affected in the US and more than 4 million in Canada.
• 10-15% of the North American population is affected.
• Most common in 40-70 year olds, with prevalence increasing with age.
• Rates are equal between males and females.
• 15% find their tinnitus intrusive, disturbing, or anxiety-provoking.
• Heller and Bergman did an experiment in 1953 where they put 80 tinnitus-free individuals in a soundproof room and asked them to report any sounds they heard.
• After 5 minutes of total silence, 93% reported tinnitus.

Classification of Tinnitus

• Subjective vs Objective.
• Pulsatile vs Non-pulsatile.
• Subjective tinnitus is most common and only perceived by the patient, is more commonly related to hearing loss, and the pitch of tinnitus may correlate with frequency of hearing loss (3-5 KHz).
• Objective tinnitus can be detected by another person, is usually caused by an internal body sound or vibration, may be exacerbated by CHL, and is more commonly related to pathology.
• Pulsatile tinnitus is usually objective tinnitus and possibly has a vascular etiology (increased or turbulent blood flow).
• Non-pulsatile tinnitus is usually subjective tinnitus and described as ringing or buzzing,.

Subjective Tinnitus: Details

• More common than objective tinnitus.
• Little is known about its physiologic mechanism, but some possibilities include hyperactive hair cells or nerves and reduced suppressive influence of the CNS.
• Possible causes include presbycusis, noise exposure/effusion, head trauma, otosclerosis, Meniere's disease, acoustic neuroma, meningitis, medications, middle ear issues, TMJ problems, syphilis, depression, metabolic problems, and cardiovascular problems.
• 75% have > 30 dB HL.
• 30% have cardiovascular disease, 20% have hypertension.
• Head injury, whiplash injury, meningitis, and multiple sclerosis are all causes of Tinnitus.
• Over 25% of individuals with show TMJ dysfunction.
• Psychological factors such as medications and depression may play a factor in roughly 50% of tinnitus cases.
• Possible medications may include Aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), aminoglycoside antibiotics, antidepressants, and other ototoxic drugs.
• Depression is more prevalent in patients with chronic tinnitus than those without tinnitus.
• Increased severity of tinnitus reported for patients with depression means the two are linked
• Tinnitus depression or depression leading to Tinnitus

Objective Tinnitus: Details

• Audible to other people/observers.
• Evaluation includes pulsatile or non-pulsatile investigation, relation to heart rate, light exercise investigation, otoscopy, auscultation of the external auditory canal, mastoid, skull, neck, audiometry,, and imaging.
• Possible causes vascular tumors; Glomus jugulare or glomus tympanicum, abdominal vascular anatomy or patulous eustachian tube include palatal myoclonus, idiopathic stapedial muscle spasm benign intracranial hypertension
• Classic vascular tumors such as glomus jugulare and tympanicum, revealed in an otoscopy, show a reddish mass behind TM that isn't altered by compression of neck blood vessels.
• Abnormal vascular anatomy may involve arterial venous malformations (AVM), high riding carotid artery arterial bruits and venous hums, persistent stapedial artery, or dehiscent jugular bulb. Arteriovenous malformations (AVM) also involves pulsatile tinnitus synchronous with heartbeat, secondary to trauma and may be managed with removal or blockage of AVM (embolization)
• Patulous eustachian tube: the Eustachian tube is abnormally open (when it should be closed), which leads to abnormal airflow between middle ear and nasopharynx, causing ear drum to potentially move leading to Autophony, hypermobile TM (moves with respiration), a clicking sound that is usually self limiting Possible causes for this include radiotherapy, significant weight loss, stroke, CN5 injury, ear surgery, associated with gum chewing, dental malocclusion, and TMJ problems. Rarely, ear tubes or ET surgery is needed
• Palatal myoclonus causes a rapid clicking sound due to contraction of palatal muscles (20-400 bpm) and Observable palatal fasciculation, Aural fullness, and hearing distortion where a common manager includes muscle relaxants or botox. Tensory tympani or Stapedius syndrome involves a Spasm or myoclonus of tensor tympani or stapedius muscles resulting in Fluttering low frequency tinnitus that is Self-limiting. Benign intracranial hypertension results in an increased ICP with a Aka pseudotumor cerebri with associatedIncreased IncreasedICP
• Benign intracranial hypertension is most common cause of pulsatile tinnitus that is common in Young overweight females that experience blurred vision and lightheadedness that can be diagnosed by lumbar puncture for elevated CSF pressureManaged with w weight loss and diuretics

Tinnitus Management & Prognosis

• Behavioral management might involve reassurance, avoidance of dietary stimulants (coffee, tea, cola,…), smoking cessation, and avoidance of medications.
• Medical management may involve alprazolam (xanax) to reduce loudness of tinnitus (but can become dependent), IV lidocaine to suppress tinnitus though impractical , or ginko biloba for some improvements that are reported.
• Psychotherapy and stress management may be useful.
• Audiological may involve hearing aids to amplify background Noise, maskers (white noise from radio or masking machine), or Tinnitus instrument: combination of hearing aid and masker Tinnitus retraining therapy may be useful because it is Based on neuropsychological model that Low-level masking with Noise counseling in addition counseling and education in order to get a good success rate.
• Tinnitus therapy involves a combination of the following:
  • Noise counseling
  • Education and self management
  • Help the patient understand what is happening with there symptoms
• There is no cure.
• Evaluate is needed as there are are a variety of etiologies.
• Therapies are directed at relieving patient anxiety and treating the underlying cause.
• Remember masking devices and tinnitus support groups can be helpful.
• Prognosis: 25% improve or disappear, 50% decrease with 25% persist