Ear, Nose and Throat
Appendix A: Supplemental Information about Specific Conditions
These disorders will be discussed together as they have a common pathophysiology and each deal with the 8th cranial nerve. Vestibular neuronitis (VN) results from inflammation of the vestibular branch of the 8th cranial nerve (8th CN), and labyrinthitis (LB) results from concomitant inflammation of the cochlear branch of the 8th CN. While the etiology is not entirely clear, these disorders are generally thought to be related to viral infections of the respective divisions of the 8th CN, though bacterial infections may also occur. The symptoms depend on which branch(es) are involved (VeDA, Labyrinthitis and Vestibular Neuritis). Symptoms usually resolve in a matter of days or weeks, but there is the potential for permanent hearing loss or balance disturbance.5 Risk of recurrence is low (about 2%), and should be no higher than that of the general population.6
Symptoms can be incapacitating, especially initially, Evaluation of VN/LB include medical history (rapid onset of symptoms, usually a single episode, presence, or absence of tinnitus and/or hearing loss, viral prodrome), and examination. On exam, horizontal nystagmus with slow component towards the affected ear is present. Testing usually consists of audiology to assess for hearing loss, electronystagmography with caloric testing, and gadolinium enhanced MRI with attention to the auditory canals to rule out other conditions including cerebellopontine angle tumors (such as acoustic neuromas), brain stem hemorrhage, or infarction. MRI may show enhancement of the vestibular nerves, consistent with inflammatory neuritis.5 If there is persistent vertigo, ENT evaluation and/or electronystagmography may be considered to assist with the return-to-duty decision. Persistent symptoms may occur in as many as 9.8% of patients.6
Treatment may consist of a course of steroids, and symptomatic treatment with antihistamines, anticholinergics, antiemetics, and benzodiazepines. Vestibular rehab may hasten resolution of slow to resolve vertigo symptoms. Medications may slow recovery, and should be discontinued as soon as possible, and especially during vestibular rehab.5,7 Return to duty should be delayed until any sedating medications (see Medications chapter) are discontinued.
Benign Paroxsymal Positional Vertigo (BPPV)
While patients with BPPV often receive extensive work up, including CT, MRI, vestibular testing, etc., the diagnosis of BPPV is usually straightforward, and can be done in the office without additional testing, unless other symptoms inconsistent with BPPV are present, indicating a need to rule out other diagnoses. Diagnostic criteria for posterior canal BPPV are based on 1) a history of vertigo provoked by changes in head position relative to gravity, and 2) vertigo associated with torsional (rotary), upbeating (toward the forehead) nystagmus is provoked by the Dix-Hallpike maneuver, performed by bringing the patient from an upright to supine position with the head turned 45° to one side and neck extended 20° with the affected ear down, 3) there is a latency period between the completion of the Dix-Hallpike maneuver and the onset of vertigo and nystagmus, 4) the provoked vertigo and nystagmus increase and then resolve within 60 seconds from the onset of the nystagmus.
Diagnosis for lateral (or horizontal) canal BPPV consists of: 1) a history of vertigo provoked by changes in head position relative to gravity; and 2) horizontal or absent nystagmus on the Dix-Hallpike maneuver, but characteristic lateral nystagmus on the supine roll test. If the diagnostic criteria are met, no further work-up is indicated.8
BPPV is the most common vestibular disorder, with an estimated lifetime prevalence of 2.4%, and a female to male predominance by a ratio of 1.5 to 2.2:1. Age of onset is typically between the 5th to 7th decades. BPPV results from otoconia that become dislodged from hair cells in the semicircular canals of the cochlea to become canaliths, and either float freely in the canals (canalithiasis) or become adherent to the cupula. With changes of head position relative to gravity, these canaliths trigger the hair cells inappropriately, causing sensations of movement. The results are episodes of vertigo, typically lasting less than a minute, and usually less severe than other forms of vertigo, occurring with predictable head movements. There are three main subtypes of BPPV: 1) posterior canal (PC) BPPV, which accounts for 85-95% of cases; 2) Lateral (horizontal) canal (LC) BPPV, which accounts for 5-15% of cases; and 3) anterior canal (AC) BPPV, which is rare. Other rare variants are multi-canal and bilateral multi-canal BPPV.8
BPPV responds well to maneuvers to reposition the canaliths, which can be taught to the patient to perform on their own.8 However, proper treatment involves first identifying which ear(s) is/are affected, and which canal(s) is/are involved. For PC BPPV, two different procedures are available and recommended. The first is the canalith repositioning maneuver (CRP), aka the Epley Maneuver (EM), and the second is the liberatory maneuver (LM), aka Semont Maneuver (SM). Studies show a high percentage of resolution of symptoms and conversion to a negative Dix-Hallpike Maneuver in patients receiving multiple treatments with EM. Resolution was 100% in studies where patients received at least 5 treatments. LM showed similar success rates. BPPV also shows a significant rate of spontaneous resolution but can take some time.
LC BPPV has not been shown to respond to the EM or SM. This would be expected based on the different planes of the canals. Maneuvers have been developed for LC BPPV, though the body of literature on effectiveness is limited at this time. The two procedures are the “barbeque roll” (BR) and Guifoni Maneuver (GM). There are limited cohort studies and case series reporting effectiveness rates of 50-100% success with the BR. Other methods have been proposed, but do not currently have adequate studies supporting their use.
A Cochrane review showed spontaneous resolution in 35-50% of cases.9 In 2006, Von Brevern et al. reported duration of symptoms to be less than 1 week in 45.0% of cases, 1-2 weeks in 11.2%, 2-4 weeks in 12.5%, 4-12 weeks in 18.8%, and >12 weeks in 12.5%. Therefore, by 1 month, 68.7% of cases had symptom resolution. It should be noted that case definition in this study was based on history alone, without Dix-Hallpike test confirmation.
Medical treatment is not considered first-line treatment for BPPV. Medications have been shown to be ineffective in shortening the duration of BPPV, although they can help with controlling symptoms. Medications may also play a role in pre-treatment for EM or LM sessions. However, medications may mask active symptoms, or suppress findings on diagnostic studies. In addition, medications may cause side effects such as somnolence or cognitive deficits, which are incompatible with the performance of safety sensitive duties.8
Very little data on impact of BPPV on work ability for safety-sensitive positions was found during literature review. Emphasis is placed on review of BPPV in other existing guidelines. A recently updated otolaryngology-head and neck surgery practice guideline on BPPV was reviewed for suggestions pertinent to clearing LEOs for duty.
BPPV is common. Von Brevern et al, calculated a lifetime prevalence of BPPV of 2.4% (3.2% in females, 1.6% in males).10 The 1-year incidence was calculated at 0.6%, with a 1-year prevalence of 1.6%. Mean age at onset was 49.4 years old. Cumulative incidence by age 80 was 10%. The median duration of an episode was reported as 2 weeks, with a range of 0.5 days to 104 weeks, though 45% of cases lasted less than a week, and 68.7% resolution by 4 weeks. Recurrence of attacks is common, with a 15% per year rate reported. This study found a recurrence rate of 56%. These numbers match fairly well with the practice guideline reviewed from Otolaryngology-Head and Neck Surgery, though the guideline indicated a recurrence rate of 36%. The guideline also indicated resolution of symptoms at 1 month in 15-85% of cases.
Eight medical standards were reviewed; seven standards addressed dizziness, vertigo, or in some cases specifically BPPV (see Appendix B). Those that addressed BPPV or vertigo were reviewed for guidance regarding BPPV. Four of these standards were specific to LEOs. Three standards, while not specific to LEOs, were for safety sensitive positions, and widely adopted consensus standards (FAA, FMCSA, and NFPA).
All standards that addressed vertigo or BPPV considered the condition to be either category A (disqualifying), or category B (possibly disqualifying). Most recommend individual assessment regarding limitations, if any, and evaluating the impact of medications (if used) on job performance/safety. BPPV can be episodic and recurrent. Active BPPV can seriously impact the ability of an individual to perform critical LEO tasks such as emergency driving, pursuit, and apprehension.11
Ménière’s disease is a diagnosis of exclusion. It is a disorder of the inner ear that presents with four main symptoms: 1) severe dizziness; 2) low frequency sensorineural hearing loss; 3) ringing of the ear (tinnitus); and 4) fullness of the ear. It is usually unilateral. It most commonly affects individuals between the ages of 40 to 60 years old. Severe cases can be subject to “drop attacks” (Tumarkin’s crises) without warning, which are reported to occur in 2 to 6% of patients. The episodes of vertigo can be severe, and typically last between 20 minutes to 12-24 hours, and are unpredictable.12,13
Usual work-up for Ménière’s disease would be a medical history (typically need at least two separate attacks of vertigo lasting at least 20 minutes each, along with the other features noted above) and clinical exam. Evaluators may wish to obtain an audiogram to assess for the presence and severity of hearing loss. Additionally, CT and/or MRI of the brain, and vestibular testing, may be requested to rule out other disorders.12,13,14
Medical treatment can be helpful in controlling symptoms during an attack of Ménière’s disease and may include medications such as antihistamines or benzodiazepines. Dietary restrictions such as reduction of salt, caffeine, chocolate, and alcohol intake may be utilized. More invasive measures include injection of steroids or gentamicin into the middle ear, or surgery. However, treatment generally does not eliminate the condition, but can provide some symptomatic relief. Treatment options may also cause debilitating symptoms, such as sedation with medications, or hearing loss with invasive treatment. These treatments would also increase the risk of impairment in relation to essential job functions as outlined above.
Other Causes of Peripheral Vertigo
- Superior semicircular canal dehiscence syndrome
- Perilymphatic fistula
- Herpes zoster oticus
- Labyrinthine concussion
- Vestibular paroxysmia
- Cogan’s syndrome
- Recurrent vestibulopathy
- Vestibular schwannoma (acoustic neuroma)
- Aminoglycoside toxicity
Causes of Central Vertigo
- Vestibular migraine
- Brainstem ischemia
- Rotational vertebral artery syndrome
- Wallenberg syndrome
- Epileptic vertigo
- Chiari malformation
- Multiple sclerosis
- Episodic ataxia type 2
- Disembarkment (mal de debarquement) syndrome
Otitis media is an infection of the middle ear space, usually bacterial, but may be viral. Symptoms include ear pain, decreased hearing, and possibly fluid draining from the ear if the tympanic membrane (TM) ruptures. Appropriate work-up of otitis media usually consists of a history and physical exam. For LEOs, an audiogram may be indicated to demonstrate adequate hearing for the essential job functions (see Hearing chapter). Where cases of OM are not responding as anticipated to treatment, further diagnostic testing with imaging studies (MRI), aspiration of fluid from the middle ear cavity, or a tympanogram, may be indicated.15
Otitis media may be treated with antibiotics, antihistamines, and, rarely, surgical intervention. Usually, ear drops are used for pain, but systemic narcotics might be used. Restrictions typically can be lifted once the condition resolves.
Chronic otitis media can lead to impaired hearing by leading to adhesive otitis (a retracted TM becomes stuck in the middle ear cavity), or a perforated TM. These complications may lead to persistent hearing loss (see hearing chapter for evaluation of permanent hearing loss), or may require restrictions for respiratory protection as noted under perforated TM.15,16
Perforated Tympanic Membrane
A perforated tympanic membrane (PTM) can result from acute trauma, foreign bodies in the ear canal, head trauma, otitis media, barotrauma, acoustic trauma, or be chronic in nature. Symptoms can include drainage or bleeding from the ear, ear pain, hearing loss, or balance disturbance. Most acute PTM heal on their own within 2 months but may become chronic.1
Work-up typically involves a history and physical exam, possibly including pneumatic otoscopy. A tympanogram may be needed in questionable cases. Rarely, imaging studies such as an MRI might be needed to evaluate for uncommon causes or to evaluate for damage to middle or inner ear structures, or associated complications such as cholesteatoma. An audiogram should be performed to assess for hearing loss (see LEO Hearing chapter). Occasionally, otomicroscopy or the bubble test (observing for a stream of bubbles during a Valsalva maneuver, after covering the TM with sterile water or saline) might be necessary for diagnosis of very small perforations.1
Treatment in most cases consists of antibiotics in the acute situation, protection against water entering the ear canal which may cause pain and/or an otitis media, and watchful waiting for spontaneous healing for up to 2 months. If healing is delayed, surgery to repair the TM may be indicated. In more complicated cases where damage to the middle or inner ear is suspected or present (head trauma, acoustic trauma, penetrating foreign body, etc.), formal clearance from the treating ENT provider, as well as evaluation/clearance for any persistent hearing loss or balance disturbance is indicated. Following surgical repair, or where perforations involve the pars flacida or the annulus of the TM, periodic evaluation for development of complications such as cholesteatoma would be indicated.1
This turned out to be one of the more interesting and difficult topics. There were differences of opinion on the task group as to whether exposure by this route was a realistic concern. We therefore undertook a review of the literature on this topic.
We found there is very little objective information available in the published literature. A literature search by a consultant returned three articles of interest. The main article was from two NIOSH researchers who studied the risk of workers with perforated tympanic membranes (PTM) being exposed to IDLH levels of hydrogen sulfide.2 Two articles were identified that discussed systemic absorption of medications instilled in the ear canal in the presence of PTM.
Ronk and White addressed the concern of potential hydrogen sulfide exposure to workers with PTM by calculating expected airflow through the Eustachian tube (ET) under various conditions, compared to the operating pressures of respirators, and to the airflow from allowable leakage of the respirator itself.2 The ET can be opened either actively (i.e., swallowing, sniffing, or blowing the nose), or passively, due to pressure differentials. Based on their literature review, the authors indicated a pressure differential of > 300 mm water pressure (320-400 mm water pressure) to passively open
a normally functioning ET. The authors identified four categories of ET dysfunction: 1) obstructed (non-patent with reduced or absent airflow); 2) non-functional (patent, no active opening, but can be passively opened); 3) non-functional and obstructed (no active or passive opening); or 4) patulous (remains open continuously). Their conclusion was that with normally functioning; obstructed; non-functional; and non-functional and obstructed ET, the likelihood of significant airflow between the nasopharynx and the middle ear would be very small, and likely less than the allowable leakage of the respirator itself. There was some concern about the potential for exposure in the case of a patulous ET with a concurrent PTM.
Current estimates of the frequency of patulous ET range from 0.3-6.6%.17 Based on Ronk and White’s analysis of the medical literature, and the operating characteristics of respirators, they felt that airflow high enough to be of concern would probably be very unpleasant, if not intolerable, to the individual.2 Given the low likelihood of having both a patulous ET and a PTM, this combination would likely be uncommon. However, for an individual identified with PTM, and assuming no increased risk for patulous ETD greater than that of the general population, there would be approximately a 1 in 20 chance of having a patulous ETD as well, with potential (though likely low) risk. Ronk and White recommended that hydrogen sulfide workers with a PTM not be restricted from an IDLH environment but use positive pressure respirators only. They reasoned that if workers with PTM/ET had airflow through the ET, it would be outward, rather than inward. They did not recommend the use of negative pressure respirators for any workers in an IDLH environment of hydrogen sulfide, likely due to concerns about PTM, as well as possible exposure of leakage of the negative pressure respirator allowing exposure.2
Two articles were identified that studied the systemic absorption of otic preparations of ciprofloxacin and pilocarpine when used in the presence of PTM. One study found that with ciprofloxacin, there were no significant blood levels noted after 7-10 days of treatment.18 In sharp contrast, Borík found that the clinical effects of pilocarpine, administered to the ear canal in the presence of PTM, were the same as when applied to the nasal or tracheal mucosa. Pilocarpine is highly soluble in water and per PubChem, 1 g can be dissolved in 0.3 mL of water (or 3,333 mg/mL).19 Ciprofloxacin, in contrast, is listed in PubChem as poorly water soluble at 36 mg/mL. Therefore, pilocarpine is almost 100 times more water soluble than ciprofloxacin. This seems to imply that the middle ear cavity mucosa has the potential for significant absorption of substances, but this may be influenced by such factors as water solubility, active transport mechanisms across the membrane, concentration, etc.
Due to the lack of available data, we reached out to national experts on respiratory protection, both within NIOSH, and with other specialists who were recommended by our NIOSH contacts. None these individuals had any additional information on this topic. In general, the consensus seemed to be a belief that the risk would be low, but without objective data, it was difficult to be certain, and that this could be an area for future research. There are no known cases of occupational injury by this route that we could identify.
Additional issues that were discussed within the task force involved the potential for liquid splashes to the ear, or the potential exposure to biological warfare agents, such as anthrax spores, which might be able to germinate on the mucosa, and release toxin. We know of no studies regarding such potential exposures by this route, but the consensus was that significant exposures were unlikely.
Based on review of the available information, and discussion with national experts, the task group would recommend the use of positive pressure respirators only for LEOs with PTM, with anticipated serious respiratory toxic exposures. The use of other personal protective equipment could also help prevent such exposures. For example, an encapsulated suit, biological/ chemical warfare ensembles, or hearing protection (such as ear plugs or muffs), would significantly reduce the likelihood of exposure of the ear canal to hazards. However, the use of personal protective equipment must be weighed against the degradation of the senses of sight and hearing, manual dexterity, speed, and thermal load/endurance. Such performance degradation could jeopardize mission completion or place the LEO or others at increased risk. Therefore, on-scene incident commanders must balance the level of protection needed, versus the known or suspected hazards, and mission requirements.
Evaluation includes a medical history, examination (may show a mass in the ear canal or behind the ear drum), audiogram, CT scan, and possibly a follow up MRI scan.4 A cholesteatoma is a cyst that forms in the middle ear or mastoid bone and can be either congenital or acquired. Symptoms arise from mass effect upon, and/or erosion into, the middle and inner ear structures. Symptoms usually include gradual hearing loss and drainage from the ear. Less common symptoms can include tinnitus, balance disturbance, ear pain, headache, and unilateral facial weakness.4
In most cases, cholesteatoma is treated surgically. Depending on the size and location of the cholesteatoma, there may be permanent hearing loss and vestibular dysfunction.3,4