Sudden Sensorineural Hearing Loss (SSNHL) Intervention

• 
  Henry Davis
  

Hearing loss is not a common healthcare issue addressed by Nurse Practitioners (NP) and Sudden Sensorineural Hearing Loss (SSNHL) occurs even less frequently. Often the onset of hearing loss (related to aging or noise exposure) is insidious, often spanning months to years and is typically bilateral. Hearing loss that occurs with advanced age is routinely compensated for with the use of electronic devices that amplify sound and this type of hearing loss is typically not cured.

SSNHL by contrast has a well-defined acute onset within 3 days and is characteristically unilateral hearing loss. Some cases of SSNHL could be cured if a diagnosis is made and treatment initiated within a short time from onset of the hearing loss

(Raghunandhan et al., 2012). Nurse practitioners may often be the first healthcare provider the patient encounters. Because of the early patient contact, nurse practitioners are uniquely poised to initiate the first line treatment after consulting with neurology, but prior to referral for follow-up care and further evaluation. Recent research supports that patients who receive early medical treatment for SSNHL recover hearing more often than those, who received delayed care

(Raghunandhan et al., 2012).

Epidemiology

Current research indicates the morbidity of SSNHL is 2-20/ 100,000 persons annually and the mean age of occurrence is 43-53 years old. Mortality as not reported other than a possible link between SSNHL and strokes. Gender does not appear to influence incidents. Risk factors for SSNHL include; advanced age, concurrent cardiovascular disease and the presence of a positive antinuclear antibody (Weber, 2014). One study indicated “…viral infection being the most common etiological factor” for SSNHL

(Raghunandhan et al., 2012, p. 229).

Etiology

The cause of SSNHL is currently considered idiopathic, however the preponderance of current research is directed at the supposition that the etiology of SSNHL is due to edema of the eighth cranial and subsequent compression of the internal auditory artery to the cochlea and circular apparatus. The likely cause of the compression is edema of the auditory nerve within the confined space of the internal auditory meatus from a viral infection

(Mom, Chazal, Gabrillargues, Gilain, & Avan, 2005). There is minimal clearance for the nerves and vessels. If any edema occurs, compression of the associated structures can result. This would be similar in nature to the pathology associated with Bell’s palsy or compartment syndrome associated with a casted extremity. The surrounding tissue swells and compresses adjacent structures.

Cause of SSNHL is currently identified as idiopathic but current treatment targets a viral infection as the causative agent. Early treatment with steroids and antiviral drugs demonstrated reduction in percentage of patients who experience total hearing loss. The nurse practitioner can begin treatment of the patient and ensure timely neurologic specialty follow-up and magnetic resonance imaging (MRI) to rule out acoustic neuroma

(Chen, Halpin, & Rauch, 2003).

Pathogenesis

Initially to understand SSNHL we first should examine the anatomy and function of the inner ear. The ear communicates with the brain via eighth cranial nerve. The eighth cranial nerve divides into two main branches, cochlear and vestibular nerves. The first cochlear nerve travels to the cochlea and the vestibular nerve travels to the semicircular ducts. The Cochlea is the portion of the inner ear responsible for the transformation of sound from a physical force, from the tympanic membrane via the malleus, incus and stapes into a nerve impulse conducted to the brain via the cranial nerve (Copstead & Banasik, 2013).

The vestibular nerve conducts impulses from the semicircular ducts. Semicircular ducts change the forces of air movement into fluid movement that in turn is changed into nerve impulses that allow for proprioception. Damage to this branch of the vestibular nerve can result in vertigo, nystagmus, vomiting and disruptions of proprioception (Copstead & Banasik, 2013).

The eighth cranial nerve passes through a relatively small opening, the internal auditory meatus, in the skull

(Weber, 2014) (Kim & Lee, 2009). This small opening also provides the arterial blood flow for the inner ear via the internal auditory artery (Kim & Lee, 2009). Even a small amount of edema in the eighth cranial nerve can result in both compression of the nerve and occlusion of the arterial blood supply to the inner ear. The result of these Sequelae would be rapid hearing loss, nystagmus and vertigo

(Weber, 2014). During the acute period, the first few hours, it would be possible to decrease the edema by administration of steroids thereby decompressing the nerve and re-establishing blood flow to the inner ear

(Narozny et al., 2006). Delays in the reduction of this edema may result in tissue necrosis and clot formation due to stasis of blood in the internal auditory artery.

Another less researched cause of SSNHL is vertebrobasilar ischemic stroke or a thrombi occlusion of the arterial supply to the inner ear

(Kim & Lee, 2009). The resultant Sequelae following the occlusion would mirror the presentation of SSNHL from edema however; the key difference would be the response to oral steroids is ineffective. Any negative effects of oral steroids, if an ischemic stroke were diagnosed would be minimal as the follow-up for MRI should be performed immediately after initial treatment.

Clinical Manifestations

Onset of SSNHL appears as idiopathic and not related to any trauma and patient denies current source of infection. The patient may report having a clogged ear or pressure in ear. There is an absence of signs and symptoms of infection such as fever, drainage and pain.

The patient may find it difficult to impossible to determine the direction of the source of a sound, as both ears are needed to identify the direction of a source of a sound. The brain normally uses the auditory input from both ears identify source location of an auditory stimulus. The occlusion of blood flow to the cochlea on one side has resulted in complete hearing loss to that side.

SSNHL may present with an acute onset of tinnitus in the affected ear. The patient may describe the sound as a ringing or roaring sound. Initial onset of tinnitus may cause difficulty in concentration. The pathology responsible for tinnitus remains unclear.

The onset of SSNHL is rapid and unilateral, proceeding from normal hearing to complete absence of hearing of the effected ear in less than 3 hours

(Weber, 2014). SSNHL is often accompanied by nystagmus, tinnitus and vertigo. This may be due to the compression of the internal auditory artery and the resultant occlusion of blood flow to the cochlea and semicircular apparatus.

In addition, when we consider the functions of the central nervous system in the perception of proprioception, multiple stimuli typically confirm the position of the body such as the semicircular apparatus and visual stimuli. With the sudden cessation of blood flow to the inner ear, a mismatch of stimuli rapidly occurs. This mismatch of stimuli among various nerves results in the perception of vertigo and often nystagmus.

The Performance of a Rinne test and Weber test enables the nurse practitioner to differentiate between bone conduction damage, as is the case with traumatic injury or nerve

damage as is the case in both SSNHL and ischemic stroke (Tintinalli, 2010). Also important is the Dix-Hallpike test, to differentiate between central or peripheral vertigo

(Furman & Barton, 2014). Central vertigo would be those with a site of origin inside the brain, were as peripheral vertigo originates outside the brain. The Dix-Hallpike test differentiates between central and peripheral vertigo. A Dix-Hallpike test is positive if vertigo and nystagmus is elicited when the head is rotated. Dix-Hallpike test also identifies unilateral vertigo, as well as it differentiates between central and peripheral causes of vertigo and nystagmus. Benign positional nystagmus is also evaluated utilizing the Dix-Hallpike test. In (BPN) the result is a delay of onset of nystagmus of >20seconds, nystagmus slowly resolves if head held in the same position, and response decreases with repeated testing

(“Dix-Hallpike Test,” 2014). A central cause of vertigo and nystagmus need to be evaluated if the Dix-Hallpike test yields atypical results of nystagmus that occurs without rotation of the head, begins without delay, and does not decrease with retesting

(“Dix-Hallpike Test,” 2014).

Treatment

The recommended treatment of SSNHL is early administration of oral glucocorticoids

(Raghunandhan et al., 2012)

(Narozny et al., 2006). This intervention is well within the scope of practice of the Nurse Practitioner. Nurse Practitioners should be encouraged to take the lead in diagnosing and initiating treatment for SSNHL. The risk associated with early treatment of suspected SSNHL is minimal however if treatment is delayed hearing loss may be permanent.

The indication for administration of steroids is to decrease edema of the eighth cranial nerve as this edema leads to loss of nerve conduction and ultimately nerve tissue death and possible arterial occlusion (Chen et al., 2003). The result of tissue death of the eighth cranial nerve is hearing loss, nystagmus, tinnitus and impaired balance (Copstead & Banasik, 2013). Current treatment of SSNHL aims at the reduction of damage to the eighth cranial nerve.

Other medications can be used to treat the after effects of SSNHL such as vertigo. Select antihistamines, which are also classified as vestibular suppressant, are often used to decrease the perception of vertigo. These drugs reduce “the activity in the vestibular nuclei and cerebellum.”

(Denner, 2013, para. 6). This class of medication is used as needed for vertigo control. Vestibular suppressant antihistamines are first line medications for vertigo.

If Vestibular suppressant antihistamines are not successful in controlling vertigo then an escalation to a low dose benzodiazepine most often resolves vertigo not controlled by first line medications. Benzodiazepines cause central nervous system depression and thereby decrease vertigo.

The treatment of choice for chronic vertigo is vestibular rehabilitation. Vestibular Rehabilitation is an exercise-based therapy used to retrain the central nervous system (CNS). Often vestibular rehabilitation is sufficient to control symptoms of vertigo without the need for daily medications.

The provider often refers the patient experiencing vertigo to physical therapy (PT) or occupational therapy (OT) for a course of progressive exercises with associated head/eye movements to retraining the CNS

(“Vestibular Rehabilitation Therapy (VRT),” 2014). Vestibular rehabilitation can greatly reduce the need for medications to reduce symptoms of vertigo and improves the quality of life.

Vestibular rehabilitation is only the first of many topics that should be addressed by the nurse practitioner to assist the patient in lessening symptoms and coping with functional loss. Patient education is targeted toward identification of limitation and practices to compensate for those limitations.

Simple functions such as body position during sleep can cause functional problems for patients. An example would be if patient sleeps on the non-affected ear toward the pillow, they would not hear sounds such as alarm clocks, smoke alarms, or other auditory products. Specialized alarms are available which provide both auditory and tactile stimuli (a strong bed vibrating unit) to awaken non-hearing or limited hearing persons. Also, educate patient that stressful situations and loud environments can exacerbate the experience of tinnitus and vertigo.

Family members of the patient would be educated on actions to compensate for patient’s hearing loss. Walking on the non-affected side and not speaking close to affected ear are two examples. Also explaining the emotional stressors for the patient and the family members as both learn to cope with the new limitations.

The Nurse Practitioner can also provide a referral to an ear, nose and throat specialist to evaluate the patient for cochlear implant for complete unilateral hearing loss. Current implants consist of a base magnet implant into the mastoid bone on the affected side. An external device is worn over the magnet and conducts sound into the magnet and across to the functional ear via bone conduction. The delay between air and bone conduction allows the patient to regain the ability to directionalize sound stimuli. The negative impacts of this option are cost, some insurances do not cover this surgery or only cover a portion of the total cost and this is a surgical intervention and all invasive procedure have associated risk factors.

Conclusion

Nurse Practitioners should broaden the scope of examination and treatment when assessing patients with sudden hearing loss. In the face of a presumptive diagnosis of SSNHL, the provider may improve outcomes by beginning treatment prior to conclusive diagnosis.

Increased early intervention for SSNHL by Nurse Practitioners and beginning steroid treatment within the first few hours after onset of hearing loss may decrease the incidence of permanent hearing loss. The Nurse Practitioner is able to discriminate between sensorineural and conductive hearing loss. A causative factor is then diagnosed to direct care.

SSNHL is an infrequently occurring health problem that can be treated with an early presumptive diagnosis. If the initial diagnosis of SSNHL is delayed for MRI to rule out Acoustic Neuroma, it increases the chance that hearing loss will become irreversible. The initial treatment with oral steroid is relatively low risk, yet this option is often omitted despite the apparent benefit.

Although the confirmation of SNNHL requires MRI to rule out a differential diagnosis of acoustic neuroma, steroid treatment could begin as a protective measure. If an Acoustic Neuroma is diagnosed the steroid therapy could be discontinued. The impact of steroid use associated with Acoustic Neuroma has not been examined in current research.

Appendix

Figure 1

(Arora, 2012, figure 5)

Figure 2

(Kim & Lee, 2009, figure 2)

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