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Case report
Bilateral inner ear damage after electrical injury: A case report George Psillas *, Marios Stavrakas, Ioanna Petrou, Dimitrios Rachovitsas, Konstantinos Markou 1st Academic ENT Department, Aristotle University of Thessaloniki, AHEPA Hospital, 1, Stilponos Kyriakidi St., GR 546 36 Thessaloniki, Greece
A R T I C L E I N F O
A B S T R A C T
Article history: Received 5 October 2016 Accepted 6 January 2017 Available online xxx
Electrical injury occurs as a result of direct contact with an electrical source. We present the case of a 62-year-old male patient, an electrician by profession, who was hit by a high-voltage electrical current while working with cables in proximity to a wet floor. The patient suffered from immediate loss of consciousness and five days later he started complaining of slight hearing loss, persistent vertigo, instability and bilateral tinnitus. A thorough audiological and vestibular examination revealed an extensive bilateral vestibulocochlear dysfunction. The exact pathogenetic mechanisms of inner ear dysfunction after electrical injury have not been fully elucidated, although it is believed that there is significant improvement with time. Long-term follow-up, medical assistance and psychological support are crucial factors for the patient management. © 2017 Elsevier B.V.. All rights reserved.
Keywords: Electrical injury Hearing loss Vertigo Pure tone audiogram Otoacoustic emissions Vestibular evoked myogenic Caloric test
1. Introduction The use of electricity for domestic and industrial purposes is increasing over the last centuries and, as a consequence, a significant number of electrical injuries are being reported. The estimated mortality rate of electrical injuries in the United States is between 3%–15% [1]. Various injuries have been recorded, with the most frequent being cardiac abnormalities and burns [2]. Neurological and neuropsychological effects have also been reported, including peripheral polyneuropathies, emotional and behavioral sequelae [3,4]. Audiovestibular sequelae of electrical injury due to lightning or electric current are probably much more common than those indicated in the literature [5]. We present a case of electrical injury which resulted in hearing loss, vertigo and imbalance,
* Corresponding author. Fax: +30 2310 994 916. E-mail address:
[email protected] (G. Psillas).
focusing on its short- and long-term effects on audiological and vestibular function tests. 2. Case presentation A 62-year-old male patient was referred to the ENT Department of “AHEPA” University Hospital by a district hospital in Northern Greece after sustaining an electrical injury. The accident happened five days prior to admission. The patient, who is a professional electrician, was mending plug cables kneeled on a wet floor, when he was hit by a current of approximately 1000 V (50 Hz AC current). He described the formation of an electric arch between his right arm and legs. For three seconds he was unable to escape the arch, until his assistant managed to pull him away from the source. A sensation of numbness remained in his right arm and legs, without troubles of mobility. As the patient suffered from an immediate loss of consciousness, he was initially admitted to the district hospital of his area for cardiac monitoring. No complications were
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Please cite this article in press as: Psillas G, et al. Bilateral inner ear damage after electrical injury: A case report. Auris Nasus Larynx (2017), http://dx.doi.org/10.1016/j.anl.2017.01.016
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observed and he was discharged five days later. When the patient went back home, he started feeling unstable and complained of persistent vertigo. He also described a few episodes of nausea and vomiting. He noticed a mild hearing loss and tinnitus, especially in his left ear. On examination, otomicroscopy revealed normal ear, with no signs of tympanic membrane perforation. Under Frenzel glasses, the patient showed second degree nystagmus towards the right; Romberg and Unterberger tests could not be carried out as he was completely unstable. Tuning fork tests were normal and the pure tone audiogram demonstrated a bilateral symmetrical, moderate threshold elevation particularly in the high frequencies (Fig. 1A). Transient otoacoustic emissions (TEOAEs) were not produced in either ear (Fig. 2). Auditory brainstem responses (ABRs, 120dBSPL click stimulus, rate 11/s) absolute and inter-peak latencies (I–III, III–V, I–V) values were within the normal limits. A directional preponderance to the right was found in the caloric test (42%, normal laboratory values <25%)
(Fig. 3A) and the cervical vestibular evoked myogenic potentials (cVEMPs, 500 Hz positive logon, 130dBSPL, 4 signals/s) (Fig. 3B) were completely absent on both sides. A rotatory pendular test (undamped rotation of 360 in 20 s) was also used. The magnetic resonance imaging (MRI) of the brain did not reveal any significant pathology. He was treated conservatively, with a short course of intravenous steroids and dimenhydrinate without showing any improvement. Moreover, he developed signs and symptoms of depression. Ten days later, his balance was improved and the patient was able to walk independently; he was discharged on a 3-month course of Betahistine (16 mg three times a day). He was also advised to perform Cawthorne–Cooksey exercises at home [6]. On the next follow-up appointment after two weeks, his balance was better, but he still suffered from dizziness, mainly during rotations of the head to the right; he also reported a feeling as walking on “broken tiles”. The nystagmus was less intense, first degree to the right and during Unterberger test he
Fig. 1. Pure tone audiogram after electrical injury: Bilateral symmetrical, moderate thresholds elevation, especially at the high frequencies, (A) on admission, (B) slightly higher one year later. -o-, -x-: air thresholds for right and left ear, respectively. ->-, -<-: bone thresholds for right and left ear, respectively.
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Fig. 2. Otoacoustic emissions after electrical injury. Abolished on both sides.
Fig. 3. Five days after electrical injury: (A) In the caloric test, directional preponderance to the right was recorded and (B) the cervical vestibular evoked myogenic potentials (cVEMPs) were completely absent on both sides.
turned to the left. Two months later, the patient had no nystagmus and a caloric test with ice-cold water revealed unilateral right paresis (55%, normal laboratory values <25%). An electroencephalography (EEG) showed suspicious theta activity in the occipital lobes, mainly at right. After one year, the patient was functional in everyday activities as he could manage his balance problems. However, the instability was deteriorated with the eyes closed; and consequently, he felt unable to work as his job required coping with heights. The hearing loss and tinnitus were still present although they did not bother him. At that time, the vestibular tests showed a persistent vestibular deficiency, including directional preponderance to the right, complete absence of VEMPs on both sides and lack of nystagmus in the rotatory pendular test. The pure tone auditory thresholds were very slightly increased, mainly at high frequencies (Fig. 1B) and the ABRs revealed prolongation of the absolute latency V and inter-peak latency III–V on the right side, respectively. 3. Discussion The International Electrotechnical Commission (IEC) defined high voltage as 1000 V for alternating current and low voltage as <1000 V (note that domestic current is 230 V across Europe and 120 V in the USA). Risk factors associated with severe
electrical injury requiring cardiac monitoring are transthoracic current, tetany longer than 1 s, loss of consciousness of any duration, or electrical source of 1000 V or more [2]. As above, our patient was exposed to a high-voltage current for 3 s before being pulled away from the electrical source. According to previous studies [7–9] hearing loss after a high-voltage electrical shock is rare and could be moderate or profound. An extensive review [3] including 28 studies with a total of 2738 victims of electrical and lightning injury, auditory disturbances, such as hearing loss and tinnitus were reported by 220 (8%) patients. The hearing loss is usually sensorineural, mainly downward-sloping [9] and less commonly conductive, secondary to tympanic membrane rupture, with the latter occurring most often after lightning strikes (usually when the exit point is the external ear canal) [5]. In most of the above cases, the sensorineural hearing loss did not improve [8–10], and less frequently hearing returned to near normal thresholds after one month [7]. In our case a downwardsloping audiogram was similarly recorded such as described after electrical injury. It is not excluded that his hearing loss might be due to aging; however, this patient complained of a bilateral mild hearing loss (mainly in his left ear) and persistent tinnitus after electrical injury without having these symptoms before the incident. It is worth noting that one year after the electrical injury a very slight deterioration of hearing was found mainly at high
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frequencies, while the patient continued to report hearing impairment and tinnitus (Fig. 1B). There is no agreement in the literature if the auditory or the vestibular system is more vulnerable to the effect of electrical injury [5]. According to a review of the literature [1], one-third of the patients presented with dizziness after low-voltage electrical contact. By contrast, Bailey et al. [2], in a short-term follow-up of 98 patients injured by domestic or industrial current (median 52 days after injury), found that 2% only of them suffered from dizziness. In our case, the vestibular tests (caloric test, VEMPs) performed, revealed extensive vestibular damage, which resulted in delayed and incomplete recovery. In a similar case, Choi et al. [9] described a 31-year-old man who received an electrical insult when a 22,900 V cable fell over him; the caloric test demonstrated a unilateral paresis and a session of Cawthorne–Cooksey exercises helped him to recover from dizziness six months later. Electric injury occurs when an electric current is directed from the “entrance” point to the “exit” point through the body; the most common entrance points are hands and the head and the most common exit points are feet, legs and the hands [3]. Through this pathway, electricity follows the tissues of low resistance, such as the nervous system and blood vessels compared to bones, fat and muscles [3]. The exact mechanism of inner ear damage occurring in electrical injury remains unclear. A possible pathway for the electrical pulse to cause damage to the cochleovestibular system is through the internal auditory meatus and low-resistant cerebrospinal fluid [5]; the perilymphatic and endolymphatic spaces are also insulted, leading to extended damage of the saccular macula and abolished VEMPs. It should be underlined that absence of VEMPs may be due to aging; however, Janky and Shepard showed only minor age effect for VEMPs amplitude [11]. The tissue injury can also result from cellular rupture induced by the presence of an electric field creation (electroporation) [2]. Moreover, as electricity creates heat, a thermal effect is also expected, resulting in denaturation of tissue proteins [9]. Two temporal bone studies following lightning strike to the neck showed widespread inner ear changes with extensive neural damage to the spiral ganglion and nerve, degeneration of vestibular neuroepithelial structures and edema of the intracanalicular portion of facial nerve [12]. Such as degenerative process might also be present in our case, explaining why the symptoms (hearing loss, vertigo, tinnitus) appeared five days later; Duff and McCaffrey [3] mentioned that such symptoms may occur days, months or even years after the electrical injury. Jindal at al [7] reported on a 26-year-old electrician who experienced diminished hearing five days after high-voltage electrical injury. Propioceptive nerves are the most prone to damage after electrical injury [4], explaining the difficulty of our patient to walk (like on “broken tiles”). Depression has also been reported, with greater frequency in electrical injury patients who experience the “no-let-go” phenomenon or tetanic spasm preventing their release from the electrical source [4]. Although in our case the arch included right hand–body–legs, it has already been demonstrated that central nervous system injury
may exist even distant to the theoretical current pathway [1]. The exact mechanism resulting in neuropsychological manifestations of central origin is also unclear. In Jindal et al. [7] study, the ABRs revealed normal interpeak latencies I–III, III–V and I–V, concluding that the sensorineural hearing loss diagnosed after the electrical injury was of cochlear origin. This is in accordance with our initial findings in OAEs and ABRs in the first days after the electrical shock; however, one year later in our case, the absolute latency V and inter-peak latency III–V were both prolonged on the right side. Similarly, Hooshmand et al. [13] found that, in more than six months after the electrical injury, the inter-peak latency I–III was prolonged in half of the cases. Moreover, the EEG of our patient showed suspicious theta activity in the occipital lobes. It is possible that gradual degenerative process is responsible for these pathological findings in the central auditory nervous system, which can be considered as longterm neurological sequelae of electrical injury [4]. In conclusion, extensive damage in both the vestibular and auditory system can occur after electrical injury. The inner ear symptoms may persist long after the patient's hospital discharge, so long-term follow-up and support, both medical and psychological, are mandatory. It is evident that larger series are required in order to draw safe conclusions.
References [1] Morse JS, Morse MS. Diffuse electrical injury: comparison of physical and neuropsychological symptom presentation in males and females. J Psychosom Res 2005;58:51–4. [2] Bailey B, Gaudreault P, Thivierge RL. Neurologic and neuropsychological symptoms during the first year after an electric shock: results of a prospective multicenter study. Am J Emerg Med 2008;26:413–8. [3] Duff K, McCaffrey RJ. Electrical injury and lightning injury: a review of their mechanisms and neuropsychological, psychiatric, and neurological sequelae. Neuropsychol Rev 2001;11:101–16. [4] Wesner ML, Hickie J. Long-term sequelae of electrical injury. Can Fam Phys 2013;59:935–9. [5] Modayil PC, Lloyd GW, Mallik A, Bowdler DA. Inner ear damage following electric current and lightning injury: a literature review. Eur Arch Otorhinolaryngol 2014;855–61. [6] Hecker HC, Haug CO, Herndon JW. Treatment of the vertiginous patient using Cawthorne’s vestibular exercises. Laryngoscope 1974;84:2065–72. [7] Jindal P, Nagarkar AN, Mann SB. Reversible hearing loss associated with high-voltage electric shock. J Laryngol Otol 2005;119:631–3. [8] Liew L, Morrison GA. Bilateral hearing loss following electrocution. J Laryngol Otol 2006;120:65–6. [9] Choi DJ, Kim BG, Park IS, Kim YB, Kim TH, Heo CY. Three cases of inner ear damage after electrical burns. Burns 2010;36:e83–6. [10] Grossman AR, Tempereau CE, Brones MF, Kulber HS, Pembrook LJ. Auditory and neuropsychiatric behaviour patterns after electrical injury. J Burn Care Rehabil 1993;14:169–75. [11] Janky KL, Shepard N. Vestibular evoked myogenic potential (VEMP) testing: normative threshold response curves and effects of age. J Am Acad Audiol 2009;20:514–22. [12] Youngs R, Deck J, Kwok P, Hawke M. Severe sensorineural hearing loss caused by lightning. A temporal bone case report. Arch Otolaryngol Head Neck Surg 1988;114:1184–7. [13] Hooshmand H, Radfar F, Beckner E. The neurophysiological aspects of electrical injuries. Clin Electroencephalogr 1989;20:111–20.
Please cite this article in press as: Psillas G, et al. Bilateral inner ear damage after electrical injury: A case report. Auris Nasus Larynx (2017), http://dx.doi.org/10.1016/j.anl.2017.01.016