AMER IC AN JOURNAL OF OT OLA RYNGOLOGY– H E A D A N D NE CK M E D ICI N E AN D S U RGE RY X X (2 0 1 5) XXX – XXX
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Sudden sensorineural hearing loss after non-otologic surgery☆,☆☆,★ Joshua Cody Page, BBA a,⁎, Bob Peters, MD b a b
UT Southwestern, Medical School, 5323 Harry Hines Blvd., Dallas, TX, USA Dallas Ear Institute, 7777 Forest Lane, Suite A-103, Dallas, TX, USA
ARTI CLE I NFO
A BS TRACT
Article history:
Sudden sensorineural hearing loss following non-otologic surgery is a rare event
Received 22 March 2015
described in the medical literature. Cardiopulmonary bypass surgery is most commonly associated with this type of hearing loss. Our case report and review of the literature describe two cases with postoperative hearing loss – neither of which are cardiac surgeries – making them exceedingly rare in the medical literature. Regardless of the rarity of this unfortunate event, the possibility for permanent hearing loss is a potentially devastating unanticipated complication and one that all surgeons should be aware. © 2015 Elsevier Inc. All rights reserved.
1.
Objective
Sudden sensorineural hearing loss (SNHL) in the postoperative setting has been reported to occur after many different types of non-otologic surgical interventions. Reported cases involve such a diversity of surgical procedures that the exact mechanism(s) by which SNHL occurs is often unclear. There are two categories of surgery that are most commonly related to reports of SNHL in the literature: cardiopulmonary bypass (CPB) surgery and procedures associated with a loss of cerebrospinal fluid (CSF). This report adds to the literature two more cases of SNHL after non-otologic surgery, one of which has previously unreported bilateral involvement, and reviews the literature to postulate mechanisms by which SNHL in this setting might occur.
2.
Patients
2.1.
Case #1
A 44-year-old female with no prior history of hearing loss underwent a total abdominal hysterectomy and an anterior and posterior repair with abdominoplasty in a combined 10-h surgery with a total blood loss of 700 ml. She noticed significant hearing loss in the right ear the morning after surgery. Her neurologic exam was otherwise normal. An audiogram was first performed three days after surgery by a referring physician demonstrating a severe-to-profound, down-sloping, high frequency predominant right ear SNHL with normal hearing in the left ear. She first presented to our clinic three weeks postoperatively for evaluation and received three .5 cc intratympanic dexamethasone injections over the
Abbreviations: SNHL, Sudden sensorineural hearing loss; CPB, cardiopulmonary bypass; CSF, cerebrospinal fluid. Consent: Written informed consent was obtained from the patient for publication of this Case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. ☆☆ Disclosure: Each author (Dr Bob Peters, Cody Page) has contributed to, read and approved the final submitted form of this manuscript. ★ Other: This manuscript is original and it, or any part of it, has not been previously published; nor is it under consideration for publication elsewhere. ⁎ Corresponding author at: 5464 Anita St, Dallas, TX, 75206. Tel.: +1 9032448508. E-mail addresses: [email protected] (J.C. Page), [email protected] (B. Peters). ☆
http://dx.doi.org/10.1016/j.amjoto.2015.04.014 0196-0709/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Page JC, Peters B, Sudden sensorineural hearing loss after non-otologic surgery, Am J Otolaryngol–Head and Neck Med and Surg (2015), http://dx.doi.org/10.1016/j.amjoto.2015.04.014
2
AMER ICA N JOURNAL OF OT OLA RYNGOLOGY– H E A D A N D N E CK M EDI CI N E AN D S U RGE RY X X (2 0 1 5) XXX – XXX
course of three weeks. Her initial and 18 month postoperative audiograms from our clinic are shown in Fig. 1 showing no significant return of hearing in the right ear. Head and temporal bone MRI and CT scans were normal.
2.2.
Case #2
A 63-year-old male underwent a left retrosigmoid craniotomy with microvascular decompression of the trigeminal nerve in the semisitting position for intractable trigeminal neuralgia. No known ototoxic medications were given perioperatively. Intra-operative bilateral auditory brainstem response (ABR) monitoring remained stable throughout the course of this two and a half hour procedure. The day after surgery, the patient reported severe bilateral hearing loss. His neurotologic exam was normal. His preoperative audiogram and those performed on postoperative days (POD) 1, 3 and 10 are compared in Fig. 2, showing a slowly resolving severe, flat bilateral SNHL. A review of all available MRI and CT scans demonstrated normal labyrinthine, cochlear aqueduct, and vestibular aqueduct anatomy.
3.
Discussion
SNHL after non-otologic surgery is an unexpected and frightening complication. Since the first report by Jaffe [1], SNHL has been reported following a variety of surgical procedures including orthopedic, abdominal, cardiovascular, ophthalmologic, dental and neurosurgical [2]. Cases have also included the use of general, spinal, and retrobulbar anesthesia [3]. Because of the wide variety of nonotologic procedures that have resulted in unexpected postoperative SNHL, several mechanisms have been postulated. Intracochlear membrane leaks, perilymphatic fistulae from implosive or explosive forces, and microvascular compromise from hemodynamic hypoperfusion or microemboli are some of the speculative theories. Two categories of surgery appear in the literature to be involved in a higher percentage of reported cases of post-operative SNHL than all others: surgeries involving cardiopulmonary bypass (CPB) and those involving loss of cerebrospinal fluid (CSF).
The well-recognized association of SNHL with CPB procedures has led to the theory that either microemboli or nonembolic hemodynamic hypoperfusion is the most likely cause in this group of patients. When evaluated retrospectively, the reported incidence is estimated at 1 to 1.8/1000 operations [4]. However, two prospective studies which compared pre and postoperative audiograms for minor hearing changes regardless of subjective patient complaints demonstrated an incidence of 8.8% and 10%, respectively [5,6]. Though our patient in Case #1 did not undergo CPB, the hypoperfusion theory can be extended to similar procedures that involve extensive, prolonged surgery with significant hemodynamic fluid displacement. SNHL after various procedures that involve the loss of CSF has been widely reported [7,8]. Dreyer et al. [9] prospectively studied 100 patients undergoing spinal anesthesia either for general surgical or urological (non-neurosurgical) procedures with pre and postoperative audiograms. Sixteen patients (16%) developed statistically significant hearing loss, typically beginning on the second postoperative day, involving only the frequencies from 125 to 2000 Hz, and resolving in all patients by the 3rd postoperative day. The audiometric pattern of hearing loss described in the vast majority of studies involving CSF procedures cited here is overwhelmingly flat or low-frequency predominant, consistent with our finding in Case #2. This audiometric pattern, which is similar to that seen in Meniere’s Disease, suggests that the loss of CSF may result in an intracochlear fluid abnormality. The loss of perilymph centrally through a patent cochlear aqueduct, leading to “perilymphatic hypotonia” and a relative endolymphatic hydrops, is a theory consistent with the clinical findings in these patients. Such an exchange of perilymph in the face of low CSF pressure does not require the presence of a radiographically enlarged cochlear aqueduct [10]. Our patient from Case #2 had completely normal temporal bone anatomy on both CT and MRI scans. Therefore it would seem impossible to predict preoperatively which patients may be at increased risk of hearing loss with procedures that involve CSF loss. Theoretically it makes sense that a patient who has a history of Meniere’s disease, and therefore may already have increased endolymphatic pressure, may be at an increased risk, but this has yet to be demonstrated.
Fig. 1 – This audiogram is from a 44-year-old woman who suffered severe-to-profound, down-sloping, high frequency predominant hearing loss in her right ear three days after total abdominal hysterectomy, anterior and posterior repair and abdominoplasty. Her hearing did not improve after 18 months. Please cite this article as: Page JC, Peters B, Sudden sensorineural hearing loss after non-otologic surgery, Am J Otolaryngol–Head and Neck Med and Surg (2015), http://dx.doi.org/10.1016/j.amjoto.2015.04.014
AMER IC AN JOURNAL OF OT OLA RYNGOLOGY– H E A D A N D NE CK M E D ICI N E AN D S U RGE RY X X (2 0 1 5) XXX – XXX
3
Fig. 2 – This audiogram is from a 63-year-old man who suffered severe, flat bilateral sensorineural hearing loss following microvascular decompression of his trigeminal nerve with resultant CSF loss. His hearing returned to baseline after 10 days, as shown here.
Bilaterality is another characteristic of Case #2 that is worth discussing. Of the theories put forth to explain SNHL after surgery, hemodynamic hypoperfusion, and relative endolymphatic hydrops via loss of CSF seem to be the etiologies most likely to have a similar effect on both ears. Etiologies such as microembolism seem extremely unlikely to affect the microcirculation of both ears in the same patient without resulting in any other neurologic sequelae. Unfortunately, cases of SNHL which are postulated to be related to hemodynamic hypoperfusion often fail to recover, as is true of our first case. A very high percentage of patients with SNHL related to CSF loss recover within a few days to 1 week, similar to our second case. Neither of our patients had tinnitus as a significant complaint. This may be partially due to the fact that in the early stages, a complaint such as tinnitus may be overshadowed by the unexpected nature of and concerns for their hearing loss. Our first patient whose SNHL remained permanent did not consider her tinnitus to be in need of intervention. This likely has nothing to do with the mechanisms of her SNHL, but rather with individual patient characteristics. In cases of acute onset unilateral SHNL such as our first patient, it is our recommendation that they wait at least 6– 12 months for maximal hearing recovery and central compensation before considering other treatment options. Over that period of time their central auditory processes make some adjustment for the loss of binaural input, after which some patients with normal hearing in the contralateral ear do not feel the need for any other intervention. For those who do however, the options include a CROS (Contralateral Rerouting of Signal) hearing aid, a BAHA (Bone Anchored Hearing Aid), or a unilateral cochlear implant (CI). Neither the CROS nor BAHA restores true binaural auditory mechanisms in those with single-sided severe to profound SNHL. They do however help mitigate the head shadow effect that occurs when attempting to hear important sounds that originate on the hearing impaired side. A cochlear implant has the potential to restore binaural mechanisms, but its use in such cases with normal contralateral hearing is still controversial and investigational.
Though the incidence of such SNHL is low, the possibility for permanence makes this a potentially devastating complication of non-otologic procedures of which all clinicians who care for these patients should be aware.
Acknowledgments N/A
REFERENCES
[1] Jaffe BF. Sudden deafness — an otologic emergency. Arch Otolaryngol 1967;86:55–60. [2] Kansu L, Yilmax I. Sudden hearing loss after dental treatment. J Oral Maxillofac Surg 2013;71:1318–21. [3] George RB, Hackett J. Bilateral hearing loss following a retrobulbar block. Can J Anaesth 2005;52:1054–7. [4] Cervantes Escarcega JL, Lopez Luciano J, Fernandez F, et al. Sudden deafness in patients undergoing cardiac surgery with extracorporeal circulation. Arch Inst Cardiol Mex 1988;58: 447–51. [5] Shapiro MJ, Purn JM, Raskin C. A study of the effects of cardiopulmonary bypass surgery on auditory function. Laryngoscope 1981;91:2046–52. [6] Phillipps JJ, Thornton AR. Audiometric changes in patients undergoing coronary artery bypass surgery. Br J Audiol 1996;30: 19–25. [7] Spirakis SE, Hurley RM. Unilateral hearing loss in children with shunt treated hydrocephalus. J Am Acad Audiol 2003; 14:510–7. [8] Walsted A, Nielsen OA, Borum P. Hearing loss after neurosurgery. The influence of low cerebrospinal fluid pressure. J Laryngol Otol 1994;108:637–41. [9] Dreyer M, Migdal H. Transient medium- and deep-tone hearing disorders following spinal anesthesia. Reg Anesth 1990;13:138–41. [10] Walsted A, Salomon G, Thomsen J. Hearing decrease after loss of cerebrospinal fluid. A new hydrops model? Acta Otolaryngol 1991;111:468–76.
Please cite this article as: Page JC, Peters B, Sudden sensorineural hearing loss after non-otologic surgery, Am J Otolaryngol–Head and Neck Med and Surg (2015), http://dx.doi.org/10.1016/j.amjoto.2015.04.014
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Sudden sensorineural hearing loss after non-otologic surgery☆,☆☆,★ Joshua Cody Page, BBA a,⁎, Bob Peters, MD b a b
UT Southwestern, Medical School, 5323 Harry Hines Blvd., Dallas, TX, USA Dallas Ear Institute, 7777 Forest Lane, Suite A-103, Dallas, TX, USA
ARTI CLE I NFO
A BS TRACT
Article history:
Sudden sensorineural hearing loss following non-otologic surgery is a rare event
Received 22 March 2015
described in the medical literature. Cardiopulmonary bypass surgery is most commonly associated with this type of hearing loss. Our case report and review of the literature describe two cases with postoperative hearing loss – neither of which are cardiac surgeries – making them exceedingly rare in the medical literature. Regardless of the rarity of this unfortunate event, the possibility for permanent hearing loss is a potentially devastating unanticipated complication and one that all surgeons should be aware. © 2015 Elsevier Inc. All rights reserved.
1.
Objective
Sudden sensorineural hearing loss (SNHL) in the postoperative setting has been reported to occur after many different types of non-otologic surgical interventions. Reported cases involve such a diversity of surgical procedures that the exact mechanism(s) by which SNHL occurs is often unclear. There are two categories of surgery that are most commonly related to reports of SNHL in the literature: cardiopulmonary bypass (CPB) surgery and procedures associated with a loss of cerebrospinal fluid (CSF). This report adds to the literature two more cases of SNHL after non-otologic surgery, one of which has previously unreported bilateral involvement, and reviews the literature to postulate mechanisms by which SNHL in this setting might occur.
2.
Patients
2.1.
Case #1
A 44-year-old female with no prior history of hearing loss underwent a total abdominal hysterectomy and an anterior and posterior repair with abdominoplasty in a combined 10-h surgery with a total blood loss of 700 ml. She noticed significant hearing loss in the right ear the morning after surgery. Her neurologic exam was otherwise normal. An audiogram was first performed three days after surgery by a referring physician demonstrating a severe-to-profound, down-sloping, high frequency predominant right ear SNHL with normal hearing in the left ear. She first presented to our clinic three weeks postoperatively for evaluation and received three .5 cc intratympanic dexamethasone injections over the
Abbreviations: SNHL, Sudden sensorineural hearing loss; CPB, cardiopulmonary bypass; CSF, cerebrospinal fluid. Consent: Written informed consent was obtained from the patient for publication of this Case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. ☆☆ Disclosure: Each author (Dr Bob Peters, Cody Page) has contributed to, read and approved the final submitted form of this manuscript. ★ Other: This manuscript is original and it, or any part of it, has not been previously published; nor is it under consideration for publication elsewhere. ⁎ Corresponding author at: 5464 Anita St, Dallas, TX, 75206. Tel.: +1 9032448508. E-mail addresses: [email protected] (J.C. Page), [email protected] (B. Peters). ☆
http://dx.doi.org/10.1016/j.amjoto.2015.04.014 0196-0709/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Page JC, Peters B, Sudden sensorineural hearing loss after non-otologic surgery, Am J Otolaryngol–Head and Neck Med and Surg (2015), http://dx.doi.org/10.1016/j.amjoto.2015.04.014
2
AMER ICA N JOURNAL OF OT OLA RYNGOLOGY– H E A D A N D N E CK M EDI CI N E AN D S U RGE RY X X (2 0 1 5) XXX – XXX
course of three weeks. Her initial and 18 month postoperative audiograms from our clinic are shown in Fig. 1 showing no significant return of hearing in the right ear. Head and temporal bone MRI and CT scans were normal.
2.2.
Case #2
A 63-year-old male underwent a left retrosigmoid craniotomy with microvascular decompression of the trigeminal nerve in the semisitting position for intractable trigeminal neuralgia. No known ototoxic medications were given perioperatively. Intra-operative bilateral auditory brainstem response (ABR) monitoring remained stable throughout the course of this two and a half hour procedure. The day after surgery, the patient reported severe bilateral hearing loss. His neurotologic exam was normal. His preoperative audiogram and those performed on postoperative days (POD) 1, 3 and 10 are compared in Fig. 2, showing a slowly resolving severe, flat bilateral SNHL. A review of all available MRI and CT scans demonstrated normal labyrinthine, cochlear aqueduct, and vestibular aqueduct anatomy.
3.
Discussion
SNHL after non-otologic surgery is an unexpected and frightening complication. Since the first report by Jaffe [1], SNHL has been reported following a variety of surgical procedures including orthopedic, abdominal, cardiovascular, ophthalmologic, dental and neurosurgical [2]. Cases have also included the use of general, spinal, and retrobulbar anesthesia [3]. Because of the wide variety of nonotologic procedures that have resulted in unexpected postoperative SNHL, several mechanisms have been postulated. Intracochlear membrane leaks, perilymphatic fistulae from implosive or explosive forces, and microvascular compromise from hemodynamic hypoperfusion or microemboli are some of the speculative theories. Two categories of surgery appear in the literature to be involved in a higher percentage of reported cases of post-operative SNHL than all others: surgeries involving cardiopulmonary bypass (CPB) and those involving loss of cerebrospinal fluid (CSF).
The well-recognized association of SNHL with CPB procedures has led to the theory that either microemboli or nonembolic hemodynamic hypoperfusion is the most likely cause in this group of patients. When evaluated retrospectively, the reported incidence is estimated at 1 to 1.8/1000 operations [4]. However, two prospective studies which compared pre and postoperative audiograms for minor hearing changes regardless of subjective patient complaints demonstrated an incidence of 8.8% and 10%, respectively [5,6]. Though our patient in Case #1 did not undergo CPB, the hypoperfusion theory can be extended to similar procedures that involve extensive, prolonged surgery with significant hemodynamic fluid displacement. SNHL after various procedures that involve the loss of CSF has been widely reported [7,8]. Dreyer et al. [9] prospectively studied 100 patients undergoing spinal anesthesia either for general surgical or urological (non-neurosurgical) procedures with pre and postoperative audiograms. Sixteen patients (16%) developed statistically significant hearing loss, typically beginning on the second postoperative day, involving only the frequencies from 125 to 2000 Hz, and resolving in all patients by the 3rd postoperative day. The audiometric pattern of hearing loss described in the vast majority of studies involving CSF procedures cited here is overwhelmingly flat or low-frequency predominant, consistent with our finding in Case #2. This audiometric pattern, which is similar to that seen in Meniere’s Disease, suggests that the loss of CSF may result in an intracochlear fluid abnormality. The loss of perilymph centrally through a patent cochlear aqueduct, leading to “perilymphatic hypotonia” and a relative endolymphatic hydrops, is a theory consistent with the clinical findings in these patients. Such an exchange of perilymph in the face of low CSF pressure does not require the presence of a radiographically enlarged cochlear aqueduct [10]. Our patient from Case #2 had completely normal temporal bone anatomy on both CT and MRI scans. Therefore it would seem impossible to predict preoperatively which patients may be at increased risk of hearing loss with procedures that involve CSF loss. Theoretically it makes sense that a patient who has a history of Meniere’s disease, and therefore may already have increased endolymphatic pressure, may be at an increased risk, but this has yet to be demonstrated.
Fig. 1 – This audiogram is from a 44-year-old woman who suffered severe-to-profound, down-sloping, high frequency predominant hearing loss in her right ear three days after total abdominal hysterectomy, anterior and posterior repair and abdominoplasty. Her hearing did not improve after 18 months. Please cite this article as: Page JC, Peters B, Sudden sensorineural hearing loss after non-otologic surgery, Am J Otolaryngol–Head and Neck Med and Surg (2015), http://dx.doi.org/10.1016/j.amjoto.2015.04.014
AMER IC AN JOURNAL OF OT OLA RYNGOLOGY– H E A D A N D NE CK M E D ICI N E AN D S U RGE RY X X (2 0 1 5) XXX – XXX
3
Fig. 2 – This audiogram is from a 63-year-old man who suffered severe, flat bilateral sensorineural hearing loss following microvascular decompression of his trigeminal nerve with resultant CSF loss. His hearing returned to baseline after 10 days, as shown here.
Bilaterality is another characteristic of Case #2 that is worth discussing. Of the theories put forth to explain SNHL after surgery, hemodynamic hypoperfusion, and relative endolymphatic hydrops via loss of CSF seem to be the etiologies most likely to have a similar effect on both ears. Etiologies such as microembolism seem extremely unlikely to affect the microcirculation of both ears in the same patient without resulting in any other neurologic sequelae. Unfortunately, cases of SNHL which are postulated to be related to hemodynamic hypoperfusion often fail to recover, as is true of our first case. A very high percentage of patients with SNHL related to CSF loss recover within a few days to 1 week, similar to our second case. Neither of our patients had tinnitus as a significant complaint. This may be partially due to the fact that in the early stages, a complaint such as tinnitus may be overshadowed by the unexpected nature of and concerns for their hearing loss. Our first patient whose SNHL remained permanent did not consider her tinnitus to be in need of intervention. This likely has nothing to do with the mechanisms of her SNHL, but rather with individual patient characteristics. In cases of acute onset unilateral SHNL such as our first patient, it is our recommendation that they wait at least 6– 12 months for maximal hearing recovery and central compensation before considering other treatment options. Over that period of time their central auditory processes make some adjustment for the loss of binaural input, after which some patients with normal hearing in the contralateral ear do not feel the need for any other intervention. For those who do however, the options include a CROS (Contralateral Rerouting of Signal) hearing aid, a BAHA (Bone Anchored Hearing Aid), or a unilateral cochlear implant (CI). Neither the CROS nor BAHA restores true binaural auditory mechanisms in those with single-sided severe to profound SNHL. They do however help mitigate the head shadow effect that occurs when attempting to hear important sounds that originate on the hearing impaired side. A cochlear implant has the potential to restore binaural mechanisms, but its use in such cases with normal contralateral hearing is still controversial and investigational.
Though the incidence of such SNHL is low, the possibility for permanence makes this a potentially devastating complication of non-otologic procedures of which all clinicians who care for these patients should be aware.
Acknowledgments N/A
REFERENCES
[1] Jaffe BF. Sudden deafness — an otologic emergency. Arch Otolaryngol 1967;86:55–60. [2] Kansu L, Yilmax I. Sudden hearing loss after dental treatment. J Oral Maxillofac Surg 2013;71:1318–21. [3] George RB, Hackett J. Bilateral hearing loss following a retrobulbar block. Can J Anaesth 2005;52:1054–7. [4] Cervantes Escarcega JL, Lopez Luciano J, Fernandez F, et al. Sudden deafness in patients undergoing cardiac surgery with extracorporeal circulation. Arch Inst Cardiol Mex 1988;58: 447–51. [5] Shapiro MJ, Purn JM, Raskin C. A study of the effects of cardiopulmonary bypass surgery on auditory function. Laryngoscope 1981;91:2046–52. [6] Phillipps JJ, Thornton AR. Audiometric changes in patients undergoing coronary artery bypass surgery. Br J Audiol 1996;30: 19–25. [7] Spirakis SE, Hurley RM. Unilateral hearing loss in children with shunt treated hydrocephalus. J Am Acad Audiol 2003; 14:510–7. [8] Walsted A, Nielsen OA, Borum P. Hearing loss after neurosurgery. The influence of low cerebrospinal fluid pressure. J Laryngol Otol 1994;108:637–41. [9] Dreyer M, Migdal H. Transient medium- and deep-tone hearing disorders following spinal anesthesia. Reg Anesth 1990;13:138–41. [10] Walsted A, Salomon G, Thomsen J. Hearing decrease after loss of cerebrospinal fluid. A new hydrops model? Acta Otolaryngol 1991;111:468–76.
Please cite this article as: Page JC, Peters B, Sudden sensorineural hearing loss after non-otologic surgery, Am J Otolaryngol–Head and Neck Med and Surg (2015), http://dx.doi.org/10.1016/j.amjoto.2015.04.014
