Sudden sensorineural hearing loss and hemodialysis.
The etiology of sensorineural hearing loss (SNHL) associated with renal failure and hemodialysis is controversial. Possible mechanisms include a shared antigenicity between the kidney and the labyrinths, osmotic alteration caused by hemodialysis, and the ototoxic effect of diuretics. We present 2 cases of SNHL associated with renal failure and its treatment. One patient was a 35-year-old man who developed profound SNHL after 5 sessions of hemodialysis, and the other was a 36-year-old woman who developed severe to profound SNHL after 7 sessions. It is our impression that both hearing losses might have been attributable to osmotic disequilibrium in the labyrinth or to an acute labyrinthine injury caused by contamination of the blood by the degraded product of an old cellulose acetate hemodialyzer membrane; the hemodialyzer had been in use for 15 years.
Sudden sensorineural heating loss (SNHL) is frequently reported in patients with renal failure who undergo hemodialysis, but its etiology in this circumstance remains controversial. (1) One possible explanation is that the kidney and the labyrinths have a shared antigenicity and, as a result, many patients with congenital renal failure have SNHL. In addition, many nephrotoxic drugs are also ototoxic. (2) Moreover, a significant decrease in cochlear microphonic and cochlear nerve action potential has been demonstrated in guinea pigs in a uremic state. (3) This finding has been corroborated in humans; lengthening of the interpeak latencies in the auditory brainstem response, collapse of the endolymphatic space, and the presence of deposits in the stria and vestibular apparatus have been documented in uremic humans. (4)
Hemodialysis also appears to have an ototoxic effect, although in some cases it is difficult to make a sharp distinction between its effects and the effects of the renal failure itself. The prevalence of hearing loss in hemodialysis-treated patients has been reported to range between 15 and 54%. (1-6)
An osmotic/electrolytic alteration caused by hemodialysis can result in (1) a loss of outer hair cells and spiral ganglion in the cochlea, (2) collapse of the endolymphatic space, and (3) edema and atrophy of the specialized auditory cells. (4-7) Also, the etiology of deafness in these patients may be related to the premature aging induced by chronic renal failure. Finally, hearing loss might be caused by contamination of the blood by remnants of old dialysis material, particularly cellulose acetate.
Our dialysis center at University College Hospital in Ibadan, Nigeria was established approximately 15 years ago. Since then, we have dialyzed more than 1,000 patients. In this article, we report 2 cases of SNHL that occurred during the course of dialysis. We believe these hearing losses were probably caused by contamination of the blood by the degraded product of an old cellulose acetate hemodialyzer membrane. We also review the literature on hearing loss and renal failure.
Patient 1. A 35-year-old man, a baker and teacher, was admitted via the accident and emergency unit with a 2-week history of diarrhea and vomiting. He had been previously seen at a private hospital, where he had been receiving treatment for oliguria, an altered level of consciousness, and a biochemical profile consistent with renal failure. He had no history of kidney disease or exposure to nephrotoxic substances, and no history of facial or pedal edema. Complete details on the drugs that had been administered at the private hospital were unavailable.
On examination, the patient was confused, drowsy, pale, anicteric, afebrile, and dehydrated. Facial swelling and mild pedal edema were present. On admission, he had an elevated blood pressure (150/80 mm Hg), serum urea nitrogen level (347 mg/dl), and creatinine level (12.5 mg/dl) and a low hematocrit (11%). Findings in other systems were essentially normal. A diagnosis of acute renal failure secondary to gastroenteritis was made, and he was prescribed dialysis.
After the fifth session of hemodialysis, the patient had experienced some clinical improvement, but he discovered that he was unable to hear. He was able to speak coherently and understand and reply to written messages and instructions. He was referred to the consultant otorhinolaryngologist, who found that the patient could not hear normal conversation at 1 meter. At closer proximity, he could barely hear a shout, and he was not able to recognize speech.
An ENT examination revealed normal anatomy. The patient exhibited no response to tuning-fork testing. Pure-tone audiometry at 500 to 8,000 Hz revealed a profound bilateral hearing loss. Bone conduction was less than 100 dB and air conduction was 90 dB. Findings on repeat audiometry 3 months later were unchanged, and the patient's speech recognition was poor. He was advised to procure a set of hearing aids. Audiometric findings at 6 months were unchanged.
Patient 2. A 36-year-old woman, a trader, was referred to the medical outpatient unit of a private hospital by her private physician with a 2-day history of generalized malaise, dizziness, vomiting, and early-morning facial puffiness. She had been diagnosed with hypertension 3 years earlier, but her blood pressure was not well controlled. She had experienced 2 episodes of spontaneous abortion, one 4 years earlier and the other the previous year; retained products had been removed by vacuum aspiration and dilation and curettage. She had a history of using oral contraceptives and abusing topical steroids for skin toning. Examination revealed that her blood pressure (170/100 mm Hg), serum urea nitrogen level (212 mg/dl), and creatinine level (26.3 mg/dl) were high and her hematocrit was low (15%). Other systems were essentially normal. The patient was diagnosed with chronic renal failure secondary to hypertensive nephrosclerosis and prescribed hemodialysis and blood transfusions. After 4 sessions of hemodialysis and transfusion of 4 pints of blood, the patient demonstrated clinical improvement. Her serum urea nitrogen level fell to 50 mg/dl, and her creatinine level dropped to 5.5 mg/dl. She was discharged home on antihypertensive and diuretic medications.
During follow-up at our outpatient clinic, we found that the patient's biochemical profile had deteriorated. She was placed on alternate-week maintenance dialysis because she could not afford regular dialysis. She also received additional blood transfusions to treat severe anemia. After the seventh session of hemodialysis, the patient complained of hearing loss. The heating loss progressed rapidly, and within 3 weeks she had become deaf.
An examination revealed that the external anatomy of the ear, nose, and throat was normal. The patient exhibited no response to tuning-fork testing or to distraction testing with a bell rung at ear level. Pure-tone audiometry revealed a profound bilateral bone-conduction hearing loss (<100 dB at all frequencies). The patient was advised to procure a set of hearing aids. She was lost to follow-up.
Hemodialysis has remarkably improved the prognosis for patients with chronic renal disease, but many complain of tinnitus, vertigo, and hearing loss. (8) The results of several investigations have suggested that permanent SNHL develops in as many as 54% of patients with nonhereditary chronic renal failure; the vast majority of affected patients had been treated with hemodialysis. (1-6)
Oda et al reported hearing loss in 43 of 290 hemodialysis patients (15%). (5) Their temporal bone studies showed that cochlear changes ranged from a mild loss of outer hair cells in patients who had undergone relatively few hemodialysis treatments and transplants to a complete absence of the organ of Corti in patients who underwent more than 250 hemodialysis treatments and multiple transplants. They concluded that the severity of the clinical and histopathologic findings was directly proportional to the number of hemodialysis treatments and transplants patients underwent.
Kligerman et al found high-frequency (>2,000 Hz) hearing loss in 15 of 28 patients (54%) treated with hemodialysis. (1) The site of the lesion was the cochlea. They reported an association between heating loss and the duration of hemodialysis; hearing losses occurred in 30% of patients who had been on hemodialysis for 18 months or less and in 67% of those who had been on hemodialysis for more than 18 months. Heating loss was also associated with the duration of individual hemodialysis sessions. Age, noise exposure, and drug ototoxicity did not contribute to hearing loss in this study.
Bergstrom et al reported that 91 of 224 patients (41%) with chronic renal disease treated with hemodialysis developed SNHL. (6) Examination of the temporal bone revealed fibrous tissue in perilymphatic spaces and degradation of the organ of Corti in one of these patients and a loss of hair cells of the organ of Corti in some others. The authors suggested that the strial deposits were calcific and possibly formed as a result of abnormal calcium-phosphorus metabolism.
Johnson and Mathog studied 61 patients with chronic renal failure undergoing hemodialysis and reported a significant high-frequency deficit early in the course of hemodialysis. (8) They also found fluctuations in hearing during single dialysis events; these fluctuations were transient and independent of changes in levels of sodium, potassium, calcium, blood urea nitrogen, glucose, blood pressure, and weight. The auditory depression reported occurred above 2 kHz.
Several other isolated cases have been reported. Rizvi and Holmes described the case of a 47-year-old man with chronic renal failure and normal hearing who experienced heating loss in "additive increments" during peritoneal dialysis and hemodialysis until he became profoundly deaf in both ears. (9) Postmortem studies revealed a collapse of his endolymphatic system and the presence of edema and atrophy in most of the specialized cell types of the auditory and vestibular sensory organs. The authors proposed that these alterations were caused by osmotic disequilibrium associated with hemodialysis. A similar conclusion was reached by Makita et al. (10)
Hutter et al observed acute-onset hearing loss and severe neurologic symptoms 7 to 24 hours after hemodialysis in 7 hospitalized patients. (11) This finding drew attention to the issue of the long-term integrity of dialysis machines and materials. The authors concluded that these injuries were associated with exposure to aged cellulose acetate dialyzer membranes, which allowed cellulose acetate degradation products to enter the bloodstream.
Many others have reported the ototoxic effect of hexadimethrine bromide (Polybrene) and other macromolecular substances. (12,13) Temporal bone examination showed severe losses of hair cells in the organ of Corti following hexadimethrine administration.
Others have found that SNHL was not related to hemodialysis. Ozturan and Lam studied 15 patients and 10 controls and compared pure-tone audiometry and distortion-product otoacoustic emissions (DPOAE) measurements before and after hemodialysis. (14) They found no difference in the pure-tone average before and after hemodialysis. They concluded that hemodialysis is safe and that the SNHL in these patients may have been attributable solely to their renal disease.
Stavroulaki et al studied the effect of hemodialysis on hearing acuity in 9 children with end-stage renal disease. (15) They found SNHL of unknown etiology in 5 of these patients (56%) on pure-tone audiometry and DPOAE measurements. They concluded that high-frequency SNHL is common in young renal failure patients who undergo multiple hemodialysis but that a single hemodialysis session does not appear to alter their hearing acuity.
Kusakari et al analyzed the heating of 37 hemodialysis patients. (16) Hearing evaluations were performed at the initiation of hemodialysis and every 3 to 12 months thereafter for at least 4 years. Only 3 patients exhibited significant hearing loss after hemodialysis. The authors concluded that hemodialysis per se does not harm the cochlea and that hearing can be maintained at pre-hemodialysis levels in most patients.
Deafness may be reversible in some patients with chronic renal failure who undergo hemodialysis, so a prolonged follow-up is necessary.
In our 2 patients, a profound, sudden-onset SNHL developed during the course of hemodialysis, and it was confirmed by pure-tone audiometry. The hearing loss was evident at all frequencies, unlike the case in many other reports, in which hearing loss was limited to the high frequencies. Although authors have reported the superiority of DPOAE measurements over pure-tone audiometry for the detection of early hearing loss, the latter is still reliable. (9,14,15)
It is our interpretation that the hearing loss in our 2 patients can be explained by (1) an acute osmotic imbalance caused by hemodialysis or (2) an acute labyrinthine injury secondary to the introduction into the bloodstream of degraded product from an old cellulose acetate membrane in a hemodialyzer that had been in use for 15 years.
In conclusion, hearing loss is a common finding in patients with chronic renal failure, and deafness may occur during the course of hemodialysis. Uremia, ototoxins, axonal uremic neuropathy, anemia, and toxic degradation products from cellulose acetate dialyzer membranes are all possible etiologic factors. We hope that a prospective study on this subject may clarify the relationship between hearing loss and chronic renal failure and its treatment.
(1.) Kligerman AB, Solangi KB, Ventry IM, et al. Hearing impairment associated with chronic renal failure. Laryngoscope 1981;91: 583-92.
(2.) Quick CA, Fish A, Brown C. The relationship between cochlea and kidney. Laryngoscope 1973;83:1469-82.
(3.) Ikeda K, Kusakari J, Arakawa E, et al. Cochlear potentials of guinea pigs with experimentally induced renal failure. Acta Otolaryngol Suppl 1987;435:40-5.
(4.) Schuknecht HF, ed. Pathology of the Ear. 2nd ed. Philadelphia: Lea & Febiger; 1993:275-8.
(5.) Oda M, Preciado MC, Quick CA, Paparella MM. Labyrinthine pathology of chronic renal failure patients treated with hemodialysis and kidney transplantation. Laryngoscope 1974;84:1489-1506.
(6.) Bergstrom L, Jenkins P, Sando I, English GM. Heating loss in renal disease: Clinical and pathological studies. Ann Otol Rhinol Laryngol 1973;82:555-76.
(7.) McDonald TJ, Zincke H, Anderson CF, Ott NT. Reversal of deafness after renal transplantation in Alport's syndrome. Laryngoscope 1978;88:38-42.
(8.) Johnson DW, Mathog RH. Hearing function and chronic renal failure. Ann Otol Rhinol Laryngol 1976;85:43-9.
(9.) Rizvi SS, Holmes RA. Hearing loss from hemodialysis. Arch Otolaryngol 1980;106:751-6.
(10.) Makita Y, Osato S, Onoyama K, et al. Idiopathic sudden sensorineural hearing loss in patients undergoing long-term haemodialysis. Int Urol Nephrol 1995;27:487-93.
(11.) Hutter JC, Kuehnert MJ, Wallis RR, et al. Acute onset of decreased vision and hearing traced to hemodialysis treatment with aged dialyzers. JAMA 2000;283:2128-34.
(12.) Kimura ET, Young PR, Barlow GH. A study with low and high molecular weights of hexadimethrine bromide--an antiheparin agent. Proc Soc Exp Biol Med 1962;111:37-41.
(13.) Ransome J, Ballantyne JC, Shaldon S, et al. Perceptive deafness in subjects with renal failure treated with haemodialysis and Polybrene. A clinico-pathological study. J Laryngol Otol 1966;80:651-77.
(14.) Ozturan O, Lam S. The effect of hemodialysis on hearing using pure-tone audiometry and distortion-product otoacoustic emissions. ORL J Otorhinolaryngol Relat Spec 1998;60:306-13.
(15.) Stavroulaki P, Nikolopoulos TP, Psarommatis I, Apostolopoulos N. Heating evaluation with distortion-product otoacoustic emissions in young patients undergoing haemodialysis. Clin Otolaryngol Allied Sci 2001;26:235-42.
(16.)Kusakari J, Hara A, Takeyama M, et al. The heating of patients treated with hemodialysis: A long term follow-up study. Auris Nasus Larynx 1992;19:105-13.
From the Department of Oto-Rhino-Laryngology (Dr. Lasisi and Dr. Olatoke) and the Department of Medicine (Dr. Salako, Dr. Kadiri, Dr. Arije, Dr. Oko-Jaja, and Dr. Ipadeola), College of Medicine, University of Ibadan, and University College Hospital, Ibadan, Nigeria.
Reprint requests: Dr. Olawale A. Lasisi, PO Box 22040, University of Ibadan, Ibadan, Nigeria. Phone: 234-805-536-9593; e-mail: firstname.lastname@example.org
Olawale A. Lasisi, MBChB; Babatunde L. Salako, MBBS; Solomon Kadiri, MBBS; Ayo Arije, MBBS; Richard Oko-Jaja, MBBS; Arinola Ipadeola, MBBS; Fatai Olatoke, MBBS
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|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Disease/Disorder overview|
|Date:||Dec 1, 2006|
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