|Year : 2022 | Volume
| Issue : 1 | Page : 129-132
Rare sudden hearing loss after lumbar spine decompression surgery: A case report and review of the literature
Shankar Acharya, Varun Khanna, Nitin Adsul, Rupinder Singh Chahal
Department of Ortho-spine Surgery, Sir Ganga Ram Hospital, New Delhi 110060, India
|Date of Submission||24-Apr-2021|
|Date of Decision||13-Jul-2021|
|Date of Acceptance||30-Jul-2021|
|Date of Web Publication||02-Feb-2022|
Department of Ortho-spine Surgery, Sir Ganga Ram Hospital, Sir Ganga Ram Hospital Marg, Rajinder Nagar, New Delhi 110060.
Source of Support: None, Conflict of Interest: None
Sensorineural hearing loss (SNHL) is a known but rare complication of non-otological surgeries. SNHL after spinal decompression also remains a rare occurrence with a handful of reports in the literature. The exact mechanism is not clearly understood. Cerebrospinal fluid leak, barotrauma, microemboli, hypoperfusion, vasospasm, traumatic event, and anesthetic agents are some of the proposed etiologies. Early diagnosis and prompt intervention have shown benefits though management lacks consensus. We report a case of profound SNHL post-lumbar decompression and fixation surgery, who showed significant recovery at 4-week follow-up, and we review the literature for hearing loss after spine surgeries.
Keywords: CSF leak, durotomy, lumbar decompression, sensorineural hearing loss
|How to cite this article:|
Acharya S, Khanna V, Adsul N, Chahal RS. Rare sudden hearing loss after lumbar spine decompression surgery: A case report and review of the literature. Indian Spine J 2022;5:129-32
|How to cite this URL:|
Acharya S, Khanna V, Adsul N, Chahal RS. Rare sudden hearing loss after lumbar spine decompression surgery: A case report and review of the literature. Indian Spine J [serial online] 2022 [cited 2022 May 25];5:129-32. Available from: https://www.isjonline.com/text.asp?2022/5/1/129/337143
| Introduction|| |
Post-operative profound sensorineural hearing loss (SNHL) can severely affect the quality of life. The complication has been described after non-otological surgeries, most noticeably cardiopulmonary bypass surgery (one in 1000 cases). Spinal surgeries leading to profound SNHL post-operatively are rare. Multiple etiologies have been proposed but the exact mechanism remains poorly understood. Complete recovery is seldom reported in the previously published reports and the management is largely inconclusive.
We report a case of sudden profound bilateral hearing loss after lumbar decompression surgery with incidental dural tear intraoperatively and review the literature. Consent of the patient was taken before sending this case report for publication.
| Case Report|| |
A 62-year-old male, known hypertensive, presented with complaints of low backache and bilateral lower limb pain since past 2 years. The patient has a history of L3-L4-L5 decompression surgery twenty years ago. His symptoms were insidious in onset and gradually progressive in nature. He had gradually developed a foot drop on the left side and was ambulating with support for the past six months with worsening neurogenic claudication. On examination, there was weakness of ankle dorsiflexion on the left side and absent ankle jerks bilaterally. Dynamic radiograph of the lumbar spine revealed L4-L5 instability with retrolisthesis and magnetic resonance imaging (MRI) showed canal stenosis [Figure 1] and [Figure 2]. After thorough evaluation and clearance, the patient underwent L3-L4-L5 posterior stabilization and L4-L5 transforaminal lumbar interbody fusion by cage and local bone graft under general anesthesia [Figure 3]. Fentanyl and propofol were used for induction, vecuronium was the muscle relaxant, and desflurane was used for the maintenance of anesthesia. Intraoperatively, there was a central opening of the L3, L4, and L5 lamina (of previous surgery), and thecal sac was seen enclosed by fibrous tissue. Scar tissue was also found to be adherent to the L4-L5 facet and while removing the medial facet, incidental durotomy and minimal cerebrospinal fluid (CSF) leak occurred which was sealed by Duragen©. The rest of the procedure was uneventful and after the leakage had completely ceased, watertight wound closure was performed.
|Figure 1: Pre-operative dynamic X-rays showing retrolisthesis at L4-L5 vertebral level|
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|Figure 2: Pre-operative MRI T2W mid-sagittal and T2W axial cuts showing lumbar stenosis at L3-L4 and L4-L5 levels|
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|Figure 3: Post-operative X-rays L3-L4-L5 posterior stabilization with L4-L5 interbody fusion with cage|
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Post-operatively, the patient was kept in bed with head end low and adequate hydration was maintained, but still the patient complained of mild headache. As the complaint of headache was persistent, oral acetazolamide 250 mg twice a day was added for 3 days to reduce CSF production. Headache improved subsequently and on post-operative day (POD) 4, the patient was mobilized in the evening. The next morning patient complained of bilateral severe hearing loss. Urgent ENT consultation was taken. On examination, there was no associated vertigo or tinnitus. External auditory meatus and tympanic membrane were normal but Weber and Rinne’s test was positive, indicating SNHL and audiometry revealed profound bilateral SNHL [Figure 4]. Non-contrast CT scan brain was done to rule out any hematoma and it was normal. Mobilization was disallowed and the patient was started on parenteral methylprednisolone 1 g for 3 days. By POD nine, the patient showed subjective hearing improvement, first in the right side and hearing markedly improved on the 10th day. He was discharged with a residual hearing deficit. At 4 weeks of follow-up, the patient had about complete recovery on the right side and 50% subjective improvement on the left side.
| Discussion|| |
Sudden SNHL is defined as hearing loss greater than 30 dB or more in three contiguous audiometric frequencies with onset within 72 h and has an approximately reported incidence of 5–20 cases per 100,000 individuals per year. Hearing loss after spine surgery is however only sparsely reported in the literature [Table 1]. CSF leak, barotrauma, microemboli, hypoperfusion, vasospasm, traumatic event, and anesthetic drugs are some of the potential proposed etiologies, although the exact mechanism is poorly understood. In our case, it can be hypothesized that mobilization on the fourth day of surgery set in motion some sequence of events which led to complete hearing loss. Also, CSF leak that occurred after incidental durotomy may have a role to play.
High incidence of incidental durotomy has been reported during revision spine surgery with rates as high as 8.1–17.4%. In our case, it was a low grade dural tear with just a few drops of CSF leak. Dural disruption and subsequent CSF leak may lead to drop in the intracranial pressure (ICP) and intracochlear pressure. Theoretically, loss of CSF pressure is transmitted to the perilymph via the cochlear aqueduct leading to perilymphatic hypotension, which in turn leads to relative high pressure in the cochlear duct creating a state that is hydrodynamically comparable to cochlear hydrops and thus loss of hearing. Persistent CSF leak seems unlikely here as surgical wound was dry on frequent inspection and symptomatically the patient had improved.
Hearing loss, both clinical and subclinical, has been frequently reported after spinal anesthesia and lumbar puncture. The precise incidence is unknown and it seems to occur more frequently than appreciated in case of general anesthesia; possible etiologies include middle ear pressure changes, vascular pathologies, CSF pressure changes, ototoxic agents, and embolism, among other causes. Nitrous oxide has often been implicated owing to its tendency to excessively increase the middle ear pressures leading to cochlear membrane breaks or perilymphatic fistulas. The increased pressures have been observed in middle ear sometimes as long as 45 min after its discontinuation. Valsalva maneuver, straining, emesis, coughing, or excessive retching during extubation, increased venous pressure due to hyperventilation may lead to increased ICP, which gets transmitted to the perilymph leading to oval or round window damage or rupture of the labyrinthine membrane. In our case, nitrous oxide was not used and the extubation was smooth without any maneuvers that would lead to increase pressure. We used oral acetazolamide (carbonic anhydrase inhibitor) to decrease the CSF production to alleviate the headache and giddiness post-operatively. Though hearing loss as direct side effect of acetazolamide has not been mentioned in the literature, in what way it might have contributed to hearing loss, if any, remains unclear.
A microembolic event triggered after mobilization can also be a potential cause of hearing loss in our case. Microembolisms are a well-explained mechanism of SNHL in bypass surgeries. The emboli (gas, thrombus, lipids, platelet aggregates, calcium) originating in the pump oxygenator system can cause occlusion of the cochlear branch of the internal carotid artery. Non-bypass cases have also been linked with microembolic phenomenon as a cause of SNHL after general anesthesia., Microembolism has been associated with irreversible hearing loss unlike our case.
The management of SNHL post-operatively is largely empirical and lacks consensus. Though use of systemic steroids is the mainstay in most reported cases of post-operative SNHL, there are no statistically significant data available in the literature. Standard dose of 1 mg/kg/day for 3–7 days is a widely accepted dose of systemic methylprednisolone for “idiopathic” SNHL. Bed rest, antiviral agents, IV fluids, vasodilators, plasma expander antidiuretics, hyperbaric oxygen therapy (HBOT), and even middle ear exploration have been used with varied success. A recent meta-analysis of 2401 patients of idiopathic SNHL concluded that HBOT as an adjuvant to the medical therapy proved to be a reasonable treatment option in cases with severe-to-profound SNHL within 3 months of symptoms, although cost and side effects are an issue. Most prudent approach seems to be prevention as much as possible. Early recognition and intervention have shown potential for recovery. Other favorable prognostic indicators are mild initial severity of symptoms, rising or flat in the middle frequencies on audiogram, and absence or presence of vestibular symptoms.
| Conclusion|| |
SNHL after spine surgery is not a usual complication and can be a frightening experience for the patient, leaving the treating surgeon perplexed. Avoiding ototoxic drugs and maneuvers increasing ICP, especially in predisposed individuals, is recommended. In the absence of any specific treatment, timely diagnosis and intervention are vital in such a complication.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]