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Oman Journal of Ophthalmology logoLink to Oman Journal of Ophthalmology
. 2023 Jun 27;16(2):366–369. doi: 10.4103/ojo.ojo_129_22

Acute reversible bilateral hearing loss after retrobulbar anesthesia

Mehmet Omer Kiristioglu 1,, Gamze Ucan Gunduz 1, Selim Doganay 1
PMCID: PMC10433043  PMID: 37602167

Abstract

This is the first reported case who had bilateral reversible hearing loss after regional anesthesia (RA) without a procedural sedoanalgesia. Furthermore, 20% lipid emulsion infusion (LEI) was first used in the treatment of a patient with hearing loss as an indicator of impending brainstem anesthesia. The ophthalmologist had performed a retrobulbar block without any difficulties to a 55-year-old the patient who undergone pars plana vitrectomy. A combination of lidocaine and bupivacaine was injected slowly through a 23G, 1.5-inch needle. Few minutes later, the patient experienced sudden bilateral hearing loss and, subsequently, mental confusion and mild respiratory distress. Local anesthetic toxicity to the predominantly brainstem was the diagnosis. Consequently, 20% LEI was administered, and his hearing loss gradually improved within a few hours. Prompt intervention is crucial in case of severe systemic complications of RA. LEI might be beneficial to halt the deepening of brainstem toxicity.

Keywords: Brainstem anesthesia, lipid emulsion infusion, local anesthetic toxicity, retrobulbar block

Introduction

In ophthalmic surgery, the most common anesthetic technique is regional ocular anesthesia. For vitreoretinal surgery, general anesthesia (GA) or regional anesthesia (RA) can be preferred; however, there has been an increasing trend toward using RA over the last decade. Sharp needle techniques (retrobulbar or peribulbar blocks) or blunt needle techniques (sub-Tenon’s blocks) can be used for RA.[1] Our clinic generally prefers retrobulbar block (RB) with or without procedural sedation and analgesia (PSA) in vitreoretinal surgery. GA is tended to be used more for children, younger patients, and patients with mental retardation.

Although life-threatening complications of the RB are rare, brainstem anesthesia with a wide variety of nonspecific neurological symptoms is not rare, which occurs in around 1:500 of the patients.[2]

To our knowledge, only one case of acute bilateral hearing loss following RB under PSA has been described so far in literature from George and Hackett.[3] However, as a difference in this report, we aim to present bilateral acute hearing loss occurring after only RB without the administration of PSA and complete recovery with lipid emulsion (LE) 20% infusion.

Case Report

Written informed consent was obtained from the patient for publication of this case report. A 55-year-old male applied to our outpatient clinic for sudden vision loss in his left eye for 2 days. His ophthalmologic examination revealed dislocated intraocular lens (IOL) and macula off rhegmatogenous retinal detachment in the left eye. Urgent pars plana vitrectomy (PPV) and IOL replacement had been planned only with RA without the administration of PSA. His medical history included type 2 diabetes and coronary artery (CA) disease with CA stenting. His medication included oral antidiabetic agents, an antihypertensive agent, and 100 mg of acetylsalicylic acid (ASA). He was referred to a cardiologist for preoperative evaluation, and ASA was ceased 7 days before the surgery without additional antithrombotic prophylaxis.

In the operating room (OR), before administration of the RB, the patient’s vital signs were pulse rate of 82 beats per min (bpm), blood pressure (BP) of 100/70 mmHg, oxygen saturation with breathing room air 99%, and normal sinus rhythm.

We administered the RB without any difficulties. No retrobulbar or peribulbar hemorrhage was detected. In our RB technique, after ensuring the patient’s eye was in primary gaze, the inferior orbital rim was palpated while the globe was gently pushed up. Then, the needle was inserted just above the rim at the lateral third of the eyelid. The needle was advanced in a bevel-up and parallel position to the orbital floor. After about 1 cm, when the needle had passed the equator, it was redirected to about 30° superonasally and advanced an additional 2.5 cm. After aspirating to ensure no blood returns, we injected a 5 mL combination of 2.5 mL 2% lidocaine and 2.5 mL 0.5% bupivacaine slowly through a 23 Gauge, 1.5 inches (38 mm) Atkinson needle. Mild pressure was applied after removing the needle to prevent hemorrhage and increase the diffusion of the agent.

Approximately 10 min after RB, the patient stated that he could not hear anything. Hearing loss appeared to be complete and bilateral since the patient did not react to any verbal stimuli. After several minutes, the respiratory difficulty with shallow respiration and mental confusion started. His oxygen saturation level started to drop to 90%. He was ventilated with a bag mask, and then, he was able to maintain normal oxygen saturation with supplemental oxygen. The patient’s pulse rate was 62 bpm, and his BP was 96/60 mmHg. He was treated with an initial intravenous bolus of 20% LE (Intralipid®) 1.5 mL/kg (for lean body mass, which is about 80 kg) and subsequently infusion of 0.25 mL/kg/min (for lean body mass) for about half an hour by the anesthesiologist according to recommendations of American Society of Regional Anesthesia.[4] The total dose of Intralipid® was 720 mL. As a result of the RB, his left eye was totally ophthalmoplegic without any light response. Light reflex was responsive in his right eye, but a detailed ophthalmologic examination could not be done due to mental drowsiness. The PPV procedure had been canceled.

Neurological examination revealed that the patient had no lateralizing signs, no cranial nerve abnormalities except RB itself. His deep tendon reflexes were normal. Computerized tomography (CT) and cranial diffusion magnetic resonance imaging (MRI) ruled out cerebrovascular accidents (CVAs). His 12-lead-electrocardiogram (ECG) and cardiac enzymes were unremarkable in the case of acute coronary syndrome. Brainstem anesthesia after an RB was the diagnosis after ruling out the major acute neurological and cardiological events.

Approximately 2 h after the onset of hearing loss, the patient noticed the return of hearing. In the following 4 h after the RB, his hearing loss had completely recovered. At this point, his vital signs, cardiac enzymes, serum electrolytes and pH, oxygen saturation, and 12-lead-ECG were within physiological limits. On the following day, his preoperative vision was maintained. An audiogram was obtained, and it was normal. He had no sign of globe perforation or optic nerve (ON) trauma. After a week, PPV with silicone oil tamponade and IOL reposition procedure was performed under GA without any complication or sequela.

Discussion

In ophthalmic surgery, different types of local anesthetics and techniques can be used with various combinations. The preferred combinations of choice vary throughout the globe. Any type of anesthesia is acceptable as long as it provides adequate patient and surgeon comfort. The decision of anesthesia depends primarily on the type of surgery, local anesthesia (LA) technique if LA is going to be administered, and the patients’ associated comorbidities.[5]

The RB is the most invasive type of RA, with the highest possible complication rate among other RA types.[1] Possible complications are either local or systemic, and they are the result of the injection technique or the anesthetic medication itself. Periorbital, subconjunctival, or retrobulbar hemorrhage is more common local complications following RB. Other local complications are chemosis, globe penetration, ON damage, ptosis, and extraocular muscle damage. Systemic complications are drug allergy, systemic anesthetic toxicity, and symptoms due to inadvertent intraarterial or intrasheath injection of the local anesthetic.[6]

The ON is an extension of the brain, and meninges surround it. These meninges are also the extension of their counterparts in the brain, brainstem, and cranial nerves and share the same embryonic origin. By this route, any given substance into the inside of the ON sheath first reaches the chiasmatic cistern in the middle cranial fossa and then can spread the subarachnoid space around the brainstem.[7] Intrasheath injections can enter either the subdural or subarachnoid space; in which space is going to be entry route probably depends on the depth of needle penetration, the force generated during injection, and volume of injected anesthetic, or individual anatomic variations [Figure 1]. However, the exact cause is unknown. Lombardi reported that 2% of the patients undergoing pressure orbitograph demonstrate contrast material in subdural space.[8] Therefore, the true incidence of intrasheath injection during RB may be higher than expected.[9]

Figure 1.

Figure 1

Suspected entry route of the Atkinson needle in the orbital apex. The dotted line represents the possible locations where the local anesthetic was injected. IR: Inferior rectus muscle, LPS: Levator palpebra superioris muscle, LR: Lateral rectus muscle, MR: Medial rectus muscle, OA: Ophthalmic artery, ON: Optic nerve, SOQ: Superior oblique muscle, SR: Superior rectus muscle

In the case of this route, the neurological signs and symptoms tend to be more sporadic and gradual onset than vascular spread.[3] Our patient experienced bilateral hearing loss and mild respiratory insufficiency, which is probably the direct result of local anesthetic tracking this route to the brainstem and cranial nerves, specifically vestibulocochlear nerves and nuclei.

Retrograde vascular spread along the ophthalmic artery and then anterograde pathway into the internal carotid artery has been suggested as a possible explanation for high brain concentrations of local anesthetic after RB.[10] If the anesthetic has entered into the central nervous system (CNS) through the vascular spread, signs and symptoms may have been more instant and devastating.

Oculocardiac reflex, vasovagal reaction, CVA, and anaphylaxis must be kept in mind when making a differential diagnosis of a systemic sign following RB. Bradycardia, diaphoresis, and hypotension, immediately after manipulation of the eyeball, can be readily explained by the oculocardiac reflex. A vasovagal reaction was unlikely because significant bradycardia was not noted, and CNS symptoms should be more delayed.[11] We ruled out the CVA with CT and MRI. Anaphylaxis criteria had not been met since there was no significant decrease in BP.

Higher pressures are needed for intrasheath injection than retrobulbar injection; however, it is not a must.[12] Hence, it should be emphasized that merely feeling no resistance during injection does not guarantee safeness. To ensure the patient’s eye is in primary gaze, not upward, is the most critical step of the RB to avoid damage to the ON. On the other hand, the length of the needle is a critical factor for preventing ON penetration. A 38 mm needle was used in our case, which was similar to the other patient who experienced bilateral hearing loss after RB.[3] Hence, we thought that shorter needles, with a length of 31 mm instead of 38 mm, could be safer for RB.

In cases of suspected spread of anesthetic into the CNS, symptomatic treatment with atropine, oxygen support, intravenous fluids and crystalloids, and the head-down (Trendelenburg) position are necessary. In the case of prolonged respiratory arrest and convulsions, endotracheal intubation will be required. The ophthalmic surgery could be done under GA if the patient could be stabilized. However, if the patient cannot be stabilized, ophthalmic surgery must be delayed.[11]

In our case, the prognosis was very similar to the first case that had been reported by George and Hackett.[3] The patient ends up with a complete recovery of signs and symptoms within a few hours without any chronic sequela. In the previous case, PSA was also administered, and this additional procedure also could have deepened the brainstem depression further.[3] Furthermore, in our case, we did not find any signs and symptoms of other cranial nerves or nucleus’ depression similar to the fore mentioned case. We also administered intravenous LE, which might have helped to decrease recovery time. LE administration is particularly effective in treating cardiovascular collapse; however, it was also reported that it might be effective in treating CNS toxicity.[12,13] However, the hearing loss may have been self-limiting, as in George and Hackett’s case.[3] The beneficial effect of the LE administration is uncertain.

Although deafness was a worrisome sign, fortunately, it was rare and utterly reversible in these two cases.[3] Nicoll et al. reported no hearing loss following any of the 6000 RBs.[13,14] Since the anesthetic drugs follow subarachnoid space as a track through the brainstem, it might affect the contralateral eye if it follows the chiasmatic cistern and may cause contralateral vision loss and third nerve palsy.[8] When intrasheath injection of anesthetic is suspected, contralateral eye movements, light reflexes, and gross vision must be checked along with other cranial nerves.[15] These examinations may give possible clues for crucial differential diagnosis. If suspicion of intrasheat injection arises, in case of hearing loss, LE administration can be considered to prevent or lessen the effects of impending brainstem anesthesia. However, further observational and experimental studies must be conducted to prove the effectiveness of the LE in the local anesthetic toxicity to the CNS.

In conclusion, bilateral hearing loss is a very rare complication of RB. Fortunately, hearing loss was completely reversible within a few hours. However, brainstem anesthesia could deepen, and life-threatening respiratory conditions could occur. We think that an anesthesiologist should be present, and the patient should be monitored in the ophthalmology OR, particularly during RB procedures. Nevertheless, an ophthalmologist should be aware of the possible complications of RB and have the ability to carry out immediate treatment.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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