Unilateral blindness following superior laryngeal nerve block for awake tracheal intubation in a case of posterior cervical spine surgery

Surgery

Before the C1-C2 posterior arthrodesis, the patient underwent an awake endotracheal intubation requiring SUPLANEB. The patient received hydroxyzine 50 mg orally, and the anesthesiologist performed a superior laryngeal nerve block. A 21-gauge needle (1 ½ inch) attached to a syringe containing 5 mL of 1% lidocaine was used once on each side (total injection of no more 10 mL of lidocaine), following which the patient was intubated using a video laryngoscope. The posterior cervical C1-C2 fusion was uneventful.

Nevertheless, after recovering from the general anesthesia, the patient complained of the left eye blindness without ocular pain, periorbital swelling, or oculomotor paresis; he also demonstrated left-sided hearing loss and facial numbness (all trigeminal territories). The direct eye examination revealed the left side anterior segment and fundus was normal, but confirmed complete left-sided visual loss, isolated direct mydriasis, and intact consensual light reflex.

Diagnostic studies

The STAT cranio-orbital computed tomography scan showed no acute intracranial or oculo-orbital lesions, but demonstrated mild bifrontal, interhemispheric, parasellar, sellar, and prepontic pneumocephalus; there was no skull base lesion [Figure 2]. The subsequent CT angiogram documented air in the left carotid sheath, near and along the carotid bifurcation, the internal carotid artery (ICA), and all around the internal jugular vein (IJV) [Figure 3]. There was also diffuse subcutaneous emphysema in the left paralaryngeal area and in the posterior cervicothoracic regions [Figure 4]. No intracranial hematomas or extraintracranial vascular lesions (no vasospasm) were present.

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Figure 2:: Axial cranial (a-c) and cervical C1 (d) computed tomography scan revealing mild pneumocephalus (arrows) at the prepontic cisterns (a), the sellar and laterosellar areas (especially next to the left optical channel) (b), and the bifrontal convexity (c). There is also a bilateral deep cervical emphysema and abnormal air in the left carotid sheath (d) (circle).

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Figure 3:: Craniocervical angiographic on sagittal (a), coronal (b), and axial (c) views demonstrating abnormal air in the left carotid sheath: the air is present nearby and along the carotid bifurcation, the internal carotid artery, and all around the internal jugular vein (arrows). The yellow circle represents these last three vessels on axial view (c).

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Figure 4:: Axial cervical (a and b) and thoracic (c and d) computed tomography scan showing diffuse subcutaneous emphysema (arrows) in the posterior cervical and thoracic regions (a-d). Note additional gas in the left paralaryngeal area (b).

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Treatment

The patient was placed in strict horizontal position and treated with inspired pure oxygen plus systemic steroid pulse therapy (120 mg of methylprednisolone each 6 h) and nimodipine (30 mg each 6 h). The 1^st postoperative day, the visual acuity remained unchanged, but nearly completely recovered the left hearing loss and facial hypoesthesia in the V2 distribution. Brain and orbital MR studies were normal. Optical coherence tomography (OCT) demonstrated postischemic retinal edema [Figure 5] with permeability of the intraocular blood vessels while retinal angiography showed delayed choroidal filling [Figure 6]. Flash visual evoked potentials were absent, while the electroretinogram revealed decreased potentials amplitudes.

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Figure 5:: Optical coherence tomography (OCT) of the left eye demonstrating a postischemic retinal edema.

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Figure 6:: Retinography (fundus photography on the 2nd postoperative day) of both eyes (left a and right b) revealing permeability of the intraocular blood vessels (especially the central retinal artery) and diffuse retinal edema on the left eye. Note the “Cherry-red spot” at the fovea (arrow) with white edematous macula around. OCT angiography features of the left eye (c) and right eye (d). There is a delayed choroidal filling in the left eye.

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The pneumocephalus and subcutaneous emphysema completely resolved on postoperative day 3. At the time of discharge on the 4^th postoperative day, there was a complete resolution of symptoms excepting for the left blindness and the V1 trigeminal hypoesthesia; the patient was sent home on nimodipine (120 mg/day) and oral steroid therapy (60 mg prednisolone) with a tapering dose over the next 4 weeks. Two months later, he remained blind in the left eye without any return of function.

Left-sided blindness

After an extensive ophthalmological exploration, it seems that our patient had postoperative ischemic retinal edema secondary to central retinal artery occlusion.

The iatrogenic intravascular infusion was likely the cause of pneumocephalus.[5,9,11,16,18,19]

Subcutaneous emphysema following a translaryngeal injection of local anesthetic has only rarely been reported in literature.[20] As there was a big air bubble in the left paralaryngeal area in this patient, our hypothesis was that the air leaked into the subcutaneous tissue through a left lateral needle track created following the superior laryngeal injection. It was then driven into the subcutaneous tissue of the cervicothoracic region and also in deep cervical and parapharyngeal areas. Another possibility was that the air was injected directly into the left carotid sheath, and it extended along the ICA and the IJV to the skull base. Thus, the pneumocephalus was due to intracranial gas extension through the carotid canal, jugular foramen, foramen lacerum, or foramen oval through the skull base.[4]

Upper cranial neuropathies

The upper cranial neuropathies (II, V1, V2, V3, and VIII cranial nerves) were likely attributed to pneumocephalus in the sellar and laterosellar regions, the abnormal extracranial air into the left carotid sheath, and the extensive cervicothoracic subcutaneous emphysema. They were also likely due to the accidental injection of the local anesthetic inside/around the ICA and/or the IJV (e.g., extending into the left cavernous sinus). This would explain the partial cavernous sinus syndrome presented by the patient. Another hypothesis is that the SUPLANEB resulted in transient vasospasm, emboli, or hypoperfusion of the ICA, thus directly resulting in occlusion of the blood supply to the left optic nerve.[3]

Future recommendations

When SUPLANEB is performed, the anesthesiologist should take care not to push the needle too far or too lateral to avoid reaching the carotid sheath.[10] It is also mandatory to draw back on the syringe and aspirate before anesthetic drugs injection. Furthermore, for patients with difficult surface anatomic landmarks, using ultrasound can be useful for performing SUPLANEB.[13]