Maxillary nerve blockade is an effective treatment for some patients with trigeminal neuralgia, which most often occurs in the V2 distribution.1 The maxillary nerve exits the foramen rotundum inferior to the ophthalmic (V1) nerve to enter the pterygopalatine fossa.2 Figure 1A 3 demonstrates its location in relation to the bony anatomy of the skull from a lateral view.
In the ensuing case report, we describe lagophthalmos as a complication after selective maxillary nerve injection performed between the mandibular condyles using a percutaneous infrazygomatic approach.
The patient gave informed written consent of the use of her medical records and images for educational purposes.
A 54-year-old woman presented with a history of right-sided trigeminal neuralgia in the V2 distribution. Her pain was refractory to multiple medications, botulinum toxin injections, and gamma knife radiation therapy. She had undergone a selective injection of the maxillary nerve with steroid and local anesthetic approximately 6 weeks before presentation. Afterwards, she described intermittent improvement of her symptoms lasting approximately 2 to 3 weeks. Given her response to this therapy, she agreed to proceed with a repeat maxillary nerve injection.
After informed written consent was obtained, the patient was positioned supine with her head turned toward the left side. Under fluoroscopic control, the patient was asked to open her mouth, and the mandibular condyles and the genu of the upper portion of the temporomandibular joint were identified. Because tactile stimulation of the area of needle insertion produced severe pain, before commencing maxillary nerve needle placement, approximately 2.5 mL of 0.5% lidocaine was administered subcutaneously. Due to severe discomfort, an additional 2.5 mL of 0.5% lidocaine was administered subcutaneously in the area between the mandibular condyles. After adequate local anesthesia was established, a 22-gauge spinal needle was advanced to the lateral pterygoid plate and “walked off” anteriorly without complaint of paresthesias and after negative aspiration for blood and cerebrospinal fluid. Figure 2 illustrates the needle placement under fluoroscopic imaging.
A combination of 80 mg (2 mL) methylprednisolone and 3 mL of 0.25% bupivacaine was administered. The patient was then returned to a recumbent position. She reported numbness and analgesia in the V2 distribution. Immediately after the procedure, however, the patient reported an inability to close her ipsilateral eye. She denied any previous episodes of this symptom. Her vital signs remained stable, and a thorough cranial nerve (CN) examination and gross neurological examination revealed no other focal deficits and otherwise normal ocular function aside from the isolated lagophthalmos.
Review of the sequence of events and drugs given during the procedure led us to conclude that the most likely cause of isolated unilateral eyelid paralysis was due to inadvertent local anesthetic blockade by lidocaine of the zygomatic branch of the facial nerve responsible for eyelid motion. A number of other diagnoses had been considered, including potential displacement of the needle during injection or a completely coincidental neurological event. Initially, we were uncertain whether this complication was caused by lidocaine or bupivacaine injection. Because we expected this complication to resolve quickly, we did not immediately consider performing a computed tomography or magnetic resonance imaging scan of the region or brain to evaluate for new pathology, although this may have been indicated if the symptoms persisted.
The patient was quite concerned about her inability to close her eyelid, despite our explanation that we felt the most likely cause of the dysfunction was from a local anesthetic effect and reassurance that this symptom would resolve quickly. Since we used lidocaine in the area of the superficial branches of the facial nerve, we expected improvement within 1 hour. The patient remained for observation after the procedure and reported improvement of her symptoms beginning 20 minutes later, with complete resolution approximately 40 minutes after the procedure was completed. She was then discharged home and scheduled for a follow-up appointment to evaluate the efficacy of the repeat injection.
The most likely explanation for the complication described in this case is the effect of lidocaine on the zygomatic motor branches of the facial nerve. The muscles that control the eyelid are innervated by branches of the oculomotor (CN III) or facial (CN VII) nerves. The oculomotor nerve innervates the levator palpebrae superioris muscle, which functions to open the eyelid. A deficit in this nerve would result in ptosis. The orbicularis oculi muscle is innervated by the zygomatic and frontal branches of the facial nerve and functions to close the eyelid. There are numerous zygomatic branches of the facial nerve, which cross superficially to the zygomatic bone to innervate the orbicularis oculi muscle.2 As illustrated in Figure 1B,3 these zygomatic motor branches are relatively superficial. Blockade of these branches can result in the inability to close the eye. Other complications associated with attempted maxillary nerve blockade, including those caused by nerve injection or needle misplacement, are noted in Table 1.4–6
The resolution of symptoms within 45 minutes is consistent with the characteristics of lidocaine, as opposed to that of bupivacaine. Furthermore, lidocaine was the only anesthetic administered subcutaneously in proximity to the zygomatic arch. The volume of lidocaine used for the repeat procedure was larger than the amount used for the patient’s previous injection. The increased volume likely contributed to the subcutaneous spread of lidocaine over the zygomatic branches of the facial nerve.
The use of 0.5% lidocaine for procedural anesthesia is a standard in our clinical practice and provides adequate analgesia for needle placement but does not typically result in motor nerve dysfunction when used in small doses. It is likely that this complication may have been avoided had a smaller volume of local anesthetic been used for skin infiltration.
Practitioners of selective maxillary nerve blockade should be aware of the proximity of superficial motor branches of CN VII to the point of needle entry. Patients should be informed of the potential complication of temporary paralysis of the eyelid so that anxiety over this event can be minimized, should it occur. If the complication occurs, patients should be advised and reassured that the duration of effect will likely be short term, based on the local anesthetic that was used. Treatment with artificial tears to the cornea to supplement the tear film should be recommended until the paralysis resolves, and the patient is able to close the eyelid. If the condition does not resolve quickly, the eye may be patched closed to protect the cornea. To avoid this complication when performing maxillary nerve blocks, it may be prudent to use a more concentrated, smaller volume of local anesthetic for skin infiltration so that there is less probability of inadvertent paralysis of the facial nerve branches.
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