Transient diplopia following maxillary local anesthetic injection

Transient diplopia following maxillary local anesthetic injection

Transient diplopia following maxillary local anesthetic injection Kelly R. Magliocca, DDS,a Neil C. Kessel, DDS, and Gerald W. Cortright, PhD, Ann Arb...

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Transient diplopia following maxillary local anesthetic injection Kelly R. Magliocca, DDS,a Neil C. Kessel, DDS, and Gerald W. Cortright, PhD, Ann Arbor, MI UNIVERSITY OF MICHIGAN SCHOOL OF DENTISTRY

A 36-year-old female paitent developed diplopia and an ipsilateral lateral rectus paresis following local anesthetic administration to remove a left maxillary second molar. Complete resolution occurred within 3 hours. The clinical examination and management plan are reviewed for this uncommon occurrence. The relevant anatomical pathways are discussed and illustrated with photographs. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:730-3)

Perhaps nothing has changed the face of dentistry more in the past century than the use of local anesthetics to make dental procedures more tolerable for patients. Although dental practitioners safely deliver millions of local anesthetic injections every year, unexpected events following anesthetic administration are likely to occur at some point in a clinician’s career. Appropriate treatment and gentle assurance are absolute necessities for patient management should a complication occur. This report details an iatrogenic paresis of the sixth cranial nerve following local anesthetic delivery and extraction of a maxillary left second molar. CASE REPORT The patient, a 36-year-old female, presented to the department of Oral and Maxillofacial Surgery with a referral for extraction of her maxillary left second molar secondary to irreversible pulpitis. She declined endodontic therapy. The examiners observed no evidence of extraoral or intraoral swelling. The patient reported no systemic symptoms, nor any medical concerns or allergies contraindicating the planned treatment. After obtaining written and verbal consent, the patient was placed into a recumbent position and two 1.7-mL cartridges of 4% articaine hydrochloride with 1:100 000 epinephrine were administered with a 25-gauge needle on an aspirating syringe. One full cartridge was delivered to anesthetize the posterior superior alveolar nerve (PSA). Since the tooth was quite large and had multiple sites of caries, three quarters of a cartridge was administered to the middle superior alveolar nerve (MSA) to maintain patient comfort should the procedure require flap reflection with extension to the area of the first molar. Finally, one quarter of a cartridge of the same anesthetic was administered to anesthetize the greater palatine nerve. Aspiration during anesthetic delivery produced no blood.

a

Adjunct Clinical Assistant Professor, Department of Oral and Maxillofacial Surgery, University of Michigan School of Dentistry, Ann Arbor, MI. Received for publication Jun 2, 2005; returned for revision Jul 14, 2005; accepted for publication Aug 15, 2005. 1079-2104/$ - see front matter Ó 2006 Mosby, Inc. All rights reserved. doi:10.1016/j.tripleo.2005.08.012

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After anesthesia was achieved, the gingival cuff of tooth #15 was reflected and the tooth was elevated, luxated, and delivered using a standard, flapless forcep technique. Following irrigation with sterile saline, the patient’s chair was slowly returned to an upright position and she was asked to bite firmly on a gauze square to control hemorrhage. The entire procedure was straightforward and lasted less than 15 minutes. A few moments after being returned to an upright position, the patient described symptoms of ‘‘double vision.’’ She denied lightheadedness, cardiac palpitations, and shortness of breath. The patient’s vital signs were stable. Cranial nerve VII remained intact bilaterally, as did sensation in the trigeminal divisions V1 and V3 bilaterally and V2 on the patient’s right side. As would be expected, the patient reported anesthesia in the distribution areas of the left PSA, MSA, and greater palatine nerves. No blanching of the facial skin was noted. Ocular examination revealed pupils that were equally round and reactive to light, with normal visual acuity and full extraocular movements in all directions with one exception— the patient’s left eye was unable to abduct past the midline (Fig. 1, Fig. 2). There was no evidence of ptosis, proptosis, conjunctivitis, or epiphora. Further physical examination of the head and neck, as well as general systems, revealed nothing unusual. It was apparent that the patient had acquired a paresis of the abducens nerve secondary to the local anesthetic injected in the left maxillary region. The patient was advised that her vision should return to normal within 2 to 3 hours, once the local anesthetic’s effects had fully dissipated. The patient was calm, alert, oriented, asked appropriate questions, and demonstrated an understanding of the event. The patient’s telephone number was obtained in order to contact her later in the day to ensure the symptoms had indeed subsided and to allow response to any questions that she might have. The left eyelid was taped in the closed position to reduce the sensation of diplopia, and she was driven home by her escort. When contacted later that evening, she reported that her vision had returned to normal. A postoperative visit the following day confirmed that the disturbance had resolved (Fig. 3).

DISCUSSION Transient abducens nerve palsy secondary to dental anesthetic injection is an uncommon complication. Several vascular and bony anatomical pathways have been proposed to explain its occurrence based on the

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Fig. 1. Immediate postoperative image. Patient is asked to direct her gaze forward. Note a very mild esotropia of left eye is present.

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Fig. 2. Immediate postoperative image. Patient attempts to gaze to her left. Note the inability of left eye to abduct past the midline.

underlying regional anatomy, the sites of injection, and the pathways of spread of the anesthetic agent.1,2 Vascular pathways Intra-arterial injection and intravenous absorption are 2 possible means of vascular transport of anesthetic into the orbital region.2 Both scenarios posit that a needle is over-inserted postero-medially at the maxillary tuberosity to enter the infratemporal fossa.3 The intra-arterial pathway is described as inadvertent needle puncture of the maxillary artery,4 followed by spread of anesthetic agent into several successive arterial branches (middle meningeal artery, then via a common anastomotic branch into the orbit to the lacrimal branch of the ophthalmic artery).1,2,5,6 Although conceivable, this route seems unlikely in the present case as careful aspiration during anesthetic administration was negative. Additionally, arterial transport of anesthetic into the orbit would also probably produce more widespread effects and not be restricted to paresis of the lateral rectus muscle.6 The venous pathway into the cavernous sinus is the most commonly cited explanation for postinjection abducens palsy.2,4-7 The pterygoid venous plexus is found within the infratemporal fossa, and any anesthetic agent reaching this location would be in close contact with numerous small, thin-walled veins.1,3,5-7 Absorption would seem relatively easy, and transport into the cavernous sinus could occur via small emissary veins passing through foramen ovale to directly enter the cavernous sinus (Fig. 4). Here, the abducens nerve is in close contact with the venous blood and vulnerable to the effects of any anesthetic agent present. Bony pathways Several bony anatomical features are often cited as responsible for allowing unintended spread of anesthetic

Fig. 3. Postoperative image 1 day after extraction. Patient successfully gazes to her left on command.

agent and resultant abducens nerve palsy. Two key points must be kept in mind regarding local anatomy. First, the inferior orbital fissure and pterygopalatine fossa are in open communication with one another in the orbital region, and the greater palatine canal is in communication with the inferior aspect of the pterygopalatine fossa. Thus, anesthetic solution may diffuse widely among these bony openings, perhaps very easily in some individuals with a unique anatomic variation. The recumbent position of the patient during anesthetic administration may also have a role.2 Second, the abducens nerve is most vulnerable in the region of the orbital apex, where it lies on the deep (intraconal) surface of the lateral rectus muscle. Anterior to this region, the nerve quickly enters the muscle, which is covered by dense fascia. Investigators have described anesthetic delivery near enough to the pterygopalatine fossa via the PSA injection, allowing for diffusion into the region of the orbital apex or inferior orbital fissure.1,2 Since the greater palatine canal is on a straight-line trajectory with the pterygopalatine fossa and orbital apex, injections at this location could introduce anesthetic into the orbital apex and induce a paresis of the abducens nerve by direct contact of the solution with the nerve at its most

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Fig. 4. Rectangle approximates the extent of the infratemporal fossa, where the pterygoid venous plexus would be found. Foramen ovale contains small emissary veins that drain into the cavernous sinus. Cavernous sinus is located in the middle cranial fosssa and surrounds the abducens nerve at that location.

Fig. 5. Local anesthetic injected posterior to the maxillary tuberosity or into greater palatine foramen may reach the orbital apex (not in view) by entering the pterygopalatine fossa. Green wire shows straight-line path from greater palatine foramen (GPF) to pterygopalatine fossa (PPF), and its continuation with the inferior orbital fissure (IOF).

vulnerable location (Fig. 5 and Fig. 6). Sved et al.8 documented the complications resulting from a technique designed to accomplish maxillary nerve anesthesia by advancing the needle into the greater palatine canal to a target depth of approximately 39 mm. Notably, the 2 most common adverse effects observed in association with this technique were diplopia and orbital muscle

Fig. 6. Anterior view of left orbit, showing the orbital apex and its relationship to the inferior orbital fissure (IOF). The green marker indicates continuity from the pterygopalatine fossa to the orbital apex, where the abducens nerve normally lies on the deep (intraconal) surface of the lateral rectus muscle but is not yet embedded within the muscle.

paresis (most commonly involving the lateral rectus muscle).8 In 2 cases, the bony greater palatine canal was constricted, which limited needle penetration to 3 mm and 6 mm, respectively.8 Maxillary anesthesia was still achieved in these cases, despite failure to reach the target depth. The authors did not state whether these 2 cases of a ‘‘constricted’’ canal resulted in

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diplopia or lateral rectus palsy.8 In the present case there was no intention or evidence of needle over-insertion during the palatal injection. Of the various pathways, 3 seem most likely to be responsible for the abducens paresis observed in this patient: (1) injection into the infratemporal fossa with subsequent absorption and transport of anesthetic into the cavernous sinus (Fig. 4); (2) injection superior and posterior to the maxillary tuberosity with subsequent spread into the pterygopalatine fossa and/or inferior orbital fissure, possibly reaching the orbital apex (Fig. 5 and Fig. 6); and (3) injection into the greater palatine canal, with spread of solution up into the region of the conjoined bony fossae near the orbital apex (Fig. 5 and Fig. 6). Regardless of how the paralysis occurred, the literature does not demonstrate any cases with permanent loss of function.1,4-7,9,10 Moreover, complete recovery was observed in nearly all reported cases within a few hours of the incident’s discovery, which is the approximate amount of time necessary for complete cessation of the anesthetic’s physiologic effects.1,4-7,9,11 After conducting a full examination, management includes reassurance as well as taping the eye closed or covering the eye for approximately 3 hours so the patient is spared the disorienting visual effects of diplopia.1,6,7 Ideally, the patient should be transported home by an escort, since operating a vehicle with the affected eye covered could be considered unsafe. A postoperative visit within 24 hours of the incident will verify cessation of symptoms. Should any visual or motor disturbances of the eye still exist, immediate referral to an ophthalmologist is recommended.11 A recent series reporting ocular disturbances resulting from the use of a 2% articaine hydrochloride with 1:100 000 epinephrine solution suggested that the improved anesthetic diffusion of this agent through soft tissue and bone could account for many of the ophthalmic findings.10 To our knowledge, this is the first reported case of transient diplopia and abducens nerve paresis that specified the use of a 4% articaine hydrochloride with 1:100 000 epinephrine solution. Although we speculate that the anatomical location of the deposited solution is responsible for this transient ophthalmologic disturbance, it is possible that further studies will implicate the chemical properties of the anesthetic agent as well.

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CONCLUSION The physical signs of an inadvertent paresis of the abducens nerve will no doubt alarm the unprepared clinician. For the patient’s benefit, a calm demeanor is imperative. The patient can be assured of a good prognosis since cessation of symptoms generally occurs within a few hours. Since there were multiple injection sites and the bony pathways are not strictly separated from one another, it is impossible to conclude which of the suspected scenarios was fully or partially responsible for the observed paresis of the lateral rectus muscle. Furthermore, it is not known whether the volume of solution injected or the specific chemical properties of 4% articaine played a role in determining this transient neurological disturbance. REFERENCES 1. Goldenberg AS. Diplopia resulting from a mandibular injection. J Endod 1983;9:261-2. 2. Walker M, Drangsholt M, Czartoski TJ, Longstreth WT Jr. Dental diplopia with transient abducens palsy. Neurology 2004;63:2449-50. 3. Malamed S. Techniques of maxillary anesthesia. In: Reinhardt RW, Baxter S, Stericker GB, editors. Handbook of local anesthesia. St Louis, MO: Mosby; 1997. p. 164-8. 4. Crean SJ, Powis A. Neurological complications of local anaesthetics in dentistry. Dent Update 1999;26:344-9. 5. Koumoura F, Papageorgiou G. Diplopia as a complication of local anesthesia: a case report. Quintessence Int 2001;32:232-4. 6. Goldenberg AS. Transient diplopia from a posterior alveolar injection. J Endod 1990;16:550-1. 7. Marinho RO. Abducent nerve palsy following dental local analgesia. Br Dent J 1995;179:69-70. 8. Sved AM, Wong JD, Donkor P, Horan J, Rix L, Curtin J, et al. Complications associated with maxillary nerve block anaesthesia via the greater palatine canal. Aust Dent J 1992; 37:340-5. 9. Fish LR, McIntire DN, Johnson L. Temporary paralysis of cranial nerves III, IV, and VI after a Gow-Gates injection. J Am Dent Assoc 1989;119:127-8; 30, discussion 29. 10. Penarrocha-Diago M, Sanchis-Bielsa JM. Ophthalmologic complications after intraoral local anesthesia with articaine. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90: 21-4. 11. McNicholas S, Torabinejad M. Esotropia following posterior superior alveolar nerve block. J Calif Dent Assoc 1992;20:33-4. Reprint requests: Kelly R. Magliocca, DDS Adjunct Clinical Assistant Professor Department of Oral and Maxillofacial Surgery University of Michigan School of Dentistry 1011 North University Drive, Room 2008 Ann Arbor, MI 48109 [email protected]