Transient unilateral oculomotor and trigeminal nerve palsy following intranasal local anesthetic infiltration: a case report

Introduction

Background

Nasal obstruction is a common rhinology problem that significantly impacts quality of life (1). Etiologies are typically classified as structural (e.g., septal deviation, hypertrophic swell bodies or turbinates), inflammatory (e.g., nasal polyposis), neoplastic, or functional (e.g., empty nose syndrome) (2). First-line treatment for structural causes includes topical intranasal corticosteroids to reduce mucosal inflammation (3). However, surgery is indicated for medically resistant nasal obstruction due to septal swell body or turbinate hypertrophy and can be non-mucosa or mucosa-preserving (3). Coblation, a mucosa-preserving method, has demonstrated efficacy in reducing turbinate and septal swell body hypertrophy while improving nasal airflow (4). In-office coblation under local anesthesia has become increasingly common over the past two decades, offering advantages such as shorter operative time and faster post-operative recovery (4). Typical complications include rhinitis, pain, congestion, bleeding, and crusting (5).

Rationale and knowledge gap

While most in-office coblation procedures are associated with minor complications, rare cases of transient oculomotor nerve palsies have been reported following inferior turbinate (IT) reduction and endoscopic sinus surgery (6-9). Similarly, trigeminal nerve palsies have been documented in dental procedures involving local anesthetic infiltration (10). However, to date, no reports have described simultaneous oculomotor and trigeminal nerve palsies following intranasal local anesthetic administered prior to coblation.

Objective

We report a transient, unilateral oculomotor nerve palsy with concurrent palsies of the ophthalmic (V1) and maxillary (V2) branches of the trigeminal nerve following local anesthetic infiltration of the ipsilateral IT and septal swell body. To our knowledge, this constellation of symptoms has not previously been reported. We present this case in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-25-8/rc).

Case presentation

A 75-year-old female patient presented with a one-year history of bilateral nasal congestion and obstruction, which was only partially alleviated by intranasal corticosteroids. No relevant medical or surgical history was reported by the patient. Bilateral hypertrophic ITs (Figure 1A,1B) and septal swell bodies (Figure 1C,1D) were visualized endoscopically. The patient’s computed tomography (CT) scan revealed a relatively straight septum and clear sinuses, in addition to hypertrophic ITs and septal swell bodies (Figure 2A). The lamina papyracea was intact without evidence of dehiscence (Figure 2B). There was an incidental finding of a small retention cyst laterally in the left frontal sinus, as well as mild bilateral proptosis. No intraorbital masses or collections were present. The patient’s Lund-Mackay score was 1/24. To address the patient’s symptoms, coblation of the hypertrophic ITs and septal swell bodies was discussed and consented to (Figure 3).

Figure 1 Endoscopic view of the left (A) and right (B) hypertrophic inferior turbinates and left (C) and right (D) hypertrophic septal swell bodies prior to the coblation procedure.

Figure 2 Coronal CT scan showing (A) hypertrophic ITs and septal swell bodies bilaterally. Axial CT scan showing an intact (B) lamina papyracea. CT, computed tomography; IT, inferior turbinate.

Figure 3 Timeline of symptom onset, interventions, and outcome.

Nine weeks later, the patient underwent an in-office bilateral coblation of the ITs and septal swell bodies. The procedure began with application of 4% lidocaine-soaked neuropatties to the relevant procedural sites, followed by infiltration of 0.25% bupivacaine hydrochloride with 1:200,000 epinephrine. Shortly after infiltration of the left IT and left septal swell body, the patient developed left-sided ptosis and was unable to adduct the left eye, while abduction was preserved. Although there was no vision loss, the patient experienced diplopia that resolved within minutes. Additionally, the patient reported paresthesia in the left forehead and left upper face regions, corresponding to the V1 and V2 dermatomes. Symptoms lasted up to 15 minutes and completely resolved by the end of the procedure.

Six weeks post-procedure, the patient was seen for follow-up. There was no sustained left-sided ptosis, diplopia, or facial paresthesia, and she was satisfied with the procedure outcomes. Overall, there was substantial improvement in her ability to breathe, and she had no other complaints. These symptoms remained absent at her six-month follow-up visit, further supporting the transient nature of the initial neurologic findings.

Ethical consideration

All procedures performed in this case were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

Numerous procedures are available to treat nasal obstruction caused by hypertrophic ITs and septal swell bodies, including both mucosa-preserving and non-mucosa-preserving methods (4). Coblation is a mucosa-preserving method typically performed using a local anesthetic, with most complications arising from the procedure itself rather than from the anesthetic agent (4). In our case, the patient developed symptoms immediately following local anesthetic infiltration into the left IT and left septal swell body, which fully resolved by the end of the procedure with no further complications. The left-sided ptosis, impaired left eye adduction, and diplopia were consistent with a left oculomotor nerve palsy, while the paresthesia involving the left forehead and upper face suggested a trigeminal nerve palsy, specifically the V1 and V2 branches.

Strengths and limitations

This case report is strengthened by its detailed documentation of a novel presentation and the proposal of three plausible mechanisms to explain the observed neurologic findings following intranasal local anesthetic infiltration. To our knowledge, no previous reports in the literature have described a similar constellation of oculomotor and trigeminal nerve involvement in this context. Limitations include the lack of ophthalmologic photo documentation and the inherent limitations of a single-patient case, which restricts generalizability.

Comparison with similar research

To our knowledge, no previously published reports have described a presentation identical to ours. However, cases of oculomotor nerve palsies post inferior turbinectomy have been described (6-9). Ravikumar et al. described a 69-year-old male who developed right-sided ptosis and diplopia following bilateral inferior turbinectomies, with symptoms persisting for five months (8). The authors proposed a potential embolic event anterior to the cavernous sinus, possibly involving the ophthalmic artery. They also considered the possibility of a vasospasm due to epinephrine infiltration. However, unlike our procedure, there was no trigeminal nerve involvement. In another case, Green et al. reported left-sided ptosis and diplopia in a six-year-old boy following submucosal diathermy to the ITs (6). A palsy of the superior division of the oculomotor nerve was diagnosed after examination. Similar to Ravikumar et al., this complication was thought to be a result of the procedure, and not due to the general anesthesia. More generally, cases of oculomotor nerve palsies post-endoscopic sinus surgery have also been reported; however, they were deemed to be related to the procedure, and not anesthetic infiltration (7,9).

In the field of dentistry, oculomotor and trigeminal nerve palsies following local anesthetic infiltration are not uncommon, although they are typically in the context of intraoral rather than intranasal administration (11-13). In a case report and review of the literature to explain ophthalmologic complications due to intraoral anesthesia, Steenen et al. proposed intra-arterial injection, intravenous injection, deep injection and infusion, and autonomic dysregulation as potential mechanisms, which are in line with our three postulated mechanisms (14). To date, the cases most comparable to our presentation involve intraoral administration of local anesthetics and vasoconstrictors, underscoring the rarity of similar complications from intranasal routes.

Explanations of findings

Although direct orbital infiltration of an anesthetic resulting in oculomotor nerve paralysis was considered, this was deemed unlikely given the intact lamina papyracea (Figure 2B) and the presence of facial paresthesia. We therefore propose three plausible mechanisms to explain the constellation of symptoms observed.

The first mechanism involves an inadvertent intravenous injection into the left sphenopalatine or anterior ethmoidal vein. From the sphenopalatine vein, the anesthetic would drain into the pterygoid venous plexus and subsequently reach the cavernous sinus via emissary veins through the foramen ovale or foramen lacerum. This could transiently affect the oculomotor nerve and the V1 and V2 branches of the trigeminal nerve on the ipsilateral side. An anesthetic in the anterior ethmoidal vein could follow a similar route via the superior ophthalmic vein and superior orbital fissure.

A second, related mechanism involves extravasation of anesthetic into the venous pathways described above, either from the IT into the sphenopalatine vein or from the septal swell body into the anterior ethmoidal vein, ultimately reaching the cavernous sinus and producing similar neurologic effects.

The third mechanism is an intra-arterial injection into the left anterior ethmoidal artery during infiltration of the left septal swell body. Previous reports have shown that injected epinephrine can induce vasospasm of the ophthalmic arteries, resulting in visual disturbances and ophthalmologic complications (15,16). It is therefore plausible to consider that an injection of 1:200,000 epinephrine may have been able to transiently induce a vasospasm of the left ophthalmic artery via retrograde flow, which would limit blood supply to cranial nerves three and five, thereby causing the symptoms reported in our patient.

Implications and actions needed

As this type of presentation has not been reported in the literature, it cannot be generalized as a common adverse event and should not be thought of as such. However, this case report highlights an important yet underrecognized complication of intranasal anesthetic use. Awareness of such transient cranial nerve palsies can help clinicians and surgeons recognize the benign and self-limited nature of these events, thereby avoiding unnecessary investigations such as imaging, consultations, or biopsies. It may also aid in reassuring patients and reducing postoperative anxiety. Additionally, this case reinforces the importance of adhering to safe injection practices, including aspirating prior to infiltration to confirm a non-intravenous or non-intra-arterial injection, and injecting the anesthetic slowly to reduce the risk of vascular compromise.

Conclusions

Although relatively low risk, local anesthetic with epinephrine infiltration of the ITs and septal swell bodies can result in complications involving cranial nerves three and five. In this case, we postulate that our patient experienced a left oculomotor nerve palsy and palsies of the left V1 and V2 branches of the trigeminal nerve due to either an intravenous injection, diffusion of injected contents into the venous system, or an intra-arterial injection. Recognizing the transient and self-limited nature of such events is essential, as it can help avoid unnecessary investigations and guide appropriate patient reassurance and injection technique optimization.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-25-8/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-25-8/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-25-8/coif). A.J. serves as an unpaid editorial board member of AME Case Reports from May 2024 to June 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this case were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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