Facial Nerve Injury Complications During Inferior Alveolar Nerve Block: A Review Article

Abstract

The Inferior Alveolar Nerve Block (IANB) is the most utilized regional anesthetic technique in dentistry, but it carries a rare risk of transient Facial Nerve (CN VII) palsy, reported at approximately 0.3\\%.This motor complication manifests as unilateral facial weakness, drooping of the corner of the mouth, and critical inability to close the ipsilateral eye (lagophthalmos). The primary etiology is a technical error: the inadvertent deposition of local anesthetic directly into the parotid gland capsule, a consequence of overly deep or posterior needle placement . While immediate palsy is a chemical conduction block, delayed presentation is hypothesized to stem from localized ischemic neuritis and secondary edema. Management is focused on immediate patient reassurance, mandatory ocular protection (lubricants and patching) to prevent corneal damage , and the use of systemic corticosteroids to mitigate inflammation . The prognosis is excellent, with complete functional recovery commonly observed within eight weeks. Prevention relies on rigorous adherence to injection protocol, including aspiration, slow injection, and strict depth control to prevent posterior needle penetration .

Introduction

The Inferior Alveolar Nerve Block (IANB) is a commonly used dental anesthetic technique but carries a rare risk (≈0.3%) of transient facial nerve (CN VII) palsy. Unlike more frequent sensory nerve injuries, this complication is motor in nature, presenting as unilateral facial weakness, drooping of the mouth, and inability to close the eye. Its rarity is attributed to a specific technical error: inadvertent deposition of anesthetic into the parotid gland, where the facial nerve lies.

Diagnosis is based on clinical history and examination, with severity and recovery monitored using the House–Brackmann Facial Nerve Grading System (Grades I–VI). Management focuses on patient reassurance, eye protection to prevent corneal damage, pharmacological therapy—commonly systemic corticosteroids—and facial physiotherapy to preserve muscle tone.

Prognosis is generally excellent, with most patients achieving complete recovery within eight weeks, and even severe cases showing significant improvement over several months. Two clinical patterns are identified: immediate onset palsy due to direct chemical neurapraxia, and delayed onset palsy, likely caused by ischemic neuritis from vascular spasm and edema. Evidence indicates no significant difference in risk between commonly used anesthetics such as articaine and lidocaine, emphasizing that anatomical misplacement, not drug choice, is the primary cause.

The discussion highlights that prevention depends on strict adherence to proper injection technique, particularly correct needle depth and contact with the mandibular ramus to avoid parotid gland penetration.

Conclusion

IANB-induced facial nerve palsy is a rare but significant iatrogenic event. Prevention is the single most effective strategy and relies exclusively on rigorous adherence to injection protocols, including mandatory aspiration, slow injection, and strict depth control to ensure the needle contacts bone (the medial aspect of the mandibular ramus). When complications occur, a combination of patient reassurance, mandatory ocular care, and corticosteroid therapy ensures high recovery rates. Future efforts should focus on defining standardized anatomical parameters and validating the ischemic neuritis hypothesis to further refine management protocols.

References

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Copyright

Copyright © 2026 Dr. Gayathri G, Dr. Mahalashmi B, Dr. Kirubavathy S, Dr. Vandhana , Dr. Afrath . This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.