Delayed Facial Nerve Paralysis following Blast Trauma
22 February 2017 (online)
Penetrating maxillofacial trauma from ballistic missiles, such as bullets, results in complex soft-tissue, bony, and neurovascular injury. The facial nerve is thus at high risk for injury by direct impact, propagated shock waves, and cavitation effects, and is further exacerbated by complex fractures, local vascular compromise, and projectile shrapnel. While guidelines for immediate paralysis associated with nerve laceration advocate for nerve exploration, the practicing facial surgeon may encounter delayed facial nerve paralysis which represents a clinical challenge. We advocate for closer follow-up for patients who may be at risk for delayed paralysis based on their mechanism of injury.
Several factors are responsible for peripheral nerve damage in the setting of ballistic injury. Blast injuries result in direct injury from crush forces of the bullet, in addition to indirect injury due to stretch of nearby tissue, vacuum effects in the cavity of the bullet's wake, and shock wave propagation, affecting peripheral nerve conduction without direct disruption of the nerve sheath. Prognosis for recovery can be evaluated by electroneurography 2 to 3 weeks following injury, or electromyography to establish whether the nerve is intact. Delayed facial nerve paralysis, initially described as within 5 to 7 days, associated with maxillofacial trauma carries a good prognosis for recovery. Delayed paralysis is likely the effect of intact nerve with conduction blocks and interruption in centrifugal flow, or first-degree injury according to Sunderland's classification, carrying a good prognosis and therefore may not warrant exploration. On the contrary, delayed edema resulting from associated displaced fracture fragments may not carry the same prognosis, and may lead clinicians to favor operative decompression. Finally, the carotid vasculature is at risk for injury in penetrating facial trauma, further compromising facial nerve function via compression by an expanding dissected internal carotid artery (ICA), or variations in the collateral nutrient arterial supply of the distal facial nerve. The facial nerve receives the majority of its blood supply from the middle meningeal branch of the internal maxillary artery, and may receive supply from the ICA. Blast injuries associated with complex fracture patterns ([Fig. 1]), bony fragments in proximity to the facial nerve, and vascular trauma ([Fig. 2]) should receive close follow-up.
In the setting of delayed facial nerve paralysis beyond 7 days, which we have encountered in our tertiary practice, the clinician is faced with a unique challenge. Conservative management is generally advocated if the suspicion for nerve transection is low, given that steroids have shown benefit in the treatment of delayed paralysis associated with temporal bone trauma. Clinical trials have shown a clear benefit of corticosteroids in the treatment of idiopathic facial nerve paralysis/Bell's palsy within the first 72 hours, with evidence for decreased inflammatory-mediated edema, enhanced regeneration, and improved overall motor function.
In summary, the clinician should be aware that delayed facial nerve paralysis even beyond 7 to 10 days may be associated with blast injury, especially in conjunction with vascular and bony trauma. If management proceeds conservatively, corticosteroids can be considered, with close follow-up for managing posttraumatic sequelae.