Pneumomediastinum after orthognathic surgery.

Pneumomediastinum, also known as mediastinal emphysema, occurs when air is found in the mediastinum. Mediastinal air may originate from the upper respiratory tract, the intrathoracic airway, the lung parenchyma, or the gastrointestinal tract. The presence of air in the mediastinum may be spontaneous, iatrogenic (eg, surgical incision or perforation of an air-filled cavity), or due to penetrating trauma. Most of the cases of pneumomediastinum that have been described in the oral and maxillofacial surgery literature result from air dissecting down the fascial planes of the neck. A case of pneumomediastinum after orthognathic surgery is presented along with a review of the pathogenesis, clinical findings, and management of pneumomediastinum. Report of a Case A 19-year-old white man with myotonic dystrophy was referred by his orthodontist for treatment of his dentofacial deformity. Past surgical history was significant for bilateral inguinal hernia repair at 17 months of age. Clinical examination revealed vertical maxillary excess, transverse maxillary deficiency, mandibular anteroposterior deficiency, and apertognathia. The surgical treatment plan included a segmental Le Fort I osteotomy with impaction and advancement as well as bilateral sagittal split osteotomies for mandibular advancement and genioplasty. Preoperative assessments included evaluation by a pediatric neurologist for myotonic dystrophy and a pediatric cardiologist for a heart murmur. The pediatric neurologist recommended avoidance of muscle relaxants, if at all possible. Patients with muscular dystrophy may develop prolonged muscular contractions after exposure to depolarizing neuromuscular blocking agents. This can lead to chest wall rigidity, which could render ventilation of these patients impossible despite intubation. Patients with myotonic dystrophy also have variable sensitivity to nondepolarizing neuromuscular blocking agents and can demonstrate a prolonged duration of blockade.1 This necessitates close monitoring of neuromuscular blockade with nerve stimulators, which can cause myotonic episodes. Evaluation by the pediatric cardiologist revealed a physiologic heart murmur for which no modifications to treatment were advised. The operative course was uneventful. Oxygen saturation was stable at 99% to 100% throughout the procedure and the peak inspiratory pressure did not exceed 25 cm of H2O. Considering the history of myotonic dystrophy, the patient was transferred intubated to the postanesthesia care unit and sedation was maintained with fentanyl and midazolam. The ventilator settings were as follows: synchronized intermittent mandatory ventilation (SIMV) at a rate of 10, tidal volume (TV) of 600 mL, and an FIO2 of 40%. A postoperative chest radiograph was not performed on arrival to the postanesthesia care unit. At 12 hours postoperatively, the patient was found to be hypotensive and tachycardic. He responded well to fluid resuscitation. On postoperative day 1, the patient was unable to be weaned off mechanical ventilation. He was found to be restless with an oxygen saturation of 90%. The airway was suctioned, and the patient was manually ventilated, which increased the oxygen saturation to 100%. The ventilator settings were adjusted as follows: SIMV, rate of 8; TV, 700 mL; peak end-expiratory pressure, 5 cm H2O; and FIO2, 40%. A portable chest radiograph revealed a pneumomediastinum with subcutaneous