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Massive Subcutaneous Emphysema and Sudden Airway Compromise After Postoperative Vomiting

1999; Lippincott Williams & Wilkins; Volume: 89; Issue: 3 Linguagem: Inglês

10.1097/00000539-199909000-00050

1526-7598

Roman Schumann, David M. Polaner,

Airway Management and Intubation Techniques

Postoperative nausea and vomiting is common, but rarely produces life-threatening symptoms. We describe a case of massive mediastinal and subcutaneous emphysema, which developed immediately after postoperative vomiting in the postanesthesia recovery unit and caused imminent airway compromise, requiring emergent fiberoptic endotracheal intubation. Case Report A 43-yr-old woman underwent an uneventful left total mastectomy for intraductal breast carcinoma. Her medical history was significant only for glaucoma and obesity (weight, 91 kg; height, 157.5 cm). General anesthesia was induced using a rapid sequence technique because of obesity. The patient's trachea was intubated using a Miller 3 blade and a 7.0 styletted endotracheal tube on the first attempt without difficulty or evident trauma. An orogastric tube was easily placed after intubation for gastric decompression, and it was removed before extubation. Anesthesia was maintained with isoflurane in 60% nitrous oxide, fentanyl, and vecuronium. At the end of surgery, the neuromuscular blockade was reversed, the patient awakened, and the trachea was extubated. Ondansetron was administered because of nausea. Fifteen minutes after arriving in the postanesthesia care unit, the patient experienced an episode of nausea and retching, and she vomited a small amount of gastric contents. Within 10 min of this event, she complained of a "funny feeling" in her neck and throat. Physical examination revealed anterior chest wall crepitus and swelling caused by subcutaneous emphysema, which, within minutes, spread cephalad to the neck and face up to the level of the eyebrows. No dyspnea, oxygen desaturation, or hemodynamic instability was noted at this time. A portable chest radiograph showed a pneumomediastinum and massive bilateral subcutaneous emphysema of the neck and chest wall (Figure 1). A pneumothorax was not present. Within the next several minutes, the patient's voice became increasingly high pitched, and she experienced more difficulty speaking. Because of the concern for impending airway compromise, fiberoptic nasotracheal intubation with a 6.0 tube was rapidly performed to secure the airway. Through the fiberoptic bronchoscope, the pharynx and supraglottic structures appeared very swollen and distorted down to the aryepiglottic folds. The vocal cords and the trachea to the level of the carina appeared normal. Figure 1: Anteroposterior chest radiograph showing the pneumomediastinum (p) and subcutaneous emphysema (e) tracking through the soft tissues of the neck.We elected to avoid positive pressure ventilation, and 5 cm H2O of continuous positive airway pressure with spontaneous ventilation was instituted. Antibiotic therapy was started, and the trachea remained intubated for 18 h. The emphysema resolved completely after several days. Diagnostic studies included a repeat flexible bronchoscopy, a barium contrast esophogram, and direct laryngoscopy, all of which were normal (except for the presence of residual emphysema in the pharynx). The patient was evaluated by the cardiothoracic surgery, pulmonary, and otolaryngology services. All efforts failed to demonstrate a clear site of injury, and the patient made an uneventful recovery. Discussion This report describes the sudden development of airway compromise caused by rapidly progressing subcutaneous emphysema after postoperative vomiting. The differential diagnosis includes alveolar rupture, spontaneous postemetic rupture of the esophagus (Boerhaave's syndrome), and trauma to the hypopharynx, trachea, or esophagus. Pneumomediastinum and subcutaneous emphysema resulting from alveolar rupture can occur after forceful vomiting. Increased alveolar pressure, produced by a valsalva maneuver during vomiting, may cause alveolar rupture into the interstitium of the lung. From there, air travels along the pulmonary vascular sheaths, where it enters the mediastinum and then dissects through the soft tissue planes of the neck, producing the subcutaneous emphysema. This has been demonstrated in experimental animals and in humans (1,2). Several other cases have been reported, but none describe the development of severe airway compromise (5–8). These cases are notable for their lack of sequelae and their spontaneous resolution. This is in contradistinction to most reported cases of Boerhaave's syndrome, in which leakage of esophageal and gastric contents into the mediastinum often causes mediastinitis with its attendant complications (3,4). Its classical presentation consists of the triad of vomiting, chest pain, and subcutaneous emphysema, although not all of these symptoms are present in many cases (3,4). Most authors agree that the high incidence of morbidity and mortality can be reduced by early diagnosis and aggressive surgical treatment; however, there are several reports of successful conservative management when leakage from the esophagus is minimal or has abated (9–11). Because of the potentially insidious nature of a small esophageal tear, it is possible that the site of rupture in our patient was impossible to locate (12). Other causes of subcutaneous emphysema in the perioperative period include trauma to the pharynx, esophagus, or trachea from laryngoscopy, intubation, overinflation of the endotracheal tube cuff, or gastric tube placement (13,14). In our patient, there was no indication that any of these procedures were difficult or caused any trauma, although occult injury cannot be entirely excluded. An initial site of injury in the pharynx or hypopharynx is unlikely in this case, because the emphysema began in the chest wall and, from there, spread cranially to the neck and head and finally produced symptoms in the airway. Furthermore, the patient's symptoms did not develop after intubation and gastric tube placement, despite several hours of positive pressure ventilation, but developed rapidly, immediately after her episode of forceful retching and vomiting, suggesting a causal relationship between those events. No pharyngeal or airway lesion was identified, although one may have been obscured by the significant swelling caused by the emphysema. In the absence of a demonstrable lesion, it was impossible to definitively establish the etiology of this patient's symptoms, but alveolar rupture is the most likely etiology. The impending loss of airway was successfully averted by immediate awake fiberoptic intubation, which may offer the best visualization of the airway and may be the easiest and least traumatic method to intubate the trachea in this situation. We conclude that subcutaneous emphysema, with extension into the soft tissue planes of the supraglottic airway, can be a rare complication of postoperative vomiting. Within minutes, this may lead to airway compromise, which may be heralded by a change in the voice. This must be promptly recognized to successfully secure the airway before distortion of the anatomy makes intubation more difficult or impossible. Investigation to identify a potential tracheoesophageal injury is warranted; if not present, alveolar rupture is the most likely diagnosis and will resolve spontaneously.