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Direct Laryngoscopy and Endotracheal Intubation Complicated by Anterior Tracheal Laceration Secondary to Protrusion of Preloaded Endotracheal Tube Stylet

Warner, Matthew A. MD; Fox, Jonathan F. MD

doi: 10.1213/XAA.0000000000000235
Case Reports: Clinical Care

Tracheal wall disruption is a rare complication of endotracheal intubation, typically occurring in the posterior (membranous) trachea lacking cartilaginous support. We present the case of a 68-year-old man who developed an anterior tracheal tear after routine endotracheal intubation, most likely occurring secondary to protrusion of a factory-preloaded stylet beyond the distal orifice of the endotracheal tube. Tracheal disruption should be considered in any patient with subcutaneous emphysema and respiratory distress after tracheal extubation and confirmed with bronchoscopy. Conservative management may be appropriate for those with small tears, hemodynamic stability, and the ability to isolate the tear from positive pressure ventilation.

From the Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota.

Accepted for publication June 16, 2015.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Jonathan F. Fox, MD, Department of Anesthesiology, Mayo Clinic, 200 1st St. SW, Rochester, MN 55905. Address e-mail to

Tracheal wall disruption occurs with an estimated incidence of 1 in 20,000 endotracheal intubations, making it a rare but often devastating iatrogenic complication.1 It is most commonly represented by longitudinal tears in the distal third of the membranous (posterior) trachea that lacks cartilaginous support.2 To our knowledge, there are no published reports describing lacerations of the anterior tracheal wall in the setting of endotracheal intubation. We present the case of a 68-year-old man who suffered a clinically significant anterior tracheal wall laceration after seemingly routine direct laryngoscopy and endotracheal intubation. Written informed consent for publication of this case report was obtained directly from the patient. In addition, the authors of this article were directly involved in the patient’s perioperative care.

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A 68-year-old man with severe mitral regurgitation, atrial fibrillation, obstructive sleep apnea, and mild esophageal dysphagia was scheduled for open mitral valve repair. The patient displayed no features predictive of difficult intubation on preoperative examination, including a Mallampati score of II, mouth opening >4 cm, thyromental distance >3 fingerbreadths, and normal range of motion of the cervical spine. After IV induction of anesthesia and succinylcholine administration, a single-lumen, 8.0-mm internal diameter oral endotracheal tube (TaperGuard™ Tracheal Tube with Stylet, Covidien) was placed by an experienced laryngoscopist on the first attempt using a Miller 2 blade with a grade 1 Cormack-Lehane view of the glottic apparatus. A transesophageal echocardiogram probe was subsequently inserted with no resistance to probe passage. In addition, a 9-French double-lumen introducer and pulmonary artery catheter were placed in the right internal jugular vein under dynamic ultrasound guidance. The operative course was uncomplicated, including unremarkable separation from cardiopulmonary bypass and no difficulties with ventilation or oxygenation. A left-sided chest tube was placed by the surgical team, in addition to a single mediastinal drain. Endotracheal intubation with IV sedation was maintained at the conclusion of the surgical procedure, and the patient was transferred to cardiac-surgical intensive care unit.

Approximately 6 hours postoperatively, the patient was discovered to have progressive subcutaneous emphysema in his neck and upper sternum and a large air leak around his endotracheal tube. Under videolaryngoscopy guidance, the periglottic and hypopharyngeal structures were visualized without evidence for injury. The cuff of the endotracheal tube was observed to be positioned at the level of the glottic inlet and was subsequently advanced with no improvement in cuff leak. Given these findings, the decision was made to exchange the endotracheal tube. With videolaryngoscopy and propofol sedation, the endotracheal tube was removed, followed by the placement of a new endotracheal tube without complication and with complete resolution of the air leak. A small perforation was noted in the cuff of the removed endotracheal tube.

After endotracheal tube exchange, the patient’s subcutaneous emphysema improved dramatically over several hours. Bedside flexible nasopharyngoscopy and formal upper endoscopy were unremarkable for any significant pharyngeal, laryngeal, or esophageal trauma. On further evaluation, the patient was discovered to have an enlarging left-sided pneumothorax, which was suspected to have contributed to his subcutaneous emphysema. A new chest tube was placed, and the patient’s trachea was extubated approximately 12 hours later after assurance of stable hemodynamics and respiratory status. However, tracheal extubation was complicated by immediate, rapid progression of subcutaneous emphysema expanding from the neck into the face and sternum. He was emergently reintubated. Fiberoptic bronchoscopy was unremarkable for lower tracheal or bronchial injury. When the endotracheal tube was retracted over the bronchoscope to the level of the false cords, an anterior tracheal laceration was noted with obvious opening of a mucosal flap with each inspiratory cycle of positive pressure ventilation (Fig. 1). The endotracheal tube was subsequently advanced distal to the mucosal disruption, and the cuff was reinflated.

Figure 1

Figure 1

After consultation with the otolaryngology service, the decision was made to maintain endotracheal intubation for 4 more days, at which time fiberoptic bronchoscopy would be repeated to look for evidence of tracheal healing. The patient had an otherwise uneventful postoperative course and was aggressively mobilized in the intensive care unit with the endotracheal tube in place. Unfortunately, there was no evidence of spontaneous tracheal healing on fiberoptic bronchoscopy by postoperative day 5. The patient was subsequently taken to the operating suite for tracheostomy. At that time, he was confirmed to have a 1.9-cm anterior tracheal wall laceration involving the second, third, and fourth tracheal rings. The patient did well postoperatively without requirement for mechanical ventilation. His tracheostomy was decannulated, and he was discharged home on postoperative day 10.

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Proposed risk factors for tracheal wall disruption after endotracheal intubation may be divided into anatomic and mechanical. Anatomic risk factors include congenital or acquired tracheal abnormalities, chronic steroid use, female sex, advanced age, and inflammatory lesions of the tracheobronchial tree, whereas mechanical factors include multiple forced attempts at intubation, double-lumen endotracheal tubes, oversized endotracheal tubes, overdistention of the endotracheal tube cuff, use of an endotracheal tube introducer, emergency intubation, repositioning of the endotracheal tube with an inflated cuff, and novice laryngoscopy.3–8 Such patients typically present with subcutaneous or mediastinal emphysema, dyspnea, dysphonia, cough, hemoptysis, or pneumothorax, the majority of which appear immediately or within hours of tracheal extubation.8–12 Interestingly, subcutaneous emphysema is considered a positive prognostic factor, likely because of faster diagnosis and treatment of an underlying tracheal disruption.8

Management of tracheal lacerations remains controversial. Early surgical repair has long been considered the standard of care3,11–13; however, many now opt for conservative treatment in patients with small tears <2 cm and in patients with nonprogressive symptoms, hemodynamic stability, and absence of air leak with spontaneous breathing.3,8,9,14–18 Conservative management includes maintenance of endotracheal intubation with the cuff distal to the injury, low-pressure ventilatory strategies, and empirical antibiotic therapy if mediastinitis is suspected.3 Most authors agree that immediate surgical repair is warranted when a laceration is detected during open chest surgery and in patients with rapid progression of air leak, hemodynamic compromise, and ventilatory deterioration.8,15

In the case presented here, the patient suffered significant trauma to the anterior cartilaginous tracheal wall despite a seemingly routine and atraumatic endotracheal intubation. Given the size, location, and linear morphology of the laceration in the absence of other tracheal inducers, we presume that this was most likely related to the protrusion of a factory preloaded stylet beyond the distal orifice of the endotracheal tube. The preloaded stylet in this case (Mallinckrodt intubating stylet, Covidien) was 4.7 mm in diameter and composed of malleable aluminum with a lubricated plastic sheath to reduce friction on stylet removal. Despite being designed to prevent stylet extension beyond the endotracheal tube orifice, preloaded stylets may inadvertently be dislodged negating their inherent safety. Although traumatic injury is a risk with any tracheal introducer or bougie, endotracheal tube stylets are more rigid structures and may carry greater potential for iatrogenic harm. It is essential that the position of a stylet be verified within the endotracheal tube before any attempts at endotracheal intubation, even with factory preloaded stylets. In addition, resistance to the passage of any tracheal introducer or endotracheal tube should prompt immediate evaluation, especially in the setting of blind advancement.

The patient in this case had a prolonged hospital course because of his injury, but ultimately had a satisfactory outcome. Abrupt progression of subcutaneous emphysema after endotracheal extubation likely occurred secondary to exposure of the tracheal laceration, which had been isolated from the effects of ventilation by an intact endotracheal tube cuff, to spontaneous air movement. Of note, positive pressure ventilation would have been similarly detrimental, as evidenced by mucosal flap opening during bronchoscopy. Given the ability to isolate the lesion from the effects of positive pressure ventilation and preserved hemodynamic stability, the decision was made to maintain endotracheal intubation distal to the lesion to facilitate healing. However, with no evidence of healing present 5 days after injury, the risk of prolonged endotracheal intubation outweighed the risks of tracheostomy. Of note, it is of great importance to maximize early mobilization and physical therapy in patients requiring prolonged endotracheal intubation, because this has many potential benefits including maintenance of motor strength, earlier ventilator liberation, and improved functional status at hospital discharge.19 Approximately 3 months postoperatively, the patient in our case has obtained complete spontaneous healing of his tracheostomy site and displays no features of residual respiratory compromise.

When preparing for endotracheal intubation, assurance of correct stylet placement must be verified even with the use of factory-issued preloaded endotracheal tube stylets. Moreover, the laryngoscopist should recognize patient-related (e.g., female sex, chronic steroid use, congenital tracheal abnormalities, advanced age) and equipment-related factors (e.g., oversized endotracheal tubes, overdistention of endotracheal cuff, protruding stylet, or introducer) associated with tracheal injury. Interestingly, a systematic review of postintubation tracheal rupture, a term that encompasses any type of tracheal wall disruption, found that approximately two-thirds of cases occurred during intubation for elective procedures, and <15% of intubations were described as difficult.8 The overall mortality was 22%. Diagnosis of tracheal wall disruption should be suspected in any patient with subcutaneous emphysema or respiratory distress after extubation and subsequently confirmed with bronchoscopy. Conservative management should be considered for patients with small tears, hemodynamic stability, and the ability to isolate the tear from the potentially harmful effects of positive pressure ventilation.

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