Obstructive shock occurs due to great vessel or cardiac ventricular obstruction . Several conditions can cause obstructive shock, such as tension pneumothorax, pneumomediastinum, cardiac tamponade, and pulmonary embolism . The most common medical causes of pneumomediastinum are asthma exacerbation and infections . Pneumomediastinum is treated with percutaneous mediastinal tube drainage or thoracotomy . In our case, obstructive shock was caused by pneumothorax and pneumomediastinum secondary to tracheal perforation due to long-term tracheostomy tube placement. Although additional thoracic drainage restored hemodynamic stability, it took 8 h for the patient’s blood pressure to recover completely because the pneumomediastinum was treated conservatively by observation. However, since the pneumomediastinum did not worsen following bridging of the tracheal perforation by the cuffed tracheostomy tube, we considered it prudent to avoid aggressive intervention for the pneumomediastinum, due to the associated risks of bleeding, cardiac puncture, and infection.
Pediatric tracheal perforations can occur as both early and delayed complications of tracheostomy and endotracheal intubation [1, 2]. Injury to the posterior tracheal wall by an endotracheal tube is a known cause of tracheal perforation . Long-term pressure on the posterior tracheal wall by the tip of the tracheostomy tube can lead to tracheo-esophageal fistula formation in children [1, 7]. Although rare, this complication is, at present, more common in immunocompromised children with poor healing who are tracheostomy dependent . Additionally, children with tracheal anomalies and severe kyphoscoliosis have a greater risk of tracheoesophageal fistulas . Our patient had severe scoliosis, and hence, his esophagus was significantly displaced to the left and was not directly behind the trachea (Fig. 3C). Since there was only soft tissue between the trachea and Th-3 vertebra, the shear stress on the soft tissue between the poorly positioned tip of the tracheostomy tube and Th-3 vertebra probably caused the perforation and subsequent pneumomediastinum and pneumothorax.
There were four possible reasons for the tracheal fragility in our case. First, our patient had cerebral palsy with undernutrition, long-term steroid replacement therapy, and severe sepsis because of an intractable cerebral abscess, making him a compromised host. Second, higher positive pressure ventilation was required during the course of treatment, which could have caused pressure injury. Use of an uncuffed tracheostomy tube during positive pressure ventilation is usually associated with some amount of air leak from the trachea. Changing to a cuffed tracheostomy tube without an air leak would result in higher pressure ventilation compared with an uncuffed tracheostomy tube with air leak despite unchanged positive pressure settings. Third, the unstable tip of the tracheostomy tube might have impinged on the posterior tracheal wall more strongly during the patient’s transfer to our hospital, which could have caused the wound that ultimately led to tracheal perforation. Fourth, it was possible that the cuff of the tracheostomy tube contacted the tracheal ulcer, causing the perforation, although we repeatedly confirmed that the cuff of the tracheostomy tube did not contact the tracheal ulcer during the course of treatment. Patients with a greater risk of tracheal perforation, such as our case, should undergo repeated assessment of the position of the tracheostomy tube not only during their hospitalization but also while being transferred, to prevent tracheal perforation.
The goal of treatment of tracheal perforation is to minimize the risk of mediastinitis and provide effective ventilation during the healing process while observing for scarring and tracheal stenosis. Generally, surgical repairs are considered when patients remain unstable or bridging the lesion is not technically feasible . If the patient’s respiration is stable, positive pressure ventilation should be terminated . A previous study showed that noninvasive positive pressure ventilatory support might be effective as transient treatment in patients with tracheal perforations . However, positive pressure ventilation could not be discontinued in our patient because of disuse syndrome and cerebral palsy. As emergency treatment for tracheal perforation, we bridged the tracheal perforation with the cuffed tracheostomy tube, which successfully prevented the deterioration of mediastinitis and provided enough ventilation.
In conclusion, we observed unexpected hypotension because of pneumomediastinum and pneumothorax secondary to tracheal perforation in a pediatric patient. Our experience suggests that tracheal perforation should be considered in the differential diagnosis in pediatric patients with long-term tracheostomy tube placement who suddenly develop hypotension.