Tracheomalacia is a condition of airway obstruction characterized by weakness of cartilaginous rings and impaired longitudinal elastic fibers of the pars membranacea.1 Previous studies have suggested that tracheomalacia is recognized as a relatively common disorder.1,2 The incidence of congenital tracheomalacia in the general population is conservatively estimated at 1 in 2100 children.3 With tracheomalacia, during the expiratory phase, the diameter of the cartilaginous rings is decreased from the normal ratio of 4–5:1, to 2–3:1, which causes respiratory symptoms (eg, expiratory stridor, wheezing, dyspnea, cyanosis, and exercise intolerance).4 Diagnosis is facilitated by pulmonary function testing, computed tomography, dynamic magnetic resonance imaging, and fiberoptic bronchoscopy augmented by a thorough clinical history and physical examination.5 However, despite advances in diagnostic equipment, a diagnosis of tracheomalacia is not straightforward.
In this report, we described the case of a 12-year-old morbidly obese boy without previous respiratory symptoms scheduled for elective laparoscopic cholecystectomy, where sudden unexpected ventilatory failure due to undiagnosed tracheomalacia was encountered.
The aim of this case report is to alert anesthesiologists that tracheomalacia is a relatively common condition and can be a cause of critical airway obstruction, especially in the setting of morbid obesity during pneumoperitoneum, even after the airway is secured with an endotracheal tube (ETT).
Written Health Insurance Portability and Accountability Act authorized consent was obtained from the patient’s family to publish this case report.
A 12-year-old morbidly obese boy (height, 168.5 cm; body weight, 102.7 kg; body mass index, 36.2 kg/m2) without previous medical history presented with recurrent right upper quadrant pain. The patient underwent a diagnostic abdominal ultrasound that revealed cholelithiasis. The preoperative liver function tests showed mildly abnormal findings (alanine transaminase, 55 U/L [reference range, 12–49 U/L]; γ-glutamyl transferase, 165 U/L [reference range, 10–42 U/L]). The patient and family denied any previous history of respiratory diseases (eg, asthma, pneumonia, bronchitis), daily symptoms (eg, shortness of breath, cough, wheezing), or obstructive sleep apnea (eg, frequent snoring, excessive daytime sleepiness) at the time of the preoperative assessment. The history was otherwise unremarkable aside from a history of hives after taking amoxicillin-clavulanate. Preoperative airway assessment showed Mallampati class II with normal mouth opening and submental space. The patient’s initial vital signs in the operating room were blood pressure, 149/61 mm Hg; heart rate, 72 beats/min; and room air oxygenation saturation, 99%. After adequate preoxygenation, IV induction was initiated with fentanyl 100 µg, propofol 300 mg, and cisatracurium 10 mg. An oral airway, a laryngeal mask airway, and a video laryngoscope were immediately available. After induction of anesthesia, bag-mask ventilation was performed easily with an oral airway, and Cormack-Lehane grade III glottic view was observed by direct laryngoscopy. The patient’s airway was secured smoothly with 6.0 mm cuffed ETT at a depth of 17 cm at the lip. The ETT placement in the trachea was confirmed by auscultation and end-tidal carbon dioxide (ETco2) capnography. The depth of the ETT was assumed appropriate by external palpation of the ETT cuff below the thyroid cartilage from the anterior portion of the patient’s neck. After the intubation, the patient was on pressure-controlled ventilation, and relatively high peak inspiratory pressures were required to ventilate the patient (tidal volume [VT], 250–300 mL; peak inspiratory pressures, 22–30 cm H2O; respiratory rate [RR], 24/min; ETco2, 53 mm Hg). At this point, bilateral respiratory sounds were clear, and there were no signs of anaphylaxis (eg, urticaria, mucosal edema, hypotension, arrhythmia). However, the ETco2 capnography waveform showed an obstructive pattern. Potential undiagnosed bronchospasm was suspected. Albuterol was administered intratracheally twice every 5 minutes. Ventilation of the patient did not improve after the administration of albuterol (VT, 350–450 mL; peak inspiratory pressures, 41–45 cm H2O; RR, 24/min; ETco2, 34 mm Hg). Immediately after pneumoperitoneum was established, the VT dramatically decreased (VT, 20–30 mL; peak inspiratory pressures, 35–40 cm H2O; RR, 27/min; ETco2, 48 mm Hg), and manual ventilation was initiated. At that point, bilateral breath sounds were confirmed. Surgeons were informed about the sudden ventilatory issue, and the pneumoperitoneum was deflated. After the desufflation of the abdomen, the VT increased (VT, 216 mL; peak inspiratory pressure, 34 cm H2O; RR, 35/min; Etco2, 37 mm Hg). At this point, a suction catheter was smoothly passed through the ETT, and no secretions were detected. The patient’s face and shoulders seemed mildly erythematous. A potential allergic reaction was suspected, and 100 µg epinephrine IV, 200 mg methylprednisolone IV, 50 mg diphenhydramine IV, and 50 mg ranitidine IV were administered. A chest x-ray was obtained, which revealed no infiltrates, collapse, and evidence of aspiration, and the ETT was in good position. Intraoperative flexible bronchoscopic exploration was performed which showed that the tip of the ETT was completely occluded by a mass of pink tissue. The flexible bronchoscope was gently pushed against this tissue to reveal what appeared to be normal tracheal tissue. The 6.0-mm cuffed ETT was exchanged to a 7.0-mm cuffed ETT via direct laryngoscopy, and the position of the ETT was adjusted under flexible bronchoscopy beyond the area of obstruction. After the reintubation, the ventilation dramatically improved (VT, 550 mL; peak inspiratory pressure, 28 cm H2O; RR, 24/min; ETco2, 40 mm Hg). Subsequently, additional doses of cisatracurium were administered. After finishing the surgery, the ETT was removed, and otolaryngology performed a microlaryngoscopy and bronchoscopy with spontaneous breathing. The examination showed moderate posterior wall tracheomalacia (Figure). At this point, there was no indication for treatment. The patient was transferred to the postanesthesia care unit without any respiratory complications.
The incidence of tracheomalacia has not been established due to the lack of a universally accepted definition.2 In addition, the diversity of the patient population makes it difficult to evaluate the incidence of tracheomalacia.2 However, these studies have suggested that tracheomalacia might be a relatively common condition.2 Boogaard et al3 estimated the incidence of primary airway malacia (tracheomalacia and bronchomalacia) as ≥1 in 2100 in the general population. In this study, the data of all flexible bronchoscopy for pediatric patients with suspected primary airway malacia were analyzed. However, it did not include the population of children with airway malacia without clinical symptoms. Therefore, the incidence of undiagnosed airway malacia in children could be higher.
Previous studies have shown several conditions related to tracheomalacia.4 In this case, the patient had no conditions related to tracheomalacia (eg, chromosomal abnormalities, laryngeal cleft, tracheoesophageal fistula, chest trauma).4
Typically, the respiratory symptoms of tracheomalacia have been described as expiratory stridor, wheezing, a barking cough, respiratory distress, and cyanosis, often beginning in infancy.1 As a differential diagnosis, refractory asthma, foreign body aspiration, and intraluminal obstruction should be considered.1 However, the diagnosis of tracheomalacia is often misdiagnosed as refractory asthma.3 In preoperative assessments, anesthesiologists have to be vigilant about respiratory symptoms that become worse with increased work of breathing and history of refractory asthma.4 Anesthesiologists might need a consultation with specialists when suspecting tracheomalacia. Intraoperatively, the diagnosis of tracheomalacia under general anesthesia has to be made promptly with flexible bronchoscopy; however, it can be challenging. In our case, relatively high peak inspiratory pressures were required to ventilate the patient after endotracheal intubation. The respiratory sounds were clear and appreciated bilaterally. However, the ETco2 monitor showed an obstructive pattern. Albuterol and IV epinephrine did not improve the ventilation. Intraoperative flexible bronchoscopy was performed, which showed that the tip of the ETT was obstructed by what appeared to be the posterior aspect of the trachea.
The impact of pneumoperitoneum on the airway dynamics in tracheomalacia is not adequately understood. Previous studies have shown that the increased intraabdominal pressure with pneumoperitoneum causes cephalic shift and stiffness of the diaphragm, resulting in increased intrathoracic pressure.6,7 In tracheomalacia, the trachea tends to be collapsed with an increase of the intrathoracic pressure, surpassing the intraairway pressure.4
Obesity in children is determined by the sex-specific body mass index-for-age–adjusted percentiles based on the growth charts of the Centers for Disease Control and Prevention in 2000.8,9 The patient was considered morbidly obese (body mass index-for-age–adjusted percentile was 99.5 percentile), and the patient’s obesity could have impaired the ventilation after initiating pneumoperitoneum. Sprung et al10 reported that both morbid obesity and pneumoperitoneum decreased static respiratory compliance (30% lower) and increased inspiratory resistance (68% higher) compared with normal weight patients.
Gupta et al11 reported that ETT migration could occur due to pneumoperitoneum. ETT migration with pneumoperitoneum likely led to the near occlusion of the ETT. The ventilatory deficiency was dramatically improved after a larger ETT was placed and advanced beyond the obstruction.
The mechanism of the sudden airway collapse caused by pneumoperitoneum was unclear. The increased intrathoracic pressure by pneumoperitoneum might have worsened the bulging of the trachea and resulted in occluding the tip of the ETT. The other potential explanation is that the tip of the ETT might have migrated to the narrowest portion of the trachea due to the cephalic migration of the diaphragm.
In conclusion, tracheomalacia has been recognized as a relatively common disease; however, it is difficult to differentiate from other obstructive disorders. Anesthesiologists should be aware of undiagnosed tracheomalacia as a cause of sudden ventilatory failure under pneumoperitoneum in obese patients.
Name: Taiki Kojima, MD.
Contribution: This author helped conceive and describe the details of the case, and draft and revise the manuscript.
Name: Ali I. Kandil, DO, MPH.
Contribution: This author helped revise the manuscript.
Name: Joseph P. Previte, MD, FAAP.
Contribution: This author helped conceive and revise the manuscript.
This manuscript was handled by: BobbieJean Sweitzer, MD, FACP.
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