Sohasky, Jerome CRNA; Chimbira, Wilson T. MD, FRCA; Nafiu, Olubukola O. MD, FRCA
From the Department of Anesthesiology, Section of Pediatric Anesthesiology, University of Michigan Health System, Ann Arbor, Michigan.
Accepted for publication April 2, 2013.
The authors declare no conflicts of interest.
Reprints will not be available from the author.
Address correspondence to Olubukola O. Nafiu, MD, FRCA, Department of Anesthesiology, Section of Pediatric Anesthesiology, University of Michigan Health System, 1500 East Medical Centre Dr., Room UH 1H247, Ann Arbor, Michigan 48109-0048. Address e-mail to email@example.com.
Video-assisted thoracoscopic surgery has become a common procedure in pediatric surgery. We present a case of accidental intraoperative bronchopleural fistula during a video-assisted thoracoscopic surgery procedure, which was first identified by the anesthesia team. We discuss differential diagnoses including the role of end-tidal carbon dioxide monitoring as an aid to prompt diagnosis.
Video-assisted thoracoscopic surgery (VATS) is a well-described technique in children, and as the technology improves more pediatric thoracic procedures are being performed in this manner.1,2 Insufflation of carbon dioxide (CO2) into the pleura (capnothorax) is commonly used during VATS to aid ipsilateral lung collapse and aid operative visualization.3 Despite being a relatively safe procedure, occasional intraoperative complications may occur. We present a case of accidental intraoperative bronchopleural fistula during a VATS procedure, which was identified by vigilance of the anesthesia team and discuss the role of end-tidal CO2 (ETCO2) monitoring and the importance of good communication with the surgical team. We are unaware of any other report of bronchopleural fistula during VATS in children. Written parental consent was obtained to report this extremely rare case.
A 7-month-old ASA physical status II girl (weight = 9.2 kg) with right upper lobe congenital cystic adenomatous malformation was scheduled for VATS resection of the right upper lobe. She was the product of full-term pregnancy complicated only by a prenatal diagnosis of a right cystic lung lesion. Postnatal follow-up with periodic ultrasonography and a recent chest computerized tomographic scan that showed increasing size of the cyst prompted a decision to operate. Her preoperative chest radiograph was unremarkable apart from apical and right hilar fullness. No definite cystic lesions were seen (Fig. 1).
Inhaled induction of anesthesia was performed with sevoflurane, and after inserting 2 peripheral IV catheters, tracheal intubation with a size 4.0, cuffed endotracheal tube (ETT) was performed. Lung isolation was established by advancing the ETT into the left main bronchus under fiberoptic visualization. A right radial arterial catheter was inserted aseptically for continuous arterial blood pressure monitoring. The patient was then placed in a left lateral decubitus position. Surgery commenced shortly thereafter, and the surgeons confirmed good lung isolation after CO2 insufflation of the pleural cavity. A basal flow of 1 L/min of CO2 and pleural pressure of 4 to 6 mm Hg was maintained to ensure lung collapse and optimal visualization. This was accompanied by a moderate increase in the ETCO2 from 35 mm Hg to about 45 mm Hg. We adjusted the ventilator settings to deliver tidal volume (VT) of 7 mL/kg and respiratory rate of 22 breaths/min. Surgery proceeded uneventfully for the first 90 minutes.
The surgeons however commented on some technical difficulty with identifying the lobar fissures. Shortly thereafter, we observed a sharp increase in the ETCO2 concentration from 45 mm Hg to 120 mm Hg and eventually to 251 mm Hg. There was no accompanying increase in the patient’s temperature, although there was associated tachycardia. At the same time, we observed a gradual decrease in the arterial blood pressure as well as the oxygen saturation as measured by pulse oximetry (SpO2). The surgical team was informed about the sudden change in the patient’s condition, and the initial thought was possible CO2 or air embolism. However, we did not observe any change in the end-tidal nitrogen concentration. We then asked the surgeons to consider the possibility of a major airway injury because this could explain the inordinately high ETCO2. The gas being insufflated into the right pleura was being entrained into the airway and being sampled by the ETCO2 sensor. At this time, the patient’s VT had decreased from 60 to 45 mL with a slight increase in the peak inspiratory pressure from 25 mm Hg to 31 mm Hg.
Due to the continued instability in the patient’s hemodynamic and ventilatory status, a decision was made to convert the procedure to open thoracotomy. Thereafter, an iatrogenic right upper lobe bronchial injury was found and bronchoplasty was performed. The ETCO2 returned to a normal range of 45 to 50 mm Hg. Arterial blood gas drawn after the patient’s status stabilized revealed severe respiratory acidosis (pH = 7.1, PaCO2 = 67 mm Hg, PO2 = 320 mm Hg, HCO3 = 25 mmol/L, BE = −3.8). Once the bronchial injury was repaired, the patient’s condition continued to improve and the remainder of the intraoperative course was relatively uneventful. The trachea was extubated, and the patient was transferred to the intensive care unit at the end of surgery. She was discharged from the hospital 10 days later to be followed up in the surgical outpatient clinic.
This case exemplifies an acute life-threatening surgical complication of VATS, which was first suspected by inordinately increasing ETCO2 and the successful outcome underscores the vigilance of the anesthesia team, knowledge of the surgical procedure, and close communication with the surgeons. The case highlights the role of ETCO2 monitoring in a patient undergoing VATS when capnothorax is used. In this instance, a 5-fold increase in ETCO2 was due to an iatrogenic major airway injury during surgical dissection.
VATS resection of congenital cystic adenomatous malformation and operative repair of other intrathoracic pathologies in children are becoming increasingly popular.1,4 Although VATS results in longer operative times, it is associated with shorter hospital stay, better cosmesis, and reduced postoperative pain.5 During VATS, CO2 pneumothorax (capnothorax) is routinely performed to ensure and maintain ipsilateral lung collapse to aid surgical exposure.6 Capnothorax is typically accompanied by a moderate increase in ETCO2 and is usually well tolerated by most children and is normally not accompanied by hemodynamic perturbations. Indeed, hypercapnia during VATS has been shown to have some hemodynamic benefit.7 This mild-to-moderate hypercapnia can usually be remedied by slightly increased respiratory rate. Our patient developed a rapid, supraphysiologic increase in ETCO2 and became progressively hypotensive. The massive increase in ETCO2 was due to a bronchopleural fistula, which produced a direct communication between CO2 being insufflated into the pleura and lung/bronchial tissue. The CO2 was then carried into the ETT in the trachea to the capnometer where high ETCO2 readings were detected. The progressive hypotension was due to rapidly developing tension pneumothorax.
VATS is a relatively safe procedure. One report of approximately 1100 consecutive VATS cases over a 12-year period identified prolonged air leak, wound infection, bleeding, and rarely conversion to open thoracotomy as the most frequent complications.8 Despite the reported low risk and efficacy of VATS,9 occasionally acute intraoperative complications that necessitate conversion to open thoracotomy may occur. Intraoperative bronchopleural fistula with tension pneumothorax is extremely uncommon but should be suspected when a supraphysiologic increase in ETCO2 with concomitant hemodynamic perturbation occurs. One additional report of intraoperative airway injury confirmed by ETCO2 has been published but this occurred in an adult patient undergoing thoracoscopic esophagectomy.10 Our case represents the only pediatric report to date.
Other possible causes of rapidly increasing ETCO2 include malignant hyperthermia, progressive hypoventilation, and thyroid storm. However, none of these differential diagnoses are accompanied by a supraphysiologic increase in ETCO2. Typically, air embolism in the early phase will cause a decrease in the ETCO2 due to an increase in dead space to tidal ventilation (VD/VT). Furthermore, during the early phase of creating capnothorax, CO2 embolism may occur. This is typically associated with tachycardia, and the increased ETCO2 is not as marked as occurred in our case and is usually transient.11 Large volume CO2 embolism may be associated with hypotension, cardiac arrhythmias, and pulmonary edema.11
In summary, this report illustrates a rare but potentially lethal intraoperative complication of VATS (bronchopleural fistula with rapidly evolving tension pneumothorax). Prompt diagnosis was aided by the rapid increase in ETCO2 and communication with the surgeons. It is essential that anesthetic caregivers are aware that capnothorax is created during VATS and that rapidly increasing ETCO2 may indicate large airway injury.
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