Contralateral Tension Pneumothorax During One-Lung Ventilation for Lobectomy: Diagnosis Aided by Fiberoptic Bronchoscopy (2002)

During one-lung ventilation, injury or compromise to the ventilated or dependent lung can progress rapidly to become a life threatening emergency. Impaired dependent-lung ventilation usually presents as abnormal respiratory mechanics, (i.e., increased airway pressure or decreased tidal volume), peripheral oxygen desaturation detected by pulse oximetry (Spo2), or both (1). Cardiovascular instability, most frequently hypotension, can also be the sign of impaired dependent-lung ventilation. We report a case of a patient who developed a tension pneumothorax during thoracic surgery and one-lung ventilation. The pneumothorax was associated with deterioration in both respiratory and cardiovascular function, and diagnosis was aided by intraoperative fiberoptic bronchoscopy. Case Report A 76-yr-old, 68-kg man was referred for right thoracotomy and resection of a right upper lobe adenocarcinoma. His medical history was significant for previous cigarette smoking (30-pack years) and previous blunt trauma to the thorax many years earlier resulting in numerous rib fractures. Treatment required a splenectomy, a tracheostomy, and placement of a right-sided chest tube. These injuries were well healed at the time of surgery. Preoperative pulmonary function testing showed a forced expiratory volume in one second of 2.4 L (86% of predicted), a diffusing capacity of 81% of predicted, and a room air Pao2 of 97 mm Hg. The chest roentgenogram showed a 3-cm mass in the right upper lobe. His preoperative blood pressure was 125/85 mm Hg and a heart rate of 90 bpm. In the operating room (OR), a right radial arterial cannula and a thoracic (T5 level) epidural were placed before the induction of anesthesia. An epidural test dose of 3 mL of 1.5% lidocaine with 1:200,000 of epinephrine was negative for intravascular or intrathecal effects. Anesthesia was induced with IV sodium thiopental 200 mg and fentanyl 250 μg, and neuromuscular blockade was achieved with rocuronium 50 mg. The trachea was intubated with an 8.0-mm ID single-lumen endotracheal tube, and anesthesia was maintained with isoflurane, fentanyl, and oxygen. After flexible fiberoptic bronchoscopy and staging mediastinoscopy, a 35F left-sided double-lumen endobronchial tube (Bronchocath®, Mallinckrodt, Great Britain) was inserted under direct laryngoscopy. Double-lumen tube placement was checked by traditional inspection and auscultation, and correct positioning was confirmed using fiberoptic bronchoscopy (2). The patient was turned into the left lateral decubitus position for the planned right posterolateral thoracotomy. Fiberoptic visualization via the tracheal and bronchial lumens again confirmed correct tube position before skin incision. During two-lung ventilation, the exhaled tidal volume was 650 mL with a peak inspiratory pressure of 16 cm H2O and a respiratory frequency of 10 breaths/min. Spo2 was 99% with an inspired fraction of oxygen of 0.98. After thoracotomy, initiation of dependent (one)-lung ventilation resulted in the peak inspiratory pressure increasing to 28 cm H2O with an exhaled tidal volume of 550 mL. Fifteen minutes later, the peak inspiratory pressure suddenly increased to 60 cm H2O together with an abrupt decrease of exhaled tidal volume to 150 mL. Spo2 decreased from 99% to 88%. Simultaneously, systolic arterial blood pressure declined from approximately 120 mm Hg to 85 mm Hg. Immediate treatment consisted of resuming two-lung ventilation with a ventilator set tidal volume of 500 mL and a respiratory frequency of 14 breaths/min. Phenylephrine 1 mg IV was titrated for 15 min. Spo2 increased to 96%, exhaled tidal volume increased to 360 mL, and peak inspiratory pressure decreased to 36 cm H2O. Systolic arterial blood pressure increased to 110 mm Hg. The breathing circuit was confirmed to be functioning correctly. Fiberoptic visualization via the tracheal lumen confirmed the bronchial cuff had not moved and remained just immediately below the carina. The fiberscope was next passed through the bronchial lumen revealing normal tube diameter and minimal secretions. Upon exiting the bronchial lumen, there was severe circumferential compression and inward bulging of the bronchial mucosa completely obstructing the left upper and lower lobe orifices (Fig. 1 A). There were no changes in bronchial dimensions during positive-pressure ventilation. The surgeon was informed and asked to inspect the dependent lung for signs of a pneumothorax, e.g., elevation of the left mainstem bronchus or mediastinal herniation into the right hemithorax. Because of extensive adhesions in the patient’s right hemithorax secondary to previous injury, inspection was inconclusive. At this point, an intraoperative cross-table lateral chest roentgenogram showed a left-sided tension pneumothorax (Fig. 2). The patient was rotated slightly to the right, and the surgeon placed a left-sided chest tube for evacuation of the pneumothorax. After tube thoracostomy, one-lung ventilation was resumed. Respiratory mechanics, Spo2, and blood pressure remained stable for the remainder of the case. Repeat fiberoptic visualization through the bronchial lumen revealed a normal bronchial carina, with patent left upper and lower lobe orifices (Fig. 1 B).Figure 1: (A) Compression of the bronchial carina by the surgeon in a different patient was used to simulate left upper and lower lobe compression as visualized via the bronchial lumen during the tension pneumothorax described in our case. (B) Bronchoscopic view via the bronchial lumen showing a normal bronchial carina with patent left upper and lower lobe orifices after release of surgical compression.Figure 2: Chest roentgenogram of the patient in the left lateral decubitus position showing left-sided tension pneumothorax with the cardiac silhouette (C on the image) increased into the right hemithorax. The double-lumen tube (DLT on the image) positioned in the trachea and left mainstem bronchus is also similarly displaced into the right hemithorax.After completion of the right upper lobectomy, the double lumen endobronchial tube was replaced with an 8.0 mm ID single-lumen tube. Fiberoptic bronchoscopic inspection did not reveal any tracheobronchial tears. The patient’s trachea was extubated in the OR, and he was transferred to the intensive care unit. The remainder of the patient’s hospital course was uneventful, and he was discharged on the ninth postoperative day. Discussion Dependent-lung tension pneumothorax during thoracotomy and one-lung ventilation is rare (3–5). The cause of the pneumothorax in our patient could not be determined with certainty, however this case illustrates that there are a variety of causes that may lead to an intraoperative pneumothorax. For example, barotrauma from excessive tidal volume and high airway pressure may occur if the left-sided double-lumen tube is positioned distally such that the entire tidal volume is directed to only one lobe (6). The relatively small-sized 35F double-lumen tube used in our patient might have permitted lobar placement. Nevertheless, peak airway pressures were not excessive during initiation of one-lung ventilation, and fiberoptic visualization showed the tube to be in good position. High tidal volumes and high airway pressures may also be delivered, especially during reexpansion of the previously collapsed surgical lung, but is not relevant in our case. Perhaps barotrauma occurred as the result of air trapping within the dependent lung, leading to hyperinflation and rupture of a sub-pleural bleb. On-line flow-volume monitoring might be useful in detecting the presence of air trapping (7). The smaller sized double-lumen tube may also have contributed to air trapping, especially during one-lung ventilation regardless of the patient’s preexisting pulmonary disease. Other causes relevant to thoracic surgery include tracheobronchial disruption after placement of the double-lumen tube, damage to the contralateral pleura during surgery, or lung injury after central venous catheter insertion or epidural placement (8,9). Pneumothorax may also occur after mediastinoscopy. Compared with two-lung ventilation, peak airway pressure normally increases by 50% when one-lung ventilation is initiated at the same tidal volume (10). Common causes of an excessive increase in airway pressure and decrease in tidal volume during one-lung ventilation include tube obstruction (from malpositioning, secretions, or blood), lung diseases (e.g., severely obstructive or restrictive), or pneumothorax (5,11). Because clinical manifestations of these different causes can be similar, an organized approach to early diagnosis and treatment is required. The combination of abnormally high peak airway pressure, decreased tidal volume, decreased Spo2, and hypotension during one-lung ventilation requires immediate intervention. In this circumstance, resumption of two-lung ventilation is required as the initial step. Because airway obstruction from tube malposition or from secretions or blood is likely, fiberoptic inspection should be undertaken. Typically, the fiberscope is passed through the tracheal lumen, first verifying a patent right main stem bronchus, then confirming correct tube position by observing the bronchial cuff in the left main bronchus, within 1 cm of the carina (2). In most cases of increased peak inspiratory pressure, repositioning the tube corrects the problem. However, in our case, because ventilation through the bronchial lumen was obstructed, fiberoptic examination through the bronchial lumen was required. The finding of a completely collapsed left bronchial carina was most likely explained by external compression from increased pressure in the pleural space, suggesting a tension pneumothorax (12). Other causes of extrinsic airway obstruction, such as disruption or dissection of the aorta or from a mediastinal mass, will usually compress the membranous portion of the airway. When visualized through a bronchoscope, the airway will seem asymmetrically compressed for only a short segment with normal anatomy distal to the obstruction (13–15). Distinguishing between a tension pneumothorax and extreme hyperinflation with intrinsic positive end-expiratory pressure may prove difficult. In both circumstances, respiratory mechanics are impaired and associated with hypoxemia and cardiovascular compromise or collapse (16). Whereas chest radiography should distinguish between these two entities, fiberoptic bronchoscopy is immediately available and should lead to the correct diagnosis (17). With a tension pneumothorax, the major bronchi are circumferentially compressed, occluding the lobar orifices (12). In contrast, with extreme hyperinflation, air trapping occurs as a consequence of loss of elastic recoil (emphysema) and/or airway narrowing from high bronchomotor tone and mucosal edema (asthma/bronchitis) (18). Thus, the obstruction occurs in smaller distal air passages not resulting in major bronchial collapse. Alternatively, flow-related collapse producing lung hyperinflation may also occur in the larger bronchi (19). In this circumstance, a ball valve effect would be present with airway patency during inspiration and dynamic airway collapse on exhalation (20). Lobar dynamic expiratory collapse might be attenuated by the bronchial portion of the double-lumen tube. In summary, compromise of dependent lung ventilation during thoracic surgery can become a life threatening situation requiring emergent intervention. Although there are many causes for impaired ventilation, fiberoptic inspection can not only diagnosis causes such as tube malposition or obstruction because of secretions, but also, as demonstrated in this case, can help diagnose a tension pneumothorax.