When unrecognized, tension pneumothorax can lead to a catastrophic outcome. It is imperative to quickly establish the diagnosis and promptly decompress the pleural space. We report a patient who developed a right-sided tension pneumothorax during left-pneumonectomy in the absence of significant hypoxemia and hemodynamic instability.
A 57-yr-old, 60 kg woman was scheduled for resection of a left lower lobe lung tumor. Her medical history was significant for diabetes and hypertension. She did not smoke, and had no known intrinsic lung disease.
In the operating room an epidural catheter was placed at the L1-2 level for postoperative analgesia. Routine monitors were applied, and a radial arterial line was inserted. Her arterial blood pressure was 120/60 and Spo2 was 100% while breathing room air. General anesthesia was induced. After two unsuccessful attempts to intubate the trachea with a right-sided 35F double-lumen tube (DLT) (BronchoCath®, Mallinckrodt Medical, Inc., Livermore, CA), a 7.0-mm endotracheal tube (ETT) was inserted by direct laryngoscopy. Using an airway exchange catheter, the ETT was replaced atraumatically with the right-sided DLT. The position of the DLT in the right bronchus was confirmed by fiberoptic bronchoscopy, but the orifice of the right-upper lobe bronchus was not visualized. Two-lung ventilation with a tidal volume VT of 500 mL produced a peak inspiratory pressure (PIP) of 20 cm H2O. PIP to each lung increased to 30–32 cm H2O with sequential one-lung ventilation.
The patient was turned to the right lateral decubitus position, and the position of the DLT in the right-main bronchus was reconfirmed by fiberoptic bronchoscopy. The left lung was selectively collapsed while one-lung ventilation of the right lung was with a VT of 450 mL. This resulted in PIP 35–38 cm H2O. Her arterial blood pressure and Spo2 remained stable.
After left thoracotomy, PIP increased over 5 min to 45–50 cm H2O and Spo2 decreased from 100% to 90%–93% on a Fio2 of 1.0. The PIP remained elevated despite suctioning. Fiberoptic bronchoscopy revealed no change in DLT position from its initial placement, with the proximal edge of the bronchial cuff visible just below the carina in the right-main bronchus. Two-lung ventilation was resumed and PIP decreased to the low 30 s cm H2O. Physical examination revealed venous congestion in the neck without subcutaneous emphysema. A portable chest radiograph was obtained and revealed an over-distended right lung.
Two-lung ventilation was maintained, the lateral thoracotomy incision was quickly closed and the patient was turned supine. At this time, PIP was in the low 30 s cm H2O, heart rate was 95, arterial blood pressure was 110/80, and Spo2 was 93%–96%. A repeat chest radiograph clearly demonstrated a right-sided tension pneumothorax (Fig. 1). A right-sided chest tube was placed resulting in a decrease in PIP to the mid 20 s cm H2O. Her arterial blood pressure and Spo2 returned to preinduction values and the venous congestion in the neck resolved.
The right-DLT was replaced with a left-DLT using a tube exchanger and the position in the left-bronchus in the left-main bronchus was confirmed by fiberoptic bronchoscopy. A chest radiograph demonstrated full re-expansion of both lungs (Fig. 2). There was no air leak via the right-sided chest tube. The patient was returned to the right lateral decubitus position, the left lung was selectively collapsed, and the right lung was ventilated with VT of 400 mL at a PIP of 26 cm H2O. A left pneumonectomy was performed without further incident.
At the completion of the procedure, the patient was breathing comfortably and was hemodynamically stable. Her trachea was extubated, and she was transferred to the intensive care unit. Her postoperative recovery was unremarkable. There was no air leak from the right-sided chest tube. She was discharged home on postoperative day 5.
Intraoperative tension pneumothorax is a relatively rare event.1–2 The lung injury that precedes a tension pneumothorax most often occurs in the prehospital setting, the emergency room, or in the intensive care unit, before actually becoming evident in the operating room.3 During general anesthesia, tension pneumothorax has resulted from central line insertion, brachial plexus blockade, thoracic epidural insertion,4 with an airway exchange catheter5 and from traumatic airway intubation.
In a mechanically ventilated patient, the clinical findings resulting from tension pneumothorax are due to shifting or compression of mediastinal structures and the lung parenchyma, or from the presence of air in anatomic spaces. This typically results in increasing PIP, subcutaneous emphysema, venous neck distension, contralateral tracheal deviation, and chest hyper-resonance, hyperexpansion, and reduced breath sounds on the affected side. In patients whose lungs are mechanically ventilated, oxyhemoglobin desaturation, marked hypotension, and tachycardia have been cited as early and reliable signs of tension pneumothorax.3
We found only six reports in the English literature of contralateral tension pneumothorax during thoracoscopy or thoracotomy.6–11 In each, significant hypoxemia or hypotension was the initial clinical finding, and in half of these reports cardiovascular collapse was present before decompression of the pneumothorax.6–8 Diagnosis is often delayed since DLT obstruction or misplacement,9,12 bronchospasm, and/or dynamic hyperinflation of the lung are usually considered first. With the patient in the lateral position, there is impaired access to the dependent hemithorax for physical examination. During thoracotomy, clinical signs can include elevation of the mediastinum and compression of the ipsilateral bronchi on fiberoptic inspection.10
Our patient had an unanticipated difficult tracheal intubation that required exchanging an ETT for a DLT. The absence of a noticeable air leak after chest decompression suggests that the catheter did not perforate the airway. Although ventilation through an airway exchange catheter is a potential cause of pneumothorax,13 the catheter was not used for that purpose in our patient.
We never visualized the right upper-lobe bronchus during bronchoscopy. To guarantee accurate placement of a right-sided DLT, patency of the right-upper lobe orifice should be confirmed. It is possible that partial occlusion of the right upper-lobe bronchus by the right-DLT with selective dynamic hyperinflation of that lobe resulted in barotrauma. Alternatively, the right upper-lobe bronchus could have been completely obstructed and the right-middle and lower lobes may have become over-distended.
We decided to proceed with the operation after chest decompression, since we had radiographic evidence of complete re-expansion of the lung without an airleak. The presence of a persistent airleak would have mandated careful bronchoscopic evaluation to exclude major iatrogenic airway injury.
Our case highlights the pathophysiology of tension pneumothorax during thoracotomy. We believe an open hemithorax relieved or delayed right heart and great vessel obstruction that would have otherwise developed due to a shifting of the mediastinal structures with increased intrapleural pressure. The tension pneumothorax was recognized and treated without the patient experiencing shock or significant hypoxemia.
In summary, we present a patient who developed a contralateral tension pneumothorax during thoracotomy. A tension pneumothorax should be considered in any patient who develops high PIP during one-lung ventilation with an open chest, even in the absence of the classic signs of hypoxemia and hypotension.
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