End-Tidal Carbon Dioxide – A Guided Tool to Diagnose a Bronchial Tree Injury in Thoracoscopic Procedures

INTRODUCTION Minimally invasive surgical techniques, such as video-assisted thoracoscopic surgeries (VATS), are commonly used to diagnose and/or treat conditions affecting the mediastinum, pleura, and lung. VATS has been widely adopted over conventional thoracic surgeries due to reduced incision size, smaller scars, less postoperative pain, faster recovery times, and shorter hospital stays. VATS requires an insufflating gas such as CO2 for surgical exposure, which has its own concerns of hypercapnia and ventilation associated with pneumothorax. Although VATS is considered a safer alternative to traditional open thoracic surgery, complications can arise during or after the procedure.[1] We hereby report a rare complication, i.e., bronchial rent developed during the VATS procedure which was timely diagnosed by a sudden rise in the end-tidal carbon dioxide (EtCO2). A written informed consent was obtained from the patient. CASE PRESENTATION A 72-year-old man diagnosed with esophageal carcinoma was scheduled for thoracoscopic esophagectomy and formation of a gastric conduit in our hospital after the pre-anesthetic checkup. The standard American Association of Anesthesiologists (ASA) monitors were attached, and a 16-G intravenous (IV) cannula was inserted into the left upper limb in the operating room. General anesthesia (GA) was induced with IV fentanyl 120 mcg, IV propofol 110 mg, and IV atracurium 30 mg. An 8.5-mm wire-reinforced endotracheal tube was inserted into the trachea for mechanical ventilation. Anesthesia was maintained with isoflurane and intermittent doses of atracurium. A triple lumen 7 French central venous catheter was inserted in the right internal jugular vein, and a 20-G arterial catheter was placed in the left radial artery for invasive blood pressure monitoring. The patient was placed in a prone position, and the VATS was started after creating a pneumothorax in the left pleural cavity with carbon dioxide (CO2) maintaining a pressure of 8–12 cm of H2O. Three ports were made, one at the 7th intercostal space on the mid-axillary line, the second at the 4th intercostal space on the anterior axillary line, and the third in front of the tip of the scapula along the posterior axillary line. While dissecting the exophages near the trachea, a sudden rise in EtCO2 was observed, exceeding the set scale value of 99 mmHg [Figure 1]. No abnormality in other ventilatory parameters was observed, and there was no change in the level of isoflurane. Lung compliance was normal. No secretions were found on endotracheal secretions. An arterial blood gas analysis done immediately revealed a partial pressure of arterial CO2 (PaCO2) of 48 mmHg. A suspicion of communication between capnothorax and a bronchial tree was made and communicated to the surgeon [Figure 2]. On surgical inspection, an injury to the bronchial tree near the right main bronchus was identified [Figure 3]. An attempt was made to seal the rent via thoracoscopy but was unsuccessful. A plan was made to close by thoracotomy. Once the insufflation of CO2 was stopped, the EtCO2 values were normalized, and the ventilator started detecting the leak in the circle system and adequate tidal volume was not able to get delivered [Figure 4]. The maintenance of GA was switched to total intravenous anesthesia with a propofol infusion from isoflurane. The patient was repositioned to a left lateral position, and a right posterolateral thoracotomy was done. The right main bronchus was approached, and the rent was repaired. The leak was no longer present, and adequate volume was being delivered. The thoracotomy site was sutured. The patient was made supine after this, and the gastric conduit was prepared on the left side of the neck. After surgical closure, the trachea was extubated without a sequel.Figure 1: Ventilator settings and parameters seen once the sudden rise in EtCO2 was detected. The leak was found to be minimal with adequate tidal volume being deliveredFigure 2: A schematic showing EtCO2 entering the airways via a right main bronchial rent measured via capnographyFigure 3: A rent (black arrow) seen in the right main bronchus after right posterolateral thoracotomy, which was subsequently repairedFigure 4: The EtCO2 levels were normalized when the insufflation of pneumothorax was stopped. A leak of ~100 mL was detected, and an adequate volume was not being deliveredDISCUSSION End-tidal carbon dioxide monitoring by capnometer is a commonly used ASA standard monitor to assess the adequacy of ventilation and circulation. It measures the concentration of CO2 in exhaled air during expiration. It provides a near estimate of the PaCO2, which is higher than EtCO2 by 2–5 mmHg in normal scenarios. However, the PaCO2-EtCO2 gradient increases in ventilation-perfusion mismatch conditions such as pulmonary embolism, pulmonary edema, pneumonia, shock, and acute respiratory disorder syndrome. Rarely, reversal of the PaCO2-EtCO2 gradient can be seen in conditions with malignant hyperthermia, large tidal volumes with low-frequency ventilation, and with low functional residual capacity such as infants, pregnant, and obese patients. This condition was first described by Nunn and Hill in 1960.[2] VATS procedures are minimally invasive thoracic procedures that are generally considered safe and have a better postoperative pain score than thoracotomy. However, it has its own complications such as bleeding, pneumothorax, atelectasis, lung or airway injury, and rhythm abnormalities. VATS approach for esophagectomy requires a thoracoscope to be inserted through a small incision in the chest to view the internal structures in real-time. It requires a CO2 insufflation to create a pneumothorax for better visualization and access. The reversal of the PaCO2-EtCO2 gradient during thoracoscopy was first described by Biles et al.[3] while operating for a mass in the right upper lobe. They found a sudden increase in EtCO2 during surgery with normal PaCO2 and hypothesized a possible capnometer detection of exogenous CO2 in the pleural cavity. A similar case was described by Karnik et al.,[4] in thoracoscopic bronchogenic cyst excision, where EtCO2 started rising from the beginning of CO2 insufflation. In both cases, the exact location of the branchial tree to pleural communication was not described. In the index case, a sudden elevation of EtCO2 with normal ventilatory parameters and normal PaCO2 levels was identified while dissecting the esophagus, causing suspicion of bronchial tree injury, which was timely identified by the surgeon, preventing further damage. There was no compromise on the amount of tidal volume being delivered to the patient during CO2 insufflation, probably due to the intrapleural pressure during capnothorax, which created an apparent seal at the site of the rent. As soon as the insufflation of CO2 was stopped, the EtCO2 levels dropped to near PaCO2 levels and a leak of approximately 100 mL was noted while delivering the tidal volume. In conclusion, a sudden rise in EtCO2 during thoracoscopic surgeries can occur due to abnormal communication between the pleura and the bronchial tree, which can be iatrogenic or a preexisting lesion. A suspicion of bronchial tree injury should be made if there is a sudden elevation in EtCO2 with normal PaCO2. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.