Case 1
A 57-year-old male with chronic obstructive lung disease was diagnosed with EGJ adenocarcinoma. There was no bulla in his preoperative chest computed tomography (CT). Laparoscopic proximal gastrectomy combined with transhiatal lower esophagectomy and thoracoscopic mediastinal lymphadenectomy followed by intra-mediastinal vEG were scheduled. General anesthesia with propofol, remifentanil, and rocuronium was provided with thoracic epidural anesthesia (T7/8). The trachea was intubated with a single lumen tube, and a bronchial blocker was inserted in the right main bronchus for one-lung ventilation.
Following anesthesia induction, the patient was turned to the prone position. Intrathoracic procedure was performed thoracoscopically via the right thorax under one-lung ventilation. After mediastinal lymphadenectomy and esophageal mobilization, the bilateral pleural spaces were connected. A 19 French thoracic tube was placed in the right pleural cavity, and both-lung ventilation was restarted at the end of the intrathoracic procedure.
The patient was then turned to the supine position. The laparoscopic procedure was started with lymphadenectomy following proximal gastrectomy. In this phase, the left crus of diaphragm was incised and esophageal hiatus was opened. The abdominal cavity and bilateral thorax were then connected. After cutting off the lower esophagus, an esophago-proximal gastrectomy was performed.
After 15 min resumption of carbon dioxide (CO2) inflation for reconstruction, peripheral arterial oxygen saturation (SpO2) gradually dropped from 99 to 94% under fraction of inspired oxygen (FIO2) 0.4, and tachycardia (heart rate 110 beats per minute) and hypotension (75/50 mmHg) appeared. Central venous pressure raised from 8 to 14 mmHg. Tidal volume simultaneously decreased from 400 to 200 ml under pressure control ventilation. We found that massive air leakage was continuously drained from the right thoracic tube independently of respiratory cycle.
We deduced that this hypoventilation and hemodynamic instability were attributed to tension pneumothorax by CO2 inflation. CO2 entered the bilateral pleural cavity via the peritoneum—left pleural cavity—right pleural cavity connection. However, the inflation management system continued providing a large amount of CO2 to keep pneumoperitoneum pressure (10 cmH2O). To treat the tension pneumothorax of this patient, stopping pneumoperitoneum and converting to laparotomy was a possible option; however, we did not stop pneumoperitoneum until the esophageal-remnant stomach anastomosis was accomplished. The reason was that the anastomosis required advanced skills if performed even by laparoscopy, much more by laparotomy. The lower esophagus was transected in the mediastinum, and the manipulation had to be performed deep in the mediastinum. In addition, thoracoabdominal incision was necessary if we stopped laparoscopic surgery. Therefore, surgeons requested to continue laparoscopic anastomosis as far as possible. In order to improve patient’s oxygenation, we raised positive end-expiratory pressure (PEEP) from 5 to 12 cmH2O and performed a lung recruitment maneuver to reopen the collapsed lung, and we increased tidal volume to 500 ml to maintain adequate ventilation. To maintain hemodynamic stability, we administered norepinephrine until the reconstruction was finished. The patient’s oxygenation, SpO2 and blood pressure returned to 100% and 110 mmHg, respectively. At the conclusion of the surgery, the second thoracic drain was inserted into the left pleural cavity. Confirming that the patient was hemodynamically stable and that no pneumothorax or atelectasis remained in the chest X-ray, the patient was extubated and transferred to the intensive care unit (ICU). The patient spent another uneventful day in the ICU and was discharged at postoperative day 17. The chest CT on post-operative day 3 showed no bulla or pneumothorax.
Case 2
A 63-year-old male with no other past history except smoking was diagnosed with EGJ adenocarcinoma. The same surgery as case 1 was scheduled. Basically, anesthesia and airway management strategies were the same as that of case 1.
The patient was stable during the thoracic and abdominal phases before laparoscopic intra-mediastinal vEG. After starting the esophagogastrostomy, paroxysmal ventricular contractions (PVCs) emerged (Fig. 1a). The PVCs then converted to non-sustained ventricular tachycardia with ST elevation in electrocardiogram (ECG) lead II (Fig. 1b). We conjectured the ECG change occurred due to impaired coronary perfusion by pericardium retraction when securing the surgical field. By adjusting the position of the pericardium retractor and administering nicorandil (4 mg/h) to maintain coronary perfusion, ECG temporarily returned to normal levels (Fig. 1c). Once the pericardium retraction became aggressive, frequent PVCs recurred with ST elevation in lead II (Fig. 1d). The ST elevation persisted after the pericardium retraction was released (Fig. 1e). Systolic blood pressure dropped to 80 mmHg. We started noradrenaline infusion (0.04 mcg/kg/h), thereby raising blood pressure and coronary perfusion pressure. ST elevation gradually improved and returned to normal levels in one hour (Fig. 1f). The surgery was performed as scheduled. The patient was transferred to the ICU under sedation and tracheal intubation. In the ICU, a 12-lead ECG showed no abnormalities including ST elevation or arrhythmia. Creatine kinase (CK) was 394 units/L, indicating a slight elevation (normal range: 59–248 units/L) with no elevation of CK-myocardial band. Troponin T was 0.286 ng/mL (normal range: 0–0.014 ng/mL). There was a possibility of transient microischemia due to transient epicardial coronary occlusion or vasospasm; however, there was no evidence of persistent cardiac infarction. We did not perform a coronary angiography. The patient was extubated the day after surgery and discharged after 11 days.
