Faculty Bibliography

Rigid bronchoscopy for chronic foreign body removal can cause rare but life-threatening complications in the form of tension pneumothorax. A two-year-old child who developed sudden cardiac arrest during the procedure required urgent chest tube insertion. Integrated team effort with effective communication prevented devastating neurological sequelae from hypoxic ischemic encephalopathy.

Mature teratoma of the mediastinum poses a significant surgical challenge due to close vicinity to vital structures causing respiratory insufficiency or hemodynamic compromise. While the malignant variety of germ cell tumors (GCT) generally present with florid symptoms, benign teratomas are detected incidentally on imaging. Large teratomas presenting as mediastinal mass syndrome have additional difficulty in airway access. Herein, we report a case of a 40-year-old-female with no significant comorbidities presenting with rapidly progressing symptoms of chest pain, dyspnea, and superior vena cava (SVC) compression. Computed tomography (CT) scan of the neck and chest confirmed a large cystic lesion with marked compression of the great veins in the neck, arch of aorta, trachea, and proximal bronchial divisions. Airway access intraoperatively was done by awake fiberoptic bronchoscopy. However, sudden hypoxia and hemodynamic deterioration warranted emergency sternotomy. Adequate preoperative preparation, as well as standby extracorporeal circulatory support, led to successful and complete excision of the tumor. The patient had an uneventful recovery and extubated in the intensive care unit (ICU) the next day. Histopathology of the mass confirmed to be mature benign cystic teratoma. At six-month follow-up, the patient was completely asymptomatic without any complications. The impact of intraoperative catastrophe on the healthcare team can be immense. Inability to achieve a secure airway and the resultant hypoxia can result in permanent neurological damage. A multidisciplinary approach leading to adequate preoperative assessment, intraoperative preparedness for an emergency sternotomy with standby extracorporeal circulatory support due to the risk of mediastinal mass syndrome, were key features in the successful management of the patient.

Extracorporeal membrane oxygenation (ECMO) has become an integral treatment option for patients as a bridge to transplant, management of post cardiotomy cardiogenic shock, and for rescue after cardiopulmonary arrest. Significant strides in ECMO technology and management cannot, however, replace the importance of maintaining and following a comprehensive safety checklist. We herein report a case of massive air entrainment from an inadvertently disconnected port of a central venous catheter (CVC) in the neck which culminated in an airlock of the ECMO circuit. Ascertaining the relative position of the tip of the CVC with respect to the venous cannula on chest X-ray, tightly securing all its ports, and appraising and educating the health-care team can prevent this rare but devastating complication of fatal air embolism.

Mitochondrial Ca²⁺ (_mCa²⁺) uptake mediated by the mitochondrial calcium uniporter (MCU) plays a critical role in signal transduction, bioenergetics, and cell death, and its dysregulation is linked to several human diseases. In this study, we report a new ruthenium complex Ru265 that is cell-permeable, minimally toxic, and highly potent with respect to MCU inhibition. Cells treated with Ru265 show inhibited MCU activity without any effect on cytosolic Ca²⁺ dynamics and mitochondrial membrane potential (ΔΨ_m). Dose-dependent studies reveal that Ru265 is more potent than the currently employed MCU inhibitor Ru360. Site-directed mutagenesis of Cys97 in the N-terminal domain of human MCU ablates the inhibitory activity of Ru265, suggesting that this matrix-residing domain is its target site. Additionally, Ru265 prevented hypoxia/reoxygenation injury and subsequent mitochondrial dysfunction, demonstrating that this new inhibitor is a valuable tool for studying the functional role of the MCU in intact biological models.