Although the incidence is not high in the general surgical population, pulmonary aspiration of gastric contents can result in serious long-term morbidity and mortality. We report a case of early use of extracorporeal membrane oxygenation (ECMO) to correct severe hypoxemia refractory to conventional mechanical ventilation in a patient with massive aspiration of gastric contents immediately followed by acute lung injury during general anesthesia induction. A 64-year-old woman diagnosed with stomach cancer was scheduled for elective diagnostic laparoscopy. Although there was no sign of gastrointestinal tract obstruction and midnight Nil per Os (NPO) was performed before the operation, pulmonary aspiration occurred during the induction of anesthesia. Despite the endotracheal intubation with mechanical ventilation, severe hypoxemia with hypercapnea persisted. Medical team agreed with applying veno-venous (VV) ECMO, and her blood gas analysis results became stable. ECMO was weaned successfully 9 days after the first aspiration event had occurred. Based on this case, early application of extracorporeal life support can have survival benefits.
Acute Lung Injury ; Anesthesia* ; Anesthesia, General ; Anoxia ; Blood Gas Analysis ; Extracorporeal Membrane Oxygenation* ; Female ; Gastrointestinal Tract ; Humans ; Incidence ; Intubation, Intratracheal ; Laparoscopy ; Middle Aged ; Mortality ; Pneumonia, Aspiration ; Respiration, Artificial ; Stomach Neoplasms

A 46-year-old female patient was admitted to the intensive care unit (ICU) after liver transplantation. About an hour later after the ICU admission, she had no pupillary light reflex. Both pupils were also fixed at 5 mm. Patients who undergo liver transplantation are susceptible to neurologic disorders including hepatic encephalopathy, thromboembolism and intracranial hemorrhage. Abnormal pupillary light reflex usually indicates a serious neurologic emergency in these patients; however, benign neurologic disorders such as peripheral autonomic neuropathy or Holmes-Adie syndrome should also be considered. We experienced a case of fixed pupillary light reflex after liver transplantation diagnosed as peripheral autonomic neuropathy.
Adie Syndrome ; Emergencies ; Female ; Hepatic Encephalopathy ; Humans ; Intensive Care Units ; Intracranial Hemorrhages ; Liver Transplantation* ; Liver* ; Middle Aged ; Nervous System Diseases ; Peripheral Nervous System Diseases* ; Pupil ; Reflex* ; Reflex, Pupillary ; Thromboembolism

We present a case of pulmonary artery catheter (PAC) placement through the right internal jugular vein, bridging vein and coronary sinus in a patient with previously unrecognized persistent left superior vena cava (LSVC) and diminutive right superior vena cava. A 61-year-old male patient was scheduled for mitral valve repair for regurgitation. Preoperative transthoracic echocardiography revealed dilated coronary sinus, but no further evaluations were performed. During advancement of the PAC, right ventricular and pulmonary arterial pressure tracing was observed at 50 and 60 cm, respectively. Transesophageal echocardiography ruled out intracardiac knotting and revealed the presence of the PAC in the LSVC, entering the right ventricle from the coronary sinus. Diminutive right superior vena cava was observed after sternotomy. The PAC was left in place for 2 days postoperatively without any complications. This case emphasizes that the possibility of LSVC and associated anomalies should always be ruled out in patients with dilated coronary sinus.
Arterial Pressure ; Catheterization, Swan-Ganz* ; Catheters ; Coronary Sinus ; Echocardiography ; Echocardiography, Transesophageal ; Heart Ventricles ; Humans ; Jugular Veins ; Male ; Middle Aged ; Mitral Valve ; Pulmonary Artery ; Sternotomy ; Vascular Malformations ; Veins ; Vena Cava, Superior*

A 46-year-old female patient was admitted to the intensive care unit (ICU) after liver transplantation. About an hour later after the ICU admission, she had no pupillary light reflex. Both pupils were also fixed at 5 mm. Patients who undergo liver transplantation are susceptible to neurologic disorders including hepatic encephalopathy, thromboembolism and intracranial hemorrhage. Abnormal pupillary light reflex usually indicates a serious neurologic emergency in these patients; however, benign neurologic disorders such as peripheral autonomic neuropathy or Holmes-Adie syndrome should also be considered. We experienced a case of fixed pupillary light reflex after liver transplantation diagnosed as peripheral autonomic neuropathy.
Adie Syndrome ; Emergencies ; Female ; Hepatic Encephalopathy ; Humans ; Intensive Care Units ; Intracranial Hemorrhages ; Liver Transplantation ; Liver ; Middle Aged ; Nervous System Diseases ; Peripheral Nervous System Diseases ; Pupil ; Reflex ; Reflex, Pupillary ; Thromboembolism

We present a case of pulmonary artery catheter (PAC) placement through the right internal jugular vein, bridging vein and coronary sinus in a patient with previously unrecognized persistent left superior vena cava (LSVC) and diminutive right superior vena cava. A 61-year-old male patient was scheduled for mitral valve repair for regurgitation. Preoperative transthoracic echocardiography revealed dilated coronary sinus, but no further evaluations were performed. During advancement of the PAC, right ventricular and pulmonary arterial pressure tracing was observed at 50 and 60 cm, respectively. Transesophageal echocardiography ruled out intracardiac knotting and revealed the presence of the PAC in the LSVC, entering the right ventricle from the coronary sinus. Diminutive right superior vena cava was observed after sternotomy. The PAC was left in place for 2 days postoperatively without any complications. This case emphasizes that the possibility of LSVC and associated anomalies should always be ruled out in patients with dilated coronary sinus.
Arterial Pressure ; Catheterization, Swan-Ganz ; Catheters ; Coronary Sinus ; Echocardiography ; Echocardiography, Transesophageal ; Heart Ventricles ; Humans ; Jugular Veins ; Male ; Middle Aged ; Mitral Valve ; Pulmonary Artery ; Sternotomy ; Vascular Malformations ; Veins ; Vena Cava, Superior

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Background: Ischemia-reperfusion (I/R) injury is inevitable during the perioperative period. The pancreas is susceptible to I/R injury. Autophagy, a self-digestion process, is upregulated during I/R injury and strongly induced by hypoxia. This study aims to determine whether dexmedetomidine can decrease pancreatic β-cell damage by regulating autophagy under hypoxia. Methods: INS-1 rat insulinoma cells were cultured in dexmedetomidine before being exposed to cobalt chloride (CoCl2)-induced hypoxia. Cell viability and the expression of autophagy-related proteins (light chain 3B [LC3B]-II, p62, and ATGs) were assessed. The expression of apoptosis-related proteins (BCL-2 and P-BAD) were also evaluated. CoCl2-treated INS-1 cells were pretreated with the autophagosome formation inhibitor, 3-methyladenine (3-MA), to compare its effects with those of dexmedetomidine. Bafilomycin-A1 (Baf-A1) that inhibits autophagosome degradation was used to confirm the changes in autophagosome formation induced by dexmedetomidine. Results: Dexmedetomidine attenuated the increased expression of autophagic proteins (LC3B-II, p62, and ATGs) and reversed the CoCl2-induced reduction in the proliferation of INS-1 cells after hypoxia. Dexmedetomidine also alleviated the decreased expression of the anti-apoptotic protein (BCL-2) and the increased expression of apoptotic protein (BAX). Dexmedetomidine reduces the activation of autophagy through inhibiting autophagosome formation, as confirmed by a decrease in LC3B-II/I ratio, a marker of autophagosome formation, in LC3B turnover assay combined with Baf-A1. Conclusions Dexmedetomidine alleviates the degree of cellular damage in INS-1 cells against CoCl2-induced hypoxia by regulating autophagosome formation. These results provide a basis for further studies to confirm these effects in clinical practice.

Although the incidence is not high in the general surgical population, pulmonary aspiration of gastric contents can result in serious long-term morbidity and mortality. We report a case of early use of extracorporeal membrane oxygenation (ECMO) to correct severe hypoxemia refractory to conventional mechanical ventilation in a patient with massive aspiration of gastric contents immediately followed by acute lung injury during general anesthesia induction. A 64-year-old woman diagnosed with stomach cancer was scheduled for elective diagnostic laparoscopy. Although there was no sign of gastrointestinal tract obstruction and midnight Nil per Os (NPO) was performed before the operation, pulmonary aspiration occurred during the induction of anesthesia. Despite the endotracheal intubation with mechanical ventilation, severe hypoxemia with hypercapnea persisted. Medical team agreed with applying veno-venous (VV) ECMO, and her blood gas analysis results became stable. ECMO was weaned successfully 9 days after the first aspiration event had occurred. Based on this case, early application of extracorporeal life support can have survival benefits.
Acute Lung Injury ; Anesthesia ; Anesthesia, General ; Anoxia ; Blood Gas Analysis ; Extracorporeal Membrane Oxygenation ; Female ; Gastrointestinal Tract ; Humans ; Incidence ; Intubation, Intratracheal ; Laparoscopy ; Middle Aged ; Mortality ; Pneumonia, Aspiration ; Respiration, Artificial ; Stomach Neoplasms