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Study Objective: To examine the change in liver-type fatty acid-binding protein (L-FABP) levels in patients undergoing aortic arch surgery and the correlation between L-FABP and postoperative acute kidney injury. Design: Prospective observational study. Setting: Operating room of a general hospital. Patients: 36 adult patients. Interventions and Measurements: Urine samples were obtained to measure urinary L-FABP at initiation of cardiopulmonary bypass (CPB) and 5 minutes after termination of hypothermic circulatory arrest. Main Results: 22 (61.1%) patients developed acute kidney injury within a 48-hour period. L-FABP increases more than a thousand-fold were found. In patients who subsequently developed acute kidney injury, significant increases in L-FABP were noted from 2.9 (3.6) ng/mg of creatinine before CPB to 62.1 (995.6) ng/mg of creatinine 5 minutes after termination of circulatory arrest. Values in patients who did not develop acute kidney injury increased from 1.1 (5.7) ng/mg before CPB to 1133.0 (6358.8) ng/mg of creatinine showing a significant mean difference (P = 0.011). The area under the L-FABP receiver operating characteristic curve at 5 minutes after termination of circulatory arrest was 0.758. A cutoff value of 75.13 ng/mg of creatinine yielded both good sensitivity (1.000) and specificity (0.546) for detecting non-acute kidney injury. Patients who developed acute kidney injury after aortic arch surgery demonstrated lower levels of urinary L-FABP. Conclusions: Low levels of urinary L-FABP may indicate kidney injury and lack of renal protection. [ABSTRACT FROM AUTHOR]

Background: Patient-ventilator asynchrony is a major cause of difficult weaning from mechanical ventilation. Neurally adjusted ventilatory assist (NAVA) is reported useful to improve the synchrony in patients with sustained low lung compliance. However, the role of NAVA has not been fully investigated. Case presentation: The patient was a 63-year-old Japanese man with acute respiratory distress syndrome secondary to respiratory infection. He was treated with extracorporeal membrane oxygenation for 7 days and survived. Dynamic compliance at withdrawal of extracorporeal membrane oxygenation decreased to 20 ml/cmH2O or less, but gas exchange was maintained by full support with assist/control mode. However, weaning from mechanical ventilation using a flow trigger failed repeatedly because of patient-ventilator asynchrony with hypercapnic acidosis during partial ventilator support despite using different types of ventilators and different trigger levels. Weaning using NAVA restored the regular respiration and stable and normal acid-base balance. Electromyographic analysis of the diaphragm clearly showed improved triggering of both the start and the end of spontaneous inspiration. Regional ventilation monitoring using electrical impedance tomography showed an increase in tidal volume and a ventilation shift to the dorsal regions during NAVA, indicating that NAVA could deliver gas flow to the dorsal regions to adjust for the magnitude of diaphragmatic excursion. NAVA was applied for 31 days, followed by partial ventilatory support with a conventional flow trigger. The patient was discharged from the intensive care unit on day 110 and has recovered enough to be able to live without a ventilatory support for 5 h per day. Conclusion: Our experience showed that NAVA improved not only patient-ventilator synchrony but also regional ventilation distribution in an acute respiratory distress patient with sustained low lung compliance. [ABSTRACT FROM AUTHOR]