Immediate postoperative non-invasive positive pressure ventilation following midface microvascular free flap reconstruction.

BACKGROUND: There is a rare need for postoperative non-invasive positive pressure ventilation (NIPPV) following microvascular reconstruction of the head and neck. In midface reconstruction, the free flap vascular pedicle is especially vulnerable to the compressive forces of positive pressure delivery. CASE: A 60 year old female with Amyotrophic Lateral Sclerosis (ALS) presented with squamous cell carcinoma of the anterior maxilla, for which she underwent infrastructure maxillectomy and fibula free flap reconstruction. To avoid tracheotomy, the patient was extubated postoperatively and transitioned to NIPPV immediately utilizing a full-face positive pressure mask with a soft and flexible sealing layer. The patient was successfully transitioned to NIPPV immediately after extubation. The free flap exhibited no signs of vascular compromise postoperatively, and healed very well. CONCLUSION: Postoperative non-invasive positive pressure ventilation can be successfully applied following complex microvascular midface reconstruction to avoid tracheotomy in select patients without vascular compromise of the free flap.

Protocol of a randomised controlled trial in cardiac surgical patients with endothelial dysfunction aimed to prevent postoperative acute kidney injury by administering nitric oxide gas.

INTRODUCTION: Postoperative acute kidney injury (AKI) is a common complication in cardiac surgery. Levels of intravascular haemolysis are strongly associated with postoperative AKI and with prolonged (>90 min) use of cardiopulmonary bypass (CPB). Ferrous plasma haemoglobin released into the circulation acts as a scavenger of nitric oxide (NO) produced by endothelial cells. Consequently, the vascular bioavailability of NO is reduced, leading to vasoconstriction and impaired renal function. In patients with cardiovascular risk factors, the endothelium is dysfunctional and cannot replenish the NO deficit. A previous clinical study in young cardiac surgical patients with rheumatic fever, without evidence of endothelial dysfunction, showed that supplementation of NO gas decreases AKI by converting ferrous plasma haemoglobin to ferric methaemoglobin, thus preserving vascular NO. In this current trial, we hypothesised that 24 hours administration of NO gas will reduce AKI following CPB in patients with endothelial dysfunction. METHODS: This is a single-centre, randomised (1:1) controlled, parallel-arm superiority trial that includes patients with endothelial dysfunction, stable kidney function and who are undergoing cardiac surgery procedures with an expected CPB duration >90 min. After randomisation, 80 parts per million (ppm) NO (intervention group) or 80 ppm nitrogen (N2, control group) are added to the gas mixture. Test gases (N2 or NO) are delivered during CPB and for 24 hours after surgery. The primary study outcome is the occurrence of AKI among study groups. Key secondary outcomes include AKI severity, occurrence of renal replacement therapy, major adverse kidney events at 6 weeks after surgery and mortality. We are recruiting 250 patients, allowing detection of a 35% AKI relative risk reduction, assuming a two-sided error of 0.05. ETHICS AND DISSEMINATION: The Partners Human Research Committee approved this trial. Recruitment began in February 2017. Dissemination plans include presentations at scientific conferences, scientific publications and advertising flyers and posters at Massachusetts General Hospital. TRIAL REGISTRATION NUMBER: NCT02836899.

The impact of closed endotracheal suctioning systems on mechanical ventilator performance.

BACKGROUND: Closed endotracheal suctioning during mechanical ventilation is increasingly used, but its impact on ventilator function has not been fully studied. METHODS: We evaluated the impact of closed suctioning with 11 critical-care ventilators, during assisted ventilation in pressure-support mode, pressure-assist/control mode, volume-assist/control mode, and during continuous positive airway pressure, with 2 suctioning pressures (-120 mm Hg and approximately -200 mm Hg), and with 2 tidal volumes (450 mL and 900 mL). We continuously measured airway pressure, flow at the airway, and pressure distal to the catheter tip, before, during, and after a single 15-second period of continuous suctioning. RESULTS: No ventilator malfunctioned as a result of the closed suctioning. During suctioning, end-expiratory pressure markedly decreased in all modes, and peak flow increased in all modes except volume-assist/control (p < 0.001). Respiratory rate increased during suctioning in pressure- and volume-assist/control (p < 0.001) but not during pressure support or continuous positive airway pressure. Gas delivery was most altered during volume-assist/control with the smaller tidal volume (p < 0.05) and least altered during pressure-assist/control with the larger tidal volume. CONCLUSION: There are large differences between the ventilators evaluated (p < 0.001). Closed suctioning does not cause mechanical ventilator malfunction. Upon removal of the suction catheter, these ventilators resumed their pre-suctioning-procedure gas delivery within 2 breaths, and, during all the tested modes, all the ventilators maintained gas delivery. However, closed suctioning can decrease end-expiratory pressure during suctioning.

Continuous positive airway pressure in new-generation mechanical ventilators: a lung model study.

BACKGROUND: A number of new microprocessor-controlled mechanical ventilators have become available over the last few years. However, the ability of these ventilators to provide continuous positive airway pressure without imposing or performing work has never been evaluated. METHODS: In a spontaneously breathing lung model, the authors evaluated the Bear 1000, Drager Evita 4, Hamilton Galileo, Nellcor-Puritan-Bennett 740 and 840, Siemens Servo 300A, and Bird Products Tbird AVS at 10 cm H(2)O continuous positive airway pressure. Lung model compliance was 50 ml/cm H(2)O with a resistance of 8.2 cm H(2)O x l(-1) x s(-1), and inspiratory time was set at 1.0 s with peak inspiratory flows of 40, 60, and 80 l/min. In ventilators with both pressure and flow triggering, the response of each was evaluated. RESULTS: With all ventilators, peak inspiratory flow, lung model tidal volume, and range of pressure change (below baseline to above baseline) increased as peak flow increased. Inspiratory trigger delay time, inspiratory cycle delay time, expiratory pressure time product, and total area of pressure change were not affected by peak flow, whereas pressure change to trigger inspiration, inspiratory pressure time product, and trigger pressure time product were affected by peak flow on some ventilators. There were significant differences among ventilators on all variables evaluated, but there was little difference between pressure and flow triggering in most variables on individual ventilators except for pressure to trigger. Pressure to trigger was 3.74 +/- 1.89 cm H(2)O (mean +/- SD) in flow triggering and 4.48 +/- 1.67 cm H(2)O in pressure triggering (P < 0.01) across all ventilators. CONCLUSIONS: Most ventilators evaluated only imposed a small effort to trigger, but most also provided low-level pressure support and imposed an expiratory workload. Pressure triggering during continuous positive airway pressure does require a slightly greater pressure than flow triggering.