Prone positioning has commonly been used for posterior spinal surgery. However, it has the potential to increase intraabdominal pressure (IAP), and adversely affects cardiovascular and pulmonary functions [1]. We describe a patient who developed severe deterioration of respiratory mechanics during anesthesia for spinal surgery in the prone position. A 64-year-old man (172 cm of height, 78 kg of weight) was presented for decompressive laminectomy L4-5 caused by spinal stenosis. He had hypertension, hypercholesterolemia, and multiple-vessel coronary artery disease, and had undergone a percutaneous coronary intervention on mid-right coronary artery (RCA) eight years ago. A transthoracic echocardiogram showed ischemic insult at RCA territory and preserved left ventricular systolic function. Anesthesia induction and endotracheal intubation were achieved using propofol, remifentanil, and rocuronium with a 7.5 mm reinforced tube. Anesthesia was maintained with sevoflurane, remifentanil, and 50% oxygen in air. Mechanical ventilation was adjusted with a tidal volume of 600 ml and respiratory rate of 12 times/min, and peak inspiratory pressure (PIP) was 17 cmH2O in the supine position. The patient’s position was changed to prone on the Wilson frame after radial artery cannulation. The surgeon lifted the Wilson frame fully and placed pads beneath the iliac crest to decrease lordosis of the lumbar spine. At that time, PIP was about 21 cmH2O. After about 30 minutes, PIP increased to 30 cmH 2O. The patient’s lung sound was clear, but decreased on both lung fields. Wheezing or rale was unremarkable. Although the possibility of reactive airway disease was low, we increased the concentration of sevoflurane and administered salbutamol inhaler (0.1 mg) via endotracheal tube 2 times to rule out bronchial asthma. PIP further increased to 33 mmHg even after administration of additional salbutamol inhaler and intravenous steroid. We changed the mode of the ventilator from volume controlled ventilation to pressure controlled ventilation with PIP of 26 cmH2O and a respiratory rate of 14 times/min, and delivered tidal volume was 270 ml. Other causes of increased airway pressure such as secretion or endobronchial intubation could be excluded through suctioning and auscultation. We increased the PIP to 28 cmH2O, but delivered tidal volume gradually decreased to less than 200 ml although SpO2 was maintained to 98% with FIO2 of 0.65. We suspected an acute rise in IAP and further increases or long-lasting intra-abdominal hypertension (IAH) might result in hypoxia and hypotension. So we changed patient’s position to supine and ventilator mode to volume controlled ventilation simultaneously. PIP decreased abruptly to less than 20 cmH2O with a tidal volume of 500 ml. The Wilson frame was changed to a Relton and Hall frame, and the patient was repositioned. Thereafter, the patient’s PIPs maintained at 19–20 cmH 20 with a tidal volume of 600 ml during the intraoperative period and the surgical procedure was uneventful. Prone positioning may be associated with an increased IAP and abdominothoracic transmission during IAH influences on multiple organ systems. Obstruction of the inferior vena cava, occurring in the prone position, is exaggerated by abdominal compression, and results in reduction of cardiac output [1]. IAH was defined as an IAP at or above 12 mmHg, and risk fac
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Feb 24, 2014
S Fernández Peña + 7
Open Access