BACKGROUND: Diaphragm dysfunction is a primary cause of ventilatory impairment after upper abdominal surgery. Laparoscopic procedures may result in less dysfunction. To test this, diaphragmatic function was studied in ten healthy adult patients undergoing elective laparoscopic cholecystectomy and in five undergoing laparoscopic hernia repair. METHODS: Respiratory gas exchange, ventilation, and breathing pattern were measured before and 3 h after surgery. Respiratory drive was evaluated from the relationship of P0.1 to end-tidal carbon dioxide (PETCO2) during tidal breathing. Diaphragm contractile function was assessed from maximal transdiaphragmatic pressure (Pdimax), and Pdi during a maximal sniff maneuver (Pdisniff). RESULTS: Oxygen consumption and carbon dioxide production did not change after surgery. Pdimax decreased by more than 50% in the laparoscopic cholecystectomy group, but Pdisniff did not change. Tidal volume and the ratio of inspiratory time over total cycle time decreased by 30% and 13%, respectively, PETCO2 increased by 9%, and minute ventilation did not change. In contrast, there was no variation in ventilatory function in patients undergoing laparoscopic hernia repair. In both groups, P0.1 did not change, which excludes depressed respiratory drive as an explanation for the decreased Pdimax in laparoscopic cholecystectomy. Contractile failure of the diaphragm was discounted as well, because Pdisniff did not change, even in the laparoscopic cholecystectomy group. CONCLUSIONS: Although laparoscopic cholecystectomy does not increase metabolic demands in the early postoperative period, it impairs diaphragm function. The internal site of surgical intervention appears to be the critical variable determining diaphragmatic inhibition after laparoscopic abdominal surgery.
BACKGROUND:Diaphragm dysfunction is a primary cause of ventilatory impairment after upper abdominal surgery. Laparoscopic procedures may result in less dysfunction. To test this, diaphragmatic function was studied in ten healthy adult patients undergoing elective laparoscopic cholecystectomy and in five undergoing laparoscopic hernia repair. METHODS: Respiratory gas exchange, ventilation, and breathing pattern were measured before and 3 h after surgery. Respiratory drive was evaluated from the relationship of P0.1 to end-tidal carbon dioxide (PETCO2) during tidal breathing. Diaphragm contractile function was assessed from maximal transdiaphragmatic pressure (Pdimax), and Pdi during a maximal sniff maneuver (Pdisniff). RESULTS:Oxygen consumption and carbon dioxide production did not change after surgery. Pdimax decreased by more than 50% in the laparoscopic cholecystectomy group, but Pdisniff did not change. Tidal volume and the ratio of inspiratory time over total cycle time decreased by 30% and 13%, respectively, PETCO2 increased by 9%, and minute ventilation did not change. In contrast, there was no variation in ventilatory function in patients undergoing laparoscopic hernia repair. In both groups, P0.1 did not change, which excludes depressed respiratory drive as an explanation for the decreased Pdimax in laparoscopic cholecystectomy. Contractile failure of the diaphragm was discounted as well, because Pdisniff did not change, even in the laparoscopic cholecystectomy group. CONCLUSIONS: Although laparoscopic cholecystectomy does not increase metabolic demands in the early postoperative period, it impairs diaphragm function. The internal site of surgical intervention appears to be the critical variable determining diaphragmatic inhibition after laparoscopic abdominal surgery.
Authors: George D Bablekos; Stylianos A Michaelides; Antonis Analitis; Konstantinos A Charalabopoulos Journal: World J Gastroenterol Date: 2014-12-14 Impact factor: 5.742