1 Adelaide, Australia 2 Tokyo, Japan
EditorIn the interesting and extensively referenced report by Ishikawa, Nakazawa and Makita,1 compression and kinking of pulmonary vessels is the suggested mechanism underlying the impressive improvement in oxygenation following surgical compression/retraction of the non-ventilated lung during right thoracotomy. However, before anaesthetists are tempted to consider compression of the non-ventilated lung as a possibly acceptable manoeuvre if hypoxaemia occurs in the early stage of one-lung ventilation, at least two questions need to be addressed. First, does avoiding or delaying absorption atelectasis by using a percentage of air in the ventilating fresh gas mixture (as the authors presumably did in conjunction with their stated FIO2 of 0.8) result in an increased need for surgical compression/retraction? Secondly, is the kinking or compression of the pulmonary vasculature more or less likely than absorption atelectasis to predispose to the life-threatening complication of postoperative acute lung injury.2
To completely avoid acute lung injury remains a major challenge for the thoracic anaesthetist. Two of the several possible predisposing events are bruising of the delicate lung tissue and hypoxia, both of which could conceivably be caused by compression or kinking of vessels in lung that already has a reduced blood flow as a consequence of hypoxic pulmonary vasoconstriction. Absorption atelectasis of the non-ventilated lung, and the need to subsequently re-expand the lung, is in theory a further potential predisposing event.
In my own practice of thoracic anaesthesia, rather than delaying or avoiding absorption atelectasis, I take positive steps to hasten the process, especially for thoracoscopic surgery.3 Also, I very rarely use air in the ventilating fresh gas mixture during a one-lung anaesthetic. Therefore, I am particularly interested to know whether Ishikawa and colleagues can direct me to any study that shows absorption atelectasis, in the context of passive lung collapse during one-lung anaesthesia, predisposes to postoperative pulmonary dysfunction or acute lung injury? I am not aware of any, but then again I cannot direct them to a study showing that lung compression/retraction is harmful. Obviously, there is still much to be learned about one-lung anaesthesia.
J. Pfitzner
Adelaide, Australia
EditorWe thank Dr Pfitzner for his interest in our study. Dr Pfitzners questions about our research1 can be summarized in two issues. First, an inspiratory fraction of oxygen (FIO2) of 0.8, which was administered to the patients in our study,1 may be inappropriate as it potentially delays or avoids absorption atelectasis. Pfitzner and colleagues showed3 that the use of nitrous oxide 50% in oxygen rather than oxygen 100% may speed collapse of the non-dependent lung, thereby facilitating thoracoscopic procedures. Secondly, we suggested in our research1 that anaesthetists can urge surgeons to compress the non-dependent lung to improve arterial oxygenation, if hypoxaemia occurs before application of the lung retractor. Pfitzner suggests that such a manoeuvre may cause postoperative acute lung injury.3
Patients who require one-lung ventilation (OLV) are routinely ventilated with an FIO2 of 0.8 and the use of nitrous oxide is usually omitted for several reasons. First, nitrous oxide is probably emetogenic.4 Secondly, the anaesthetic effect of a low concentration of nitrous oxide (e.g. FIN2O = 0.2) is small. Lastly, nitrous oxide probably diffuses into cuffs of double-lumen tubes and causes overinflation.5 At the begining of OLV, arterial oxygen partial pressure (PaO2) rapidly decreases. However, arterial oxygen saturation monitored by pulse oximetry rarely decreases below 90% with an FIO2 of 0.8. In our experience, the use of a lower FIO2 is associated with hypoxaemia even if it is short-lived. The use of nitrous oxide 50% may be helpful during thoracoscopic surgery. However, we have no data demonstrating whether or not it decreases the need for surgical compression/retraction of the non-dependent lung during oesophagectomy through a thoracotomy.
Facilitating exposure of the surgical field by compressing the non-dependent lung using a retractor has been performed routinely during oesophagectomy for more than 30 yr (2040 cases per yr) in our institution. All the patients who undergo oesophagectomy are routinely sedated and mechanically ventilated after the surgical procedure, and the tracheas of most patients are successfully extubated the next day. Neither surgeons nor anaesthetists feel that such a manoeuvre causes acute lung injury postoperatively. Since the oesophagus lies in the posterior mediastinum, anterior compression/retraction of the right lung may be unavoidable for better exposure of the surgical field. Compression of the non-dependent lung by skilled surgeons may therefore be acceptable. But we agree that such a manoeuvre may not be permissible in other surgical procedures or by unskilled surgeons, purely for the purpose of improving arterial oxygenation, due to the potential risk of acute lung injury.
S. Ishikawa
K. Nakazawa
K. Makita
Tokyo, Japan
References
1 Ishikawa S, Nakazawa K, Makita K. Progressive changes in arterial oxygenation during one-lung anaesthesia are related to the response to compression of the non-dependent lung. Br J Anaesth 2003; 90: 216
2 Jordan S, Mitchell JA, Quinlan GJ, Goldstraw P, Evans TW. The pathogenesis of lung injury following pulmonary resection. Eur Respir J 2000; 15: 7909
3 Pfitzner J, Peacock MJ, Pfitzner L. Speed of collapse of the non-ventilated lung during one-lung anaesthesia: the effects of the use of nitrous oxide in sheep. Anaesthesia 2001; 56: 9339[CrossRef][ISI][Medline]
4 Kenny GNC. Risk factors for postoperative nausea and vomiting. Anaesthesia 1994; 49 (Suppl.): 610[ISI][Medline]
5 Stanley TH. Nitrous oxide and pressure and volume of high- and low-pressure endotracheal-tube cuffs in intubated patients. Anesthesiology 1975; 42: 63740[ISI][Medline]