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* From the Division of Operative Critical Care, Department of Anesthesia; and
the Division of Cardiothoracic Surgery, University Hospital Basel, Basel, Switzerland.
Address correspondence to: Dr. Wolfgang Ummenhofer, University Hospital Basel, Spitalstrasse 21, CH-4031 Basel, Switzerland. Phone: +41 61 265 25 25; Fax: +41 61 265 73 20; E-mail: wummenhofer{at}uhbs.ch
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Abstract |
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Clinical features: A 15-yr-old girl developed severe post-traumatic ARDS. After all conventional treatment strategies failed, we inserted a pumpless extracorporeal lung assist device. This device consists of an arterial cannula inserted into the femoral artery, and a membrane oxygenator with a venous cannula that returns the oxygenated blood back to the patient’s femoral vein. Since the driving force is the patient’s blood pressure, a roller pump with its negative side effects is not needed. The device allowed removal of excessive PaCO2 and, by applying minimal ventilation, minimization of further ventilator-induced lung injury. The pumpless extracorporeal lung assist device remained in situ for ten days without any adverse side effect. During this time, the lung recovered such that mechanical ventilation could be reinstalled cautiously. The device was then removed and, after a prolonged period of intensive care, the patient recovered without any sequelae.
Conclusion: In this case of a severely damaged lung, an arteriovenous pumpless extracorporeal lung assist was a helpful device to remove elevated CO2 and reduce mechanical stress by applying minimal ventilation. This device is simple to operate and has the potential of being used routinely in the treatment of severe ARDS.
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Introduction |
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Case report |
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A few days after her arrival in the intensive care unit, a multiple organ dysfunction syndrome occurred with renal failure, ARDS, and hemodynamic instability. Two weeks after recovery from multiple organ dysfunction syndrome, a bacterial pneumonia evolved, and a second, and more severe case of ARDS developed. It was necessary to reinsert pleural drainage on both sides due to ventilator-induced pneumothoraces. Despite pressure-controlled ventilation, high respiratory rate and low-tidal volumes, prone positioning, inhaled bronchodilators, and inhaled nitric oxide, the blood gases and lung compliance continuously deteriorated. Application of higher levels of positive end-expiratory pressure failed due to a dramatic increase of air leakage through the pleural drainages. During this time, the patient was sedated to a sedation agitation score of 1 with high doses of midazolam (300 µg·min–1 iv) and morphine (100 µg·min–1 iv). No muscle relaxants were administered. When arterial blood gas analysis showed a critical PaO2 of 60 mmHg (FIO2 1.0), a PaCO2 of 145 mmHg, and all conventional therapeutic efforts were exhausted; we decided to use a new lung assist device (NovaLungTM) as a last attempt to save the patient (Figure
). The Table presents the course of blood gas analyses and the respiratory parameters before and after the introduction of this device.
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), and hemodynamic parameters, diuresis, and temperature (37°C) remained stable. We did not change the ventilator settings over the course of the next five days, with the exception that FIO2 was carefully reduced to 0.7, and the patient was gradually weaned off the nitric oxide. The sedation level was then reduced, spontaneous respiration gradually resumed, the patient awakened. On day eight following insertion of the lung assist device, the expiratory pressure level was reduced step by step to 14 cm H2O with a mechanical respiratory rate of 25 breaths·min–1. On day ten, FIO2 was 0.4, expiratory pressure level was decreased to 12 cm H2O inspiratory pressure level was unchanged at 26 cm H2O and mechanical respiratory rate was 25 breaths·min–1. Blood flow through the NovaLungTM device was always between 0.9 and 1.2 L·min–1. We next stopped the O2 supply to the membrane oxygenator and, as there was no change in arterial PaCO2, a surgeon removed the cannulae and sutured the insertion sites of the vessels. The following weeks were complicated by several episodes of sepsis; but 104 days after admission our patient was transferred to a peripheral hospital, and ten weeks later she returned home without any further sequelae.
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Discussion |
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This technique is attractive because of its simplicity and independence from machines. It is based on a low resistance lung assist device designed for pulsatile blood flow with tight diffusion membranes and a protein matrix coating. The gas exchange surface amounts to 1.3 m2. Blood-flow resistance across the membranes is reduced to an arteriovenous pressure gradient of approximately 15 mmHg between inflow and outflow of the system, with pressure gradient being cannulae dependent but providing a trans device blood flow of up to 4 L·min–1.10 The rationale for using such a device was not primarily to improve oxygenation, but more to minimize ventilator-associated lung injury, and to ameliorate and eliminate the inflammatory process that is enhanced by mechanical ventilation. With this method, complete removal of CO2 is possible within minutes by increasing O2 flow, but the drop in CO2 should be guided by the change in pH. PaO2 values did not change after extra-corporeal circulation was initiated, and an O2 flow of 6 L·min–1 was applied, but fell dramatically when we tried to incorporate apneic ventilation.
There might be several reasons for the observed decrease in PaO2. First, a blood flow of 1 L·min–1 through the membrane oxygenator is quite low. This equals about 25% of the patient’s cardiac output. The membrane oxygenator of the NovaLungTM device is based on the QuadroxTM heparin coated hollow fibre technology. Its low resistance produces a pressure gradient of only 10 to 15 mmHg between inflow and outflow, providing a transmembrane oxygenator flow of up to 4 L·min–1, depending on the diameters of the cannulae. Since we were treating a young teen-ager with a femoral artery diameter of only 5 mm, we had to insert a small 13-French cannula, resulting in a correspondingly low blood flow. Secondly, it is more difficult to oxygenate arterial blood than to use unsaturated venous blood, as is done in venovenous ECMO systems. Thirdly, the decrease of oxygen pressure in the blood was most prominent after we stopped ventilation completely, which caused the concentration of the simultaneously applied nitric oxide to increase and probably resulted in a further ventilation-perfusion mismatch. Once the increase was noted, it was resolved by providing minimal ventilation with a respiratory rate of 4 breaths·min–1, with inspiratory and expiratory pressures of 26 and 22 cm respectively. After resolution, the concentrations of nitric oxide and arterial remained stable. During the entire critical phase, the patient was ventilated in the biphasic positive airway pressure and assisted spontaneous breathing mode of an Evita 4 respirator (Draeger, Lübeck, Germany). This mode consists of pressure-controlled ventilation with tube compensation that allows spontaneous breaths during the entire mechanical cycle. The spontaneous efforts of the patient are pressure supported with tube compensation during the mechanical expiration phase.
Since the pulmonary parameters stabilized, we did not change the mechanical ventilatory settings for the next five days. Our intent was to allow the lungs to recover without the stress of repeated mechanical distension by the respirator. During this period, we only reduced FIO2 to 0.7, based upon the PaO2 values, and the patient was weaned off nitric oxide. Because there is little experience on the best method to wean a patient from such a lung assist device, we had to define one. After five uneventful days of apneic ventilation, we reduced sedation and our patient began to spontaneously breathe with a respiratory rate of 25 breaths·min–1. During the course of the next five days, we reduced the expiratory level of the bi-level positive airway pressure ventilation step-by-step to 14 cm H2O. The mechanical respiratory rate was adapted to the patient’s initial spontaneous respiratory rate of 25 breaths·min–1. Thus, tidal volumes were care-fully augmented. Finally, on the tenth day of using the membrane oxygenator, a bi-level positive airway pressure modus was set at an of FIO2 0.4, inspiratory pressure level of 26 cm H2O, expiratory pressure level of 12 cm H2O, and a mechanical respiratory rate of 25 breaths·min–1, which resulted in tidal volumes of 350 to 400 mL and a minute volume of 8 to 9 L·min–1. After cessation of the external O2 supply to the membrane oxygenator, arterial blood gases remained stable over several hours. At this time, we decided to remove the NovaLungTM.
In conclusion, arteriovenous pumpless extracorporeal lung assist is a reasonable complementary therapeutic option in the treatment of severe ARDS. Insertion can be done by an intensivist and, after an initial intensive monitoring phase, the NovaLung is a simple device to operate. Adverse events were not observed. Routine application in critically ill patients with ARDS appears possible, but future studies will be needed to demonstrate this, as well as to determine the indications that are optimal for its use.
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Acknowledgments |
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Footnotes |
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References |
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2 Pulmonary Artery Catheter Consensus Conference Participants. Pulmonary artery catheter consensus conference: consensus statement. Crit Care Med 1997; 25: 910–25.[Medline]
3 Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998; 338: 347–54.
4 Putensen C, Mutz NJ, Putensen-Himmer G, Zinserling J. Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 159: 1241–8.
5 Gattinoni L, Tognoni G, Pesenti A, et al. Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med 2001; 345: 568–73.
6 Lundin S, Mang H, Smithies M, Stenqvist O, Frostell C. Inhalation of nitric oxide in acute lung injury: results of a European multicentre study. The European Study Group of Inhaled Nitric Oxide. Intensive Care Med 1999; 25: 911–9.[Medline]
7 Gadek JE, DeMichele SJ, Karlstad MD, et al. Effect of enteral feeding with eicosapentaenoic acid, gammalinolenic acid, and antioxidants in patients with acute respiratory distress syndrome. Enteral Nutrition in ARDS Study Group. Crit Care Med 1999; 27: 1409–20.[Medline]
8 Michaels AJ, Schriener RJ, Kolla S, et al. Extracorporeal life support in pulmonary failure after trauma. J Trauma 1999; 46: 638–45.[Medline]
9 David M, Heinrichs W. High-frequency oscillatory ventilation and an interventional lung assist device to treat hypoxaemia and hypercapnia. Br J Anaesth 2004; 93: 582–6.
10 Liebold A, Reng CM, Philipp A, Pfeifer M, Birnbaum DE. Pumpless extracorporeal lung assist - experience with the first 20 cases. Eur J Cardiothorac Surg 2000; 17: 608–13.
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