THORACIC

Extracorporeal Removal CO2 Using a Venovenous, Low-Flow System (Decapsmart) in a Lung Transplanted Patient: A Case Report
F. Ruberto, F. Pugliese, A. DAlio, S. Perrella, B. DAuria, S. Ianni, M. Anile, F. Venuta, G.F. Coloni, and P. Pietropaoli ABSTRACT Background. Primary graft dysfunction (PGD) is a syndrome that may occur after lung transplantation. In some cases of severe PGD, conventional therapies like ventilatory support, administration of inhaled nitric oxide (iNO), and surfactant and intravenous prostacyclins are inadequate to achieve adequate gas exchange. The only lifesaving option is to use an extracorporeal membrane oxygenator. The Decapsmart is a new venovenous, low-ow extracorporeal device to removal carbon dioxide (CO2). It does not need a specialized staff. Herein we have presented a case report of a patient who underwent single lung transplantation and experienced respiratory failure. Methods. On November 2007, a 52-year-old woman underwent a single right lung transplantation, and developed severe PGD in the postoperative period. After institution of conventional treatments, including ventilatory and hemodynamic support, iNO, and prostaglandine E1, we started treatment with Decapsmart to remove CO2. Hemodynamic and respiratory parameters were assessed at baseline and after 3, 12, 24, and 48 hours. Results. No adverse events occurred. From baseline to 48 hours, pH values increased and partial pressure of CO2 reduced. At the same time ventilatory support was reduced, thereby mitigating barotrauma and risk of overdistension. Conclusion. The use of Decapsmart may be an important aid for patients with severe respiratory acidosis in association with conventional therapy during the perioperative period after lung transplantation.
RIMARY GRAFT DYSFUNCTION (PGD) refers to an injury that may occur after lung transplantation. It represents about 50% of the early mortality among these patients.1,2 The case history of PGD is characterized by an inadequacy of gas exchange. The International Society for Heart and Lung Transplantation has recently described a grading system for the severity of PGD as well as a synopsis of its etiology, outcome, and treatment.3 In some cases of severe PGD, conventional therapies like ventilatory support, administration of inhaled nitric oxide (iNO), surfactant and intravenous prostacyclins are inadequate to achieve adequate gas exchange. The only lifesaving treatFrom the Dipartimento di Scienze Anestesiologiche, Medicina Critica e Terapia del Dolore (F.R., A.D., S.P., S.I., B.D., P.P.) and Cattedra di Chirurgia Toracica (M.A., F.V., G.F.C.), Universita Degli Studi di Roma La Sapienza, Viale del Policlinico N 188, 00144 Roma, Italia. Address reprint requests to Dott Franco Ruberto, Viale del Policlinico 188, 00144 Roma, Italia. E-mail: rube2005@libero.it 2009 Published by Elsevier Inc. 360 Park Avenue South, New York, NY 10010-1710 Transplantation Proceedings, 41, 14121414 (2009)

0041-1345/09/$see front matter doi:10.1016/j.transproceed.2009.03.048 1412

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Table 1. Hemodynamic and Blood Gas Analysis Data, Ventilator Setting During the Study
T0 T1 T2 T3 T4

ment option for these patients is the use of an extracorporeal membrane oxygenator (ECMO). The Decapsmart is a new low-ow venovenous device that removes about 20% to 25% of carbon dioxide (CO2) from plasma.4,5 Herein we have presented a case report of a patient with pulmonary brosis who underwent a single lung transplantation, and then developed respiratory failure in the immediate postoperative period with severe respiratory acidosis.
CASE REPORT
The study was performed in our posttransplant intensive care unit. A 52-year-old woman, weighing 60 kg and of 160 cm height was affected by idiopatic pulmonary brosis. She underwent a single right lung transplantation in November 2007. Before anesthesia induction, the patient was monitored with a radial artery cannula for arterial pressure and periodic blood sampling for gas analysis as well as a thoracic epidural catheter to control postoperative pain, a double-lumen cannulated subclavian vein, and a Swan Ganz catheter to evaluate continuous cardiac output and hemodynamic changes with Monitor Vigilance (Edwards Lifesciences, Irvine, Calif). We employed pressure-controlled mechanical ventilation with ventilator settings modied on the basis of gas analysis values after endotracheal intubation and during the intraoperative period, which lasted about 6 hours. In particular, during the monopulmonary period, we allowed a condition of permissive hypercapnia, seeking to reduce barotrauma and overination risk. Simultaneously was administered dobutamine (5 g/kg/min) and prostaglandine E1 intavenuosly, iNO (10 ppm) to reduce pulmonary artery pressure. Reperfusion edema appeared when the pulmonary artery were declamped; it exacurbated the respiratory gas exchange. In the immediate postoperative period, the patient developed a severe form of PGD as documented by radiography with a progressive decline in clinical condition. A transesophageal echocardiography was performed to exclude pulmonary vascular problems. A severe form of hypercapnia and respiratory acidosis persisted despite the use of pressurecontrolled mechanical ventilation with an inspiratory peak pressure (PIP) 35 cm H2O, limitation of positive end-expiratory pressure (PEEP) to 10 cm H2O, and delivery of 100% FiO2. Standard medical therapy including iNO (10 ppm) and intravenous prostacyclins. Thus we initiated treatment with the Decapsmart system (Decapsmart, Medica srl, Medolla [Modena], Italy) which was connected via a large-gauge venous access obtained via a doublelumen catheter inserted into subclavian vein using Seldingers technique. A bolus of 5000 UI of heparin was administered intravenously followed by titrated administration to maintain the active clotting time value between 150 and 200. Administration of uids, as well as vasopression or inotropic agents was targeted to maintain a mean arterial pressure (MAP) 65 mm Hg. CO2 removal treatment was maintained for 48 hours. We monitored the following variables: pH, pressure partial CO2, PIP, MAP, respiratory rate, and PaO2/FiO2 ratio at baseline (T0) as well as at 3 (T1), 12 (T2) 24 (T3), and 48 hours from the beginning of the treatment. Moreover, at the same time we performed blood gas analysis and blood samples for coagulation, serum electrolyte, and hemochrome.

pH PaCO2 (mm Hg) PaO2/FiO2 PIP (cm H2O) PEEP (cm H2O) Vt (mL) RR (b/min) MAP (mm Hg) APm (mm Hg) HR (r/min)

7.15 73 100 35 10 650 18 94 69 96

7.24 69 230 25 8 600 16 95 60 95

7.25 62 240 25 8 600 14 88 50 88

7.29 52 250 25 8 600 12 90 48 85

7.31 48 280 25 8 600 12 90 48 85

PIP, peak inspiratory pressure; PEEP, positive end espiratory pressure; Vt, tidal volume; RR, respiratory rate; MAP, medium arterial pressure; APm, medium pulmonary artery pressure; HR, hearth rate.

Decapsmart treatment in terms of bleeding, circuit clotting, severe hemodynamic instability, or venous embolism. Unfortunately, the patient died on the postoperative day 6 because of multiple organ failure.
DISCUSSION

RESULTS

Hemodynamic and ventilatory settings data are shown in Table 1. We observed a reduction in PaCO2 and an increase in pH values at each sampling time. PaO2/FiO2 ratio also increased. No adverse events were observed during or after

In our rst experience, the use of Decapsmart was shown to be simple; the assembly of circuit did not show particular difculty. The insertion of a venous catheter was performed without problems. No adverse event occurred during the treatment: coagulopathy, thrombocytopenia, or leukocytopenia. The hemodynamic impact has been negligible so that there were no hypotensive episodes or changes in the heart rate after the application of an extracorporeal pump with a ow of 400 mL/h. PGD still remains an important cause of death after lung transplantation.1 Standard medical therapy including the administration of iNO, surfactant, prostaglandins, and corticosteroids. The presence of permissive hypercapnia and hypoventilation is useful to limit barotrauma caused by the mechanical ventilation. In acute and severe cases that do not respond to medical therapy, the only way to improve gas exchanges is represented by the application of ECMO. Several studies have reported the use of ECMO both as a treatment of PGD and as a bridge to the lung transplantation with interesting results in terms of survival.6 8 Unfortunately, ECMO is a complex and invasive procedure that is possible only in specialized centers with a trained and competent staff. It is characterized by numerous complications. More recently some studies have examined the efcacy and safety of new arterovenous devices to selectively remove CO2.9-10 These new techniques may reduce the disadvantages associated with ECMO, such as bleeding, high costs, and the need for a specialized staff. However, they are also characterized by complications, such as prolonged ischemia, increased left-right shunt, and lack of direct control of the blood ow. Interesting prospects for clinical work come from the study of Livigni et al,4 who observed the efcacy and safety of a new venovenous device with a low-ow CO2 removal system in animal models. Our case report documented the use of the system in a patient

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RUBERTO, DALIO, PERRELLA ET AL 2. Prekker ME, Nath DS, Walker AR, et al: Validation of the proposed International Society for Heart and Lung Transplantation grading system for primary graft dysfunction after lung transplantation. J Heart Lung Transplant 25:371, 2006 3. Fischer S, Boha D, Rycus P, et al: Extracorporeal membrane oxygenation for primary graft dysfunction after lung transplantation: analysis of the Extracorporeal Life Support Organization (ELSO) registry. J Heart Lung Transplant 26:472, 2007 4. Livigni S, Maio M, Ferretti E, et al: Efcacy and safety of low-ow veno-venous carbon dioxide removal device: results of an experimental study in adult sheep. Crit Care 10:R151, 2006 5. Mielck F, Quintel M: Extracorporeal membrane oxygenation. Curr Opin Crit Care 11:87, 2005 6. Jackson A, Cropper J, Pye R, et al: Use of extracorporeal membrane oxygenation as a bridge to primary lung transplant: 3 consecutive, successful cases and a review of the literature. J Heart Lung Transplant 27:348, 2008 7. Hartwig MG, Appel JZ 3rd, E Cantu 3rd, et al: Improved results treating lung allograft failure with venovenous extracorporeal membrane oxygenation. Ann Thorac Surg 80:1872, 2005; discussion 1879 8. Oto T, Rosenfeldt F, Rowland M, et al: Extracorporeal membrane oxygenation after lung transplantation: evolving technique improves outcomes. Ann Thorac Surg 78:1230, 2004 9. Bein T, Weber F, Philipp A, et al: A new pumpless extracorporeal interventional lung assist in critical hypoxiemia/hypercapnia. Crit Care Med 34:1372, 2006 10. Kopp R, Dembinski R, Kuhlen R: Role of extracorporeal lung assist in the treatment of acute respiratory failure. Minerva Anestesiol 72:587, 2006

who underwent single lung transplantation. We observed a reduction in CO2, and hence an improvement of plasma pH. These data certainly suggested its use in various stages of lung transplantation. Indeed, elective intraoperative and postoperative use, with minimal hemodynamic impact due to the low ow, would particularly benet the negative effects of mechanical ventilation. However, we must stress that this new system should not be considered to be a replacement for traditional ECMO, because the yield is not comparable in terms of removing CO2 and especially improving oxygenation. In conclusion, the Decapsmart is a low-ow venovenous device, that has low invasive properties and does not require surgical cannulation of large vessels. Its management does not require the presence of specialized personnel (perfusionist), and it requires minimum administration of heparin. The employment of this system could be particularly useful to improve gases exchange during various stages of a lung transplant.
REFERENCES
1. Christie JD, Sager JS, Kimmel SE, et al: Impact of primary graft failure on outcomes following lung transplantation. Chest 127:161, 2005