Extracorporeal membrane oxygenation in severe trauma patients with bleeding shock

Extracorporeal membrane oxygenation in severe trauma patients with bleeding shock

Resuscitation 81 (2010) 804–809 Contents lists available at ScienceDirect Resuscitation journal homepage: www.elsevier.com/locate/resuscitation Cli...

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Resuscitation 81 (2010) 804–809

Contents lists available at ScienceDirect

Resuscitation journal homepage: www.elsevier.com/locate/resuscitation

Clinical paper

Extracorporeal membrane oxygenation in severe trauma patients with bleeding shock夽 Matthias Arlt ∗ , Alois Philipp, Sabine Voelkel, Leopold Rupprecht, Thomas Mueller, Michael Hilker, Bernhard M. Graf, Christof Schmid University Hospital Regensburg, Germany

a r t i c l e

i n f o

Article history: Received 15 October 2009 Received in revised form 3 February 2010 Accepted 20 February 2010

a b s t r a c t Aim of the study: Death to trauma is caused by disastrous injuries on scene, bleeding shock or acute respiratory failure (ARDS) induced by trauma and massive blood transfusion. Extracorporeal membrane oxygenation (ECMO) can be effective in severe cardiopulmonary failure, but preexisting bleeding is still a contraindication for its use. We report our first experiences in application of initially heparin-free ECMO in severe trauma patients with resistant cardiopulmonary failure and coexisting bleeding shock retrospectively and describe blood coagulation management on ECMO. Methods: From June 2006 to June 2009 we treated adult trauma patients (n = 10, mean age: 32 ± 14 years, mean ISS score 73 ± 4) with percutaneous veno-venous (v-v) ECMO for pulmonary failure (n = 7) and with veno-arterial (v-a) ECMO in cardiopulmonary failure (n = 3). Diagnosis included polytrauma (n = 9) and open chest trauma (n = 1). We used a new miniaturised ECMO device (PLS-Set, MAQUET Cardiopulmonary AG, Hechingen, Germany) and performed initially heparin-free ECMO. Results: Prior to ECMO median oxygenation ratio (OR) was 47 (36–90) mmHg, median paCO2 was 67 (36–89) mm Hg and median norepinephrine demand was 3.0 (1.0–13.5) mg/h. Cardiopulmonary failure was treated effectively with ECMO and systemic gas exchange and blood flow improved rapidly within 2 h on ECMO in all patients (median OR 69 (52–263) mm Hg, median paCO2 41 (22–85) mm Hg. 60% of our patients had recovered completely. Conclusions: Initially heparin-free ECMO support can improve therapy and outcome even in disastrous trauma patients with coexisting bleeding shock. © 2010 Elsevier Ireland Ltd. All rights reserved.

1. Introduction Severe trauma is a leading cause of death in young adults.1,2 Fatal injuries without any treatment option (e.g., cervical spinal injury and aortic rupture) result in immediate death at the scene. Lifethreatening complications in the early course are bleeding shock and/or severe respiratory failure following chest trauma or massive blood transfusion. The early goal in trauma care is to combat shock. Bleeding shock can be treated effectively on scene by controlling the source of bleeding and rapidly initiating fluid resuscitation. In cases of severe trauma, early damage control surgery and extensive blood transfusion are immediately necessary.3 About 15% of polytrauma patients are in need of massive blood transfusion (MBT)

夽 A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2010.02.020. ∗ Corresponding author at: Department of Anesthesiology, University Hospital Regensburg, Franz-Josef-Strauss Alle 11, 93042 Regensburg, Germany. Tel.: +49 941 9440; fax: +49 941 9447802. E-mail address: [email protected] (M. Arlt). 0300-9572/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2010.02.020

defined as more than 10 units of packed red blood cells (PRBC). The prognosis of trauma patients receiving MBT is considered to be poor.4–8 Even if massive blood transfusion (MBT) is effective in the treatment of hemorrhagic shock, it is associated with potential complications9,10 like severe acidosis and hypothermia. Hypothermia (body temperature < 34 ◦ C) has deleterious effects on blood coagulation in trauma patients and when occurring in conjunction with metabolic acidosis can result in a mortality rate up to 90%.11–14 MBT can overwhelm the patient’s cardiocirculatory function resulting in the early decrease of cardiac output and pulmonary gas exchange. Late complications can appear as transfusion-related lung injury (TRALI) which magnifies the impairment of pulmonary gas exchange by blunt chest trauma and pulmonary contusions.12 Both-, MBT and pulmonary contusion can lead to acute respiratory distress syndrome (ARDS). ARDS is most frequently observed in the early course of intensive care in patients with severe trauma and shock. The mortality rate in these patients reaches up to 40% despite advanced ventilatory treatment.15,16 The use of extracorporeal membrane oxygenation (ECMO) as lifesaving treatment in respiratory failure was introduced by the pioneer work of Robert Bartlett in 197217 and revolutionised the treatment of resistant

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Table 1 Median and minimum–maximum of arterial pressure, blood pH, blood lactate and vasopressor support before, 2 h and 24 h on ECMO (n = 10). MAP: mean arterial pressure; OR: oxygenation ratio (paO2 [mm Hg]/FiO2 ). Measurement

Before ECMO

2 h on ECMO

24 h on ECMO

MAP [mm Hg] Norepinephrine [mg/h] Lactate [mg/dl] OR [mm Hg] paCO2 [mm Hg] pH

68 (45–90) 3.0 (1.0–13.5) 60 (25–105) 47 (36–90) 67 (36–89) 7.21 (6.89–7.47)

74 (56–92) 0.9 (0.0–5.0) 68 (11–122) 69 (52–263) 41 (22–85) 7.41 (7.30–7.61)

72 (52–84) 0.75 (0.0–2.5) 73 (9–126) 144 (48–218) 34 (29–45) 7.43 (7.30–7.59)

hypoxemia in patients worldwide.18,19 Depending on the site of cannulation, ECMO takes over the gas exchange function of the lung (veno-venous ECMO) or provides additional circulatory support (veno-arterial ECMO).17–19 Despite ongoing technical improvement of ECMO devices like centrifugal pumps and heparin coating of the circuits (which allows a reduction of systemic heparinisation), bleeding is still the most common complication in patients on ECMO. Bleeding can be induced by cannulation of the vessels, underlying coagulation disorders or the full-dose heparinisation commonly used.20 Since the first ECMO in a trauma victim was performed by Hill et al.,20 there have been several reports on ECMO in the subsequent course of post-traumatic respiratory failure in patients with blunt chest trauma.21,22 However, the use of ECMO in severe trauma victims with preexisting bleeding shock is still unusual.23 A recently published report on ECMO support in post-traumatic ARDS patients highlights the effort to extend this lifesaving technology to trauma patients.23 We report our first experiences in application of initially heparin-free ECMO in severe trauma patients with resistant cardiopulmonary failure and coexisting bleeding shock. We reviewed our data retrospective and describe cannulation procedures and blood coagulation management during emergency v-v and v-a ECMO.

2. Methods In addition to being a level I trauma centre, our institution provides an interdisciplinary specially trained ECMO team consisting of a senior perfusionist, consultant anaesthesiologist with special skills in cardiothoracic anaesthesia and emergency medicine and on demand one cardiac surgeon. This specialised team allows round-the-clock extracorporeal life support for indoor and out-of-centre use.19 The indication for v-v ECMO support in this report was resistant hypoxemia (OR < 100 mm Hg) despite advanced respiratory and positive end-expiratory pressure management, transfusion regime and chest tube placement. Indications for v-a ECMO support were persisting shock despite fluid resuscitation, blood transfusion and vasopressor support. Shock was defined as inadequate blood flow with signs of tissue hypoperfusion despite fluid resuscitation and vasopressor support. If massive blood transfusion MBT (defined > 10 units of packed red blood cells PRBC) was necessary shock was defined as bleeding shock. Contraindications for extracorporeal life support in our trauma patients were fatal cerebral lesions and states of observed prolonged hypoxemia (e.g., resuscitation on scene in cases of vehicle entrapment) or potentially fatal preexisting disease. When possible, we performed trauma CT-scan before the decision was made regarding extracorporeal life support to identify injury patterns (e.g., unstable cervical spine injury), as well as options for clinical improvement and main vessel pathology (e.g., aortic dissection). We thus assessed the patient’s options for clinical improvement. In cases of severe trauma without complete trauma CT-scan, it is necessary to protect the patient’s cervical spine especially during emergency cannulation procedures using jugular vessel access. Before setting a patient “on-pump”, the ECMO team must be convinced that no

improvement in cardiopulmonary function by other means is possible. Depending on the patient’s priority in trauma care and his actual cardiopulmonary deterioration, we initiated extracorporeal life support in our patient group either in the emergency room (ER) or the operating room (OR) during damage control surgery. The percutaneous cannulation procedure was carried out by Seldinger technique without routinely use of skin incision to prevent cannula site bleeding. In leading hypoxic pulmonary failure with preserved cardiocirculatory function, we used femoro-jugular veno-venous (v-v) cannulation. In cases of circulatory failure or cardiopulmonary resuscitation (CPR) we performed femoral–femoral veno-arterial (v-a) cannulation. Depending on the patient’s biometric data, we used a 21 or 23 Fr cannula (Femoral cannula, DLP Medtronic, Minneapolis) for venous outflow in v-v and v-a ECMO and a 15 or 17 Fr cannula (NovaportTM , Novalung, Talheim, Germany) for venous and arterial backflow in v-v and v-a ECMO. In femoro-jugular venovenous ECMO, the tip of the outflow cannula was placed in the inferior vena cava and the inflow cannula was placed in the superior vena cava superior. To avoid recirculation within the ECMO circuit, it is necessary to prevent venous “inflow” proximity to venous “outflow”. For veno-arterial ECMO, the tip of the arterial cannula (inflow) was positioned in the common iliac artery or the distal abdominal aorta, whereas the tip of the venous cannula (outflow) was placed in the inferior vena cava. To initiate extracorporeal membrane oxygenation, we used a new miniaturised ECMO device (PLS-Set, MAQUET Cardiopulmonary AG, Hechingen, Germany) and performed initially heparin-free ECMO. The PLS-Set has a priming volume less than 600 ml normal saline and consists of a plasma-resistant polymethylpentene membrane oxygenator (Quadrox PLSTM ) and a centrifugal pump (RotaflowTM ). The system is heparin-coated (BiolineTM ) “tip-to-tip” and has a 14 days CE approval. The Rotaflow drive and steering unit incorporates flow sensing and bubble detecting. The circuit includes a special shunt line for drug and volume application and, if required, an effective high-speed fluid resuscitation line. The centrifugal pump and the membrane oxygenator are mounted on a specialised lightweight holder system which allows fixation in close proximity to the patient. The Rotaflow drive unit has an integrated battery pack and can act as a standalone device during patient transfer. The oxygenator also acts as a heating or cooling device to control the patient’s blood temperature. In ECMO, pump flow rates were up to 4.5 l/min and gas supply to the oxygenator was initially pure oxygen with a flow rate of up to 12 l/min to utilise maximum gas exchange capacity. Shortly after successful implementation of the ECMO pump, gas flow rates were adjusted to the patient’s actual requirements and gas exchange function. The blood flow achieved with v-a ECMO support should be in the range of physiologic cardiac output, adapted to the patient’s biometric data. Gas supply to the oxygenator is regulated to achieve blood gas values in the normal arterial range to avoid the adverse effects of hyperoxygenation or hypocapnia. For patients on ECMO assistance, lung protective ventilation including reduction of high inspiratory oxygen concentration was performed as soon as possible. Blood temperature was maintained between 33 and 35 ◦ C in patients who had suffered cerebral injury or those who had episodes of cardiopulmonary resuscitation. In all other

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Table 2 Patient characteristics, treatment on ECMO, blood transfusion demand and outcome. Trauma

Diagnosis

Scores ISS/SOFA

Norepinephrine [mg/h] pre-ECMO

H.R./m/22 years

v-v

Car crash

66/13

41

50

5.0

K.M./m/30 years

v-v

Car crash

75/14

39

80

1.0

D.V./m/56 years

v-v

Car crash

75/12

58

59

1.1

B.S./m/27 y

v-v

Car crash

Polytrauma Bleeding shock ARDS Polytrauma Bleeding shock ARDS Aspiration Polytrauma ICB Bleeding shock ARDS Polytrauma Bleeding shock ARDS

75/14

64

36

1.4

W.T./m/21 years

v-v

Car crash

Polytrauma Bleeding shock ARDS

75/10

36

84

2.0

K.P./m/17 years

v-v

Motorcycle crash

75/12

48

67

13.5

K.N./f/24 years

v-v

Car crash

66/12

69

38

1.0

T.P./m/39 years

v-a

Truck crash

75/10

46

53

5.6

P.S./f/23 years

v-a

Suicid fall

Polytrauma Open chest Bleeding shock ARDS Polytrauma Bleeding shock ARDS Polytrauma Bleeding shock ARDS Polytrauma ICB Bleeding shock ARDS

75/10

40

85

5.0

A.S./m/62 years

v-a

Open chest trauma

29/11

105

89 g

4.0

Treatment on ECMO

Blood transfusion units on ECMO

Days on ECMO

Outcome

Damage control surgery CT-scan Damage control surgery CT-scan Kinetic therapy Damage control surgery CT-scan

PRBC: 33 FFP: 54 PLTC: 6 PRBC: 2

4

Survived without handicap

6

Survived without handicap

PRBC: 10 FFP: 22 PLTC: 3

5

Survived without handicap

CT-scan Kinetic therapy

PRBC: 12 FFP: 19 PLTC: 2

2

Died 20 days post-ECMO in septic multiple organ failure

Damage control surgery CT-scan Kinetic therapy CT-scan Kinetic therapy

PRBC: 54 FFP: 102 PLTC: 11

3

Died on ECMO in septic multiple organ failure

PRBC: 10 FFP: 27 PLTC: 2

5

Died on ECMO in septic multiple organ failure

Laparatomy Trauma surgery

PRBC: 7

7

Survived without handicap

Trauma surgery Kinetic therapy CT-scan Damage control surgery

PRBC: 12 FFP: 24 PLTC: 2 PRBC: 25 FFP: 12

7

Survived without handicap

0.5

Died on ECMO intractable retroperitoneal bleeding

Damage control chest surgery

PRBC: 12 FFP: 3

11

Survived without handicap

M. Arlt et al. / Resuscitation 81 (2010) 804–809

ECMO type

CPR open heart Bleeding shock

paO2 /FiO2 pre-ECMO

PaCO2 [mm Hg] pre-ECMO

Patient/ gender/age

M. Arlt et al. / Resuscitation 81 (2010) 804–809

patients, we maintained normal blood temperature to preserve blood coagulatory function. Coexisting haemorrhagic shock was treated before and on ECMO support with fluid resuscitation and massive blood transfusion using units of packed red blood cells, fresh frozen plasma, platelets and single blood coagulation factor replacement (e.g., prothrombin complex and fibrinogen) until blood clot formation on site of the wounds could be monitored. A specially designed integrated high-speed fluid resuscitation line facilitates volume application in ECMO. Our treatment of severe bleeding in trauma patients requiring ECMO support did not differ from treatment of haemorrhagic shock and coagulopathy in trauma patients without extracorporeal life support. If bleeding and signs of shock had been treated effectively during ECMO assistance, we applied low-dose heparin (5000 I.E. units i.v.) to achieve a PTT of double the normal range or an ACT value above 150 s. Dependent on the patient’s clinical course, blood coagulation was assessed every 4 h and anti-thrombin (AT III) levels were kept within the normal range. In femoral–femoral veno-arterial ECMO support, we monitored limb perfusion by using clinical examination, pulseoximetry and ultrasonic flow measurement. If limb ischemia was detected, the arterial cannula was switched to the right subclavian artery and the femoral artery was reconstructed surgically. All patients were kept in a state of general anaesthesia. Patient monitoring included capnography, pulse oximetry, temperature and central venous pressure measurement. Transoesophageal echocardiography was performed for diagnosis of cardiac and aortic pathology, volume load and outflow cannulas positioning if required. We used arterial lines in all patients to monitor arterial blood gases, electrolytes and blood pressure. In femoral–femoral v-a ECMO, arterial blood gas samples were taken from the right radial artery to monitor blood flow and oxygen supply to the supraaortic vessels, ensuring adequate cerebral perfusion. Catecholamine administration was lowered to maintain a mean arterial pressure between 50 and 70 mm Hg, dependent on the underlying diseases and modes of extracorporeal assistance. In veno-arterial ECMO support, pulsatile arterial pressure was regarded favourably as it indicates residual left ventricular myocardial contractility and unloading. Maintaining residual left ventricular ejection may also reduce the risk of intra-cardiac clot formation.18 If mechanical CPR is necessary on va ECMO (e.g., ECMO system failure), we recommend clamping the venous outflow line to prevent pendulous blood flow in the ECMO circuit.

3. Results From June 2006 to June 2009 we treated n = 10 adult patients with severe trauma-associated cardiopulmonary failure (mean age: 34.8 years [21–62], mean ISS score 73 ± 4) with percutaneous veno-venous (n = 7) and veno-arterial (n = 3) ECMO support and reviewed our datas retrospectively. Diagnoses included severe trauma (defined as ISS score > 16) with coexisting bleeding shock and respiratory failure (n = 7) as well as severe trauma with bleeding shock and cardiocirculatory failure (n = 3). Massive blood transfusion before and during (not because of) ECMO implementation was necessary in all patients. The implementation of ECMO was carried out in the emergency department (n = 5) or under damage control surgery in the OR (n = 3). Percutaneous cannulation using Seldinger technique was successful in all patients without cannula or guide wire associated vessel injuries. Despite this we observed temporary limb ischemia after v-a ECMO implementation in two patients. We solved this problem by surgical cannula switch to the right arteria subclavia. Before ECMO the median mean arterial pressure was 68 mm Hg (45–90) with a median norepinephrine demand of 3.0 mg/h (range 1.0–13.5). Median oxygenation ratio was 47 mm Hg (36–90) and median CO2 of 67 mm Hg

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Fig. 1. Miniaturised ECMO device (PLS-Set, MAQUET Cardiopulmonary AG, Hechingen, Germany). (1) Quadrox PLS membraneoxygenator; (2) centrifugal pump; (3) rotaflow control and steering unit; (4) multifunctional holder; (5) heat exchange unit.

(36–89). Two hours on ECMO, median mean arterial pressure was 74 mm Hg (56–92) with a median norepinephrine demand of 0.9 mg/h (0.0–5.0) and gas exchange improved to a median oxygenation ratio of 69 mm Hg (52–263) and median CO2 of 41 mm Hg (22–85) (Table 1). Mean duration on ECMO was 5 days (range 0.5–11) (Table 2). Overall hospital survival rate was 60%. These patients who survived, had recovered completely. Reasons for death were intractable retroperitoneal bleeding after suicide fall (n = 1) and septic multiple organ failure in the later course (n = 3). Despite initially heparin-free ECMO support and simultaneous massive blood transfusion on ECMO, we observed no thromboembolic events or unexpected blood clot formation. No part of the ECMO circuit (i.e., centrifugal pump, circuits, membrane oxygenator and cannulae) showed any decrease in function (Fig. 1). 4. Discussion Severe trauma causes about 5 million deaths per year worldwide, of which 1 million are in Europe.1,12 Acute medical care of disastrous trauma patients is challenging and requires an excellent multidisciplinary approach. To combat potentially evolving shock, rapid control of bleeding, appropriate use of damage control surgery, the use of blood products and the maintenance of tissue oxygenation are of the utmost importance. However, with recent improvements in prehospital care trauma specialists face more challenging cases than ever before.24 Many patients are properly pretreated by emergency care physicians performing fluid resuscitation, ventilator support and chest tube drainage if necessary. Despite these efforts certain trauma patients are rapidly developing severe cardiopulmonary failure with increased mortality rates up to 90%.1,3,8 Especially severe trauma patients with coexisting incapacitating bleeding shock exhibit poor outcomes. Extracorporeal membrane oxygenation has proven to be lifesaving in respiratory failure, even among trauma victims.19 ECMO in trauma victims with severe extensive injury patterns is a new field of application and potential survival benefit has recently been reported.23,25,26 Despite ongoing improvement in extracorporeal gas exchange technique (e.g., centrifugal pumps and heparin-bonded circuits), to our knowledge, heparin (or the use of other anti-coagulants) administration was reported in all patients on ECMO. Severe coagulopathy and preexisting bleeding are mostly accepted as contraindications for setting trauma patients on ECMO. We have not seen reports on ECMO support in

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severe trauma patients with pulmonary and/or cardiopulmonary failure and coexisting bleeding shock. To provide ECMO support in resistant pulmonary and/or cardiopulmonary failure in patients with disastrous trauma, even in the context of bleeding shock, we started initially heparin-free v-v and v-a ECMO support. Treatment of haemorrhagic shock and coagulation disorders was carried out according to the recommendations for blood component transfusion in trauma patients12 using PRBC, platelets and cryoprecipitate if necessary. In awareness of the high volume demand, we integrated a specially designed high-speed fluid resuscitation line into the ECMO circuit. Using this special port about 4000 ml of volume can be given within 30 min in addition to volume infused over large bore central venous lines.27 There was no need to order constriction of supporting blood coagulation in patients on the pump. Damage control surgery was carried out on ECMO and blood coagulation support was carried out until bleeding stopped and clinical signs of blood clot formation on the wound sites occurred. Restoration of blood coagulation is a main goal in the care of severe trauma patients in a state of haemorrhagic shock with or without extracorporeal life support. After haemorrhagic shock was treated successfully, clot formation was clinically observed during trauma surgery, we administered a first-time low-dose (5000 I.E. units) of heparin in our ECMO patients to keep the ACT within a range of 120–140 s. In general, hemostatic function is strongly affected by blood temperature. In hypothermia, both platelet function and clotting factors are impaired. Hypothermia in trauma patients is frequent and the causes are multifactorial including decreased heat production due to tissue hypoperfusion in shock, exposure to low ambient temperature, infusion of inadequately warmed resuscitation fluids and massive transfusion. Furthermore, coagulation disorders are aggravated by persistent respiratory acidosis, caused by respiratory failure and severe metabolic acidosis induced by inadequate tissue oxygen supply in shock. Optimised tissue oxygen supply is an early goal in interrupting the vicious cycle of haemorrhagic shock and coagulopathy in severe trauma patients. We were able to avoid the lethal triad of haemorrhagic shock, hypoxia and circulatory failure effectively in our patient group by using this newly developed ECMO system and performing initially heparin-free ECMO as well as allowing full support of blood coagulation. The ECMO support provides sufficient blood flow, oxygen delivery and blood warming to treat accidental hypothermia or mild blood cooling for cerebral protection. Despite these additional treatment options, ECMO can be associated with potential side effects. Cannulation has to be carried out smouth and gently even in emergency situations because guide wire and/or cannula perforation is life-threatening and increases morbidity and mortality rate dramatically. v-a ECMO requires femoral artery cannulation and is associated with risk of limb ischemia. Monitoring of limb perfusion is therefore essential and cannula switch options (e.g., right subclavia artery) have to be provided. Setting a patient on ECMO has certain specific requirements and needs preplanning by physicians and perfusionists. Evaluation of patient’s hemodynamic function, gas exchange and biometric data is essential to provide the best extracorporeal life support as possible on scene.28 In trauma patients it is crucial to perform cervical spine immobilisation during cannulation procedures, if the CT-trauma scan is not completed or spine injury is detected. Coexisting fatal injuries (e.g., spleen or liver disruption) have to be anticipated, recognised and managed rapidly. In general, ECMO support in trauma patients shall clearly not delay or handicap advanced trauma care, including damage control surgery-otherwise, the outcome will be poore. If major aortic vessel injury is detected (e.g., aortic dissection) and requires urgent surgical repair, the patient has to be transferred for cardiac surgery using a conventional heart and lung machine. If extracorporeal assistance is required it will be performed postoperatively as a bridge to recovery in pulmonary and/or cardiopulmonary failure. In

the subsequent course on ECMO it is essential to treat the traumaassociated injuries in a careful manner to facilitate full recovery. 5. Conclusion Previously, severe trauma patients with coexisting bleeding shock were mostly excluded from ECMO support. However, our first experiences with initially heparin-free ECMO in severe trauma patients with coexisting bleeding shock are suggesting that v-v and v-a ECMO can be a safe and highly effective rescue treatment for these patients. ECMO in severe trauma patients with resistant pulmonary and/or cardiopulmonary failure can be first-time instituted alongside conventional management of bleeding shock and damage control surgery. In as much as we continue to extend the application of live saving ECMO technology, even trauma victims with disastrous injuries will have another chance at survival. Conflict of interest statement Dr. M. Arlt received honoraries for lectures from the MAQUET Cardiopulmonary AG, Hechingen, Germany. References 1. Roissant R, Cerny V, Coats T, et al. Key issues in advanced bleeding care in trauma. Shock 2006;26:322–31. 2. Krug EG, Sharma GK, Lozano R. The global burden of injuries. Am J Public Health 2000;90:523–6. 3. Schreiber MA. Damage control surgery. Crit Care Clin 2004;20:101–18. 4. Huber-Wagner S, Qvick M, Mussack T, et al. Working Group on Polytrauma. German Trauma Society (DGU). Vox Sang 2007;92:69–78. 5. Hakala P, Hiippala S, Syrjala M, Randell T. Massive blood transfusion exceeding 50 units of plasma poor red cells or whole blood: the survival rate at the occurrence of leucopenia and acidosis. Injury 1999;30:619–22. 6. Drummond JC, Petrovitch CT. The massively bleeding patient. Anesthesiol Clin North America 2001;19:633–49. 7. Crosson JT. Massive transfusion. Clin Lab Med 1996;16:873–82. 8. Groskowicz R. The complications of massive transfusion. Anesthesiol Clin North America 1999;17:959–78. 9. Dunne JR, Malone DL, Tracy JK, Napolitano LM. Allogenic blood transfusion in the first 24 hours after trauma is associated with increased systemic inflammatory response syndrome (SIRS) and death. Surg Infect (Larchmt) 2004;5:395–404. 10. Silverboard H, Aisiku I, Martin GS, Adams M, Rozycki G, Moss M. The role of acute blood transfusion in the development of acute respiratory distress syndrome in patients with severe trauma. J Trauma 2005;59:717–23. 11. Cosgriff N, Moore EE, Sauaia A, et al. Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidosis revisited. J Trauma 1997;42:857–61. 12. Spahn DR, Rossaint R. Coagulopathy and blood component transfusion in trauma. Br J Anaesth 2005;95:130–9. 13. Ferrara A, Mac Arthur JD, Wright HK, et al. Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion. Am J Surg 1990;160:515–8. 14. Krause KR, Howells GA, Buhs CL, et al. Hypothermia-induced coagulopathy during hemorrhage shock. Am Surg 2000;66:348–54. 15. Cohn SM. Pulmonary contusion: review of the clinical entity. J Trauma 1997;42:973–9. 16. Yuang K-C, Fang J-F, Chen M-F. Treatment of endobronchial hemorrhage after blunt chest trauma with extracorporeal membrane oxygenation (ECMO). J Trauma 2008;65:1151–4. 17. Bartlett RH, Gazzaniga AB, Jefferies MR, et al. Extracorporeal membrane oxygenation (ECMO) cardiopulmonary support in infancy. Trans Am Soc Artif Intern Organs 1976;22:80–93. 18. Arlt M, Philipp A, Zimmermann Z, et al. First experiences with a new miniaturised life support system for mobile percutaneous cardiopulmonary bypass. Resuscitation 2008;77:345–50. 19. Arlt M, Philipp A, Zimmermann M, et al. Emergency use of extracorporeal membrane oxygenation in cardiopulmonary failure. Artif Organs 2009;33:696–703. 20. Hill JG, O’Brien TG, Murray JJ, et al. Extracorporeal oxygen for acute posttraumatic respiratory failure (shock-lung syndrome): use of the Bramson membrane lung. N Engl J Med 1972;286:629–34. 21. Sasadeusz KJ, Long WB, Kemalyan N, et al. Successful treatment of a patient with multiple injuries using extracorporeal membrane oxygenation and inhaled nitric oxide. J Trauma 2000;49:1126–8. 22. Perchinsky MJ, Long WB, Hill JG, et al. Extracorporeal cardiopulmonary life support with heparin-bonded circuitry in resuscitation of massively injured trauma patients. Am J Surg 1995;169:488–91.

M. Arlt et al. / Resuscitation 81 (2010) 804–809 23. Cordell-Smith JA, Roberts N, Peek GJ, Firmin RK. Traumatic lung injury treated by extracorporeal membrane oxygenation (ECMO). Injury, Int J Care Injured 2006;37:29–32. 24. Maani CV, Desocia PA, Holcomb JB. Coagulopathy in trauma patients: what are the main influence factors? Curr Opin Anaesthesiol 2009;22:255–60. 25. Madershahian N, Wittwer T, Strauch J, et al. Application of ECMO in multitrauma patients with ARDS as rescue therapy. J Card Surg 2007;22:180–4.

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26. Michaels A, Schriener R, Kolla S, et al. Extracorporeal life support in pulmonary failure after trauma. J Trauma 1999:46. 27. Arlt M, Philipp A, Iesalnieks I, et al. Successful use of a new hand-held ECMO system in cardiopulmonary failure and bleeding shock after thrombolysis in massive post-partal pulmonary embolism. Perfusion 2009;24:49–50. 28. Mueller T, Philipp A, Luchner A, et al. A new miniaturized system for extracorporeal membrane oxygenation in adult respiratory failure. Crit Care 2009;13:R205.