Abdominal Compartment Syndrome Due to Extracorporeal Membrane Oxygenation in Adults Pascal Augustin, MD, Sigismond Lasocki, MD, PhD, Guillaume Dufour, MD, Julie Rode, MD, Alexandre Karsenti, MD, Nawwar Al-Attar, MD, Romain Bazeli, MD, and Philippe Montravers, MD, PhD Departments of Anesthesiology and Surgical Intensive Care Unit, Thoracic and Vascular Surgery, Cardiac Surgery, and Radiology, Hôpital Bichat-Claude Bernard, Assistance Publique-Hôpitaux de Paris, Université Paris VII, Paris, France
Extracorporeal membrane oxygenation (ECMO) improves the outcome of refractory cardiogenic shock. Few studies in adult populations have specifically addressed the complications of ECMO. Abdominal compartment syndrome (ACS) has been previously described in the pediatric literature, but it has never been directly attributed to ECMO alone. The authors describe two cases of ACS directly induced by venoarterial ECMO. In one case, decompressive laparotomy restored an adequate hemodynamic status. The authors hypothesize that ECMO contributed to ACS by inducing massive fluid overload and subsequent tense ascites. In conclusion, when ECMO dysfunction or hemodynamic impairment occurs, ACS should be considered and a decompressive laparotomy should be performed. (Ann Thorac Surg 2010;90:e40 –1) © 2010 by The Society of Thoracic Surgeons
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enoarterial extracorporeal membrane oxygenation (ECMO) improves the prognosis of refractory cardiogenic shock, but many complications induced by this assistance device have been described [1]. Nevertheless, the majority of articles published on ECMO are cases of success or new indications and perspectives. Very little literature is available on cases of failure or specifically addressing ECMO complications. Abdominal compartment syndrome (ACS) has never been described as a complication of ECMO. We report two cases of ACS induced by venoarterial ECMO for cardiogenic shock.
Case Reports Patient 1 Angioplasty in a 72-year-old woman was complicated by left anterior descending coronary artery rupture and tamponade with cardiac arrest. Cardiopulmonary resuscitation was performed followed by beating-heart coronary artery bypass grafting. Postoperative transthoracic echocardiography (TTE) showed a left ventricular ejection fraction (LVEF) of 15% with aortic flow time-velocity of 8 cm. Multi-organ failure (MOF) required the use of venoarterial ECMO by cannulation of the femoral vessels with surgical dissection. The correct position of the venous cannula was verified on chest roentgenogram and TTE. Massive fluid loading was necessary to achieve satisfactory venous return on ECMO and a pump flow Accepted for publication June 7, 2010. Address correspondence to Dr Augustin, Hôpital Bichat-Claude Bernard, 46, rue Henri Huchard, Paris Cedex 18, 75877, France; e-mail:
[email protected].
© 2010 by The Society of Thoracic Surgeons Published by Elsevier Inc
rate greater than 3 L/min. Fluid (20 L) was infused with a 16-L positive fluid balance. After 48 hours, organ functions improved and ECMO was explanted after a positive weaning trial with an LVEF of 45% on TTE. Two hours later, the patient had generalized mottled skin develop with MOF. Cardiogenic shock and hypovolemia were excluded with an LVEF of 40% on TTE and an aortic flow time-velocity of 16 cm. A computed tomographic scan was performed, due to the presence of abdominal distension, which showed ascites and mucosal enhancement compatible with mesenteric ischemia. A laparotomy was performed, which revealed tense ascites with major bowel edema, but no sign of ischemia. The patient’s hemodynamic status dramatically improved. No other intervention was performed, apart from decompression. Postoperative intra-abdominal pressure was still 19 mm Hg, suggesting the presence of ACS [2]. The postoperative hemodynamic course was uneventful with decompression alone, confirming the diagnosis of ACS, but the patient died 7 days later of anoxic brain damage.
Patient 2 A 50-year-old woman underwent bilateral lung transplantation for emphysema. The right lung was removed first. The donor right lung was implanted without any surgical problem. After declamping the right pulmonary artery, the patient had ventricular tachycardia develop with circulatory arrest. Internal cardiac massage and internal defibrillation restored spontaneous circulation after 3-minute resuscitation. Continuous infusion of epinephrine (2 mg/hr) restored an adequate hemodynamic status (blood pressure, 120/70 mm Hg; cardiac output, 7 L/min; central venous oxygen saturation, 87%). On transesophageal echocardiograpy, the patient’s LEVF was 50% with inferolateral hypokinesia. The patient was admitted to the intensive care unit for postoperative care. Five hours after intensive care unit admission, her hemodynamic status dramatically worsened with MOF and hyperlactatemia (peak serum lactate, 11 mmol/L), despite an epinephrine infusion of 10 mg/hr. The TTE showed global hypokinesia with an LEVF of 15%. It was hypothesized that this patient had stunned myocardium develop secondary to cardiac arrest. She was placed on venoarterial ECMO with femoral cannulation, rapidly allowing discontinuation of the epinephrine infusion with return to normal serum lactate level (1 mmol/L). Large fluid volumes were required to ensure adequate ECMO pump flow, with a positive fluid balance of 23 L in 4 days. Her LEVF improved after 4 days. During an ECMO weaning trial, a TTE showed an LEVF of 45% with low cardiac output (3.5 L/min). It was decided to delay the ECMO withdrawal. On the following day, although her cardiac function had improved continuously for the first 4 days, her hemodynamic status worsened with severe vasoplegia and MOF. Extracorporeal membrane oxygenation dysfunction was observed with impaired venous return and pump flow of less than 1.5 L/min, despite massive fluid loading and epinephrine infusion. Correct positioning of the venous cannula was verified. Infection and colonic ischemia were ruled out. Finally, it was observed that intra-abdominal pressure of 35 mm Hg was leading to a diagnosis of ACS, but the patient died before a decompressive laparotomy could be performed. The patient was on ECMO for a total of 5 days. 0003-4975/$36.00 doi:10.1016/j.athoracsur.2010.06.039
Ann Thorac Surg 2010;90:e40 –1
Comment These two cases of ACS were clearly induced by venoarterial ECMO for cardiogenic shock. The common feature of these two cases was the need for massive fluid overload to achieve appropriate flow rates. It can be hypothesized that this massive positive fluid balance was responsible for tense ascites with intra-abdominal hypertension and subsequent ACS. No alternative diagnosis could be considered in the first case, as decompressive laparotomy dramatically improved hemodynamic status, and ACS was subsequently confirmed. In the second case, intra-abdominal hypertension was accompanied by MOF and secondary ECMO dysfunction, although the device initially functioned adequately. Abdominal compartment syndrome is a known cause of ECMO dysfunction and five pediatric cases of ECMO dysfunction caused by ACS with impaired venous return have been published [3– 6]. In these cases, the link between ACS and ECMO dysfunction was confirmed because decompressive laparotomy restored adequate blood flow. In some cases, intra-abdominal hemorrhage was the cause of ACS and, in other cases, ascites with ACS was explained by peritoneal extravasation in a context of sepsis. Association between ECMO and significant fluid overload is known in the pediatric literature [7]; therefore we can assume that in addition to sepsis, ECMO may be involved in fluid overload. In fact, relative hypovolemia during ECMO is the major cause of inappropriate low pump flow, with suction and collapse of the right atrial wall by the venous cannula. Fluid loading usually restores pump flow. This phenomenon explains how ECMO alone can induce fluid overload. Massive fluid overload was necessary in both of the cases reported here, despite correct positioning of the venous cannula. A large positive fluid balance is associated with general edema, pleural effusion, and ascites known to be a cause of ACS [8].
CASE REPORT AUGUSTIN ET AL ABDOMINAL COMPARTMENT SYNDROME AND ECMO
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Intra-abdominal hypertension and ACS can occur during ECMO and can cause secondary ECMO failure and deterioration of hemodynamic status. By promoting massive fluid overload, ECMO can contribute to tense ascites and ACS. Therefore, intra-abdominal pressure should be measured in the case of unexplained deterioration, especially in the presence of large fluid overload.
References 1. Combes A, Leprince P, Luyt CE, et al. Outcomes and longterm quality-of-life of patients supported by extracorporeal membrane oxygenation for refractory cardiogenic shock. Crit Care Med 2008;36:1405–11. 2. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. I. Definitions. Intensive Care Med 2006;32:1722–32. 3. Lam MC, Yang PT, Skippen PW, Kissoon N, Skarsgard ED. Abdominal compartment syndrome complicating paediatric extracorporeal life support: diagnostic and therapeutic challenges. Anaesth Intensive Care 2008;36:726 –31. 4. McKee CT, Vricella LA, Harris ZL, Easley RB. Abdominal compartment syndrome contributing to failure of extracorporeal membrane oxygenation in an infant with congenital heart disease and sepsis. Pediatric Crit Care Med 2006;7: 180 –2. 5. Wu ET, Huang SC, Chiu IS, Ko WJ. Abdominal compartment syndrome caused failure of venous return in a neonate during extracorporeal membrane oxygenation support. Pediatric Crit Care Med 2006;7:400 –1. 6. Okhuysen-Cawley R, Prodhan P, Imamura M, Dedman AH, Anand KJ. Management of abdominal compartment syndrome during extracorporeal life support. Pediatric Crit Care Med 2007;8:177–9. 7. Hoover NG, Heard M, Reid C, et al. Enhanced fluid management with continuous venovenous hemofiltration in pediatric respiratory failure patients receiving extracorporeal membrane oxygenation support. Intensive Care Med 2008;34: 2241–7. 8. Bailey J, Shapiro MJ. Abdominal compartment syndrome. Crit Care 2000;4:23–9.
