Abdominal compartment syndrome after endovascular repair of

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CASE REPORT

Interactive CardioVascular and Thoracic Surgery 14 (2012) 897–899 doi:10.1093/icvts/ivs030 Advance Access publication 27 February 2012

Abdominal compartment syndrome after endovascular repair of ruptured iliac artery aneurysm† Joana Ferreira*, Alexandra Canedo, Paulo Barreto and António Vaz Department of Vascular Surgery, Hospital Vila Nova de Gaia/Espinho, Vila Nova de Gaia/Espinho, Portugal * Corresponding author. Rua do Bolhão, n 268, 4505-314 Fiães VFR, Portugal. Tel: +351-96-2958421; e-mail: [email protected] ( J. Ferreira). Received 13 November 2011; received in revised form 3 January 2012; accepted 5 January 2012

Abstract Abdominal compartment syndrome is a possible complication after aneurysm repair and has a high mortality rate. Although there has been an increment in patient survival rates after aneurysm repair, there has also been an increase in this entity. However, there are few data about the incidence and management of this complication after endovascular repair of a ruptured iliac artery aneurysm. The objective of this report is to describe a case of abdominal compartment syndrome after endovascular correction of a ruptured iliac artery aneurysm, emphasizing the importance of the accurate monitoring of intra-abdominal pressure, medical therapy and timely laparotomy. An 85-year old male was submitted to the endovascular repair of a ruptured iliac artery aneurysm. On the first day after the intervention, he developed abdominal compartment syndrome which did not resolve with medical therapy. Consequently, on the second postoperative day, a decompressive laparotomy was performed, removing the retroperitoneal haematoma, which was the main cause of the high intra-abdominal pressure and the abdominal compartment syndrome. At 12 months of follow-up, there was no evidence of complications. This case stresses the importance of early recognition of abdominal compartment syndrome. Keywords: Isolated iliac artery aneurysm • Abdominal compartment syndrome • Endovascular repair

INTRODUCTION Isolated iliac artery aneurysm (IAA) has a prevalence of 0.03% and a mortality rate of 30–60% on rupture [1]. Endovascular repair of IAA has evolved to be minimally invasive and has been shown to be safe and durable at mid-term follow-up [2]. With the improvement in endovascular techniques and, consequently, patient survival, there has been an increase in previously unrecognized complications, such as abdominal compartment syndrome (ACS) [3, 4]. It occurs in 18–30% of patients with ruptured abdominal aortic aneurysm a with mortality rates of 57–70% [4–6].

nasogastric and rectal tube were inserted and rectal enemas were performed. He was infused with colloids and 2 units of red blood cells. On the second day his intra-abdominal pressure rose to 29 mmHg. He underwent an angio-CT scan, which revealed a retroperitoneal haematoma measuring 9.8 cm × 8.0 cm, with some areas of recent haemorrhage (Fig. 2). A surgical decompression was undertaken by a McBurney incision. Almost 2000 ml of retroperitoneal haematoma was removed. The fascia was kept open and the muscles were closed. On the second day, after decompression, intra-abdominal pressure was 15 mmHg, and there was progressive normalization of the diuresis. At 12 months of follow-up the endoprosthesis stayed without fractures, endoleaks, evidence of infection or migration.

CASE REPORT

† Presented at the Fifth World Congress on the Abdominal Compartment Syndrome, 10–13 August 2011, Florida, USA.

DISCUSSION Primary ACS is defined as a sustained intra-abdominal pressure of >20 mmHg that is associated with new organ failure, and in which abdominal decompression has beneficial effects [7]. In the case described above, on the first day after the intervention, the intra-abdominal pressure was 26 mmHg, and there was evidence of kidney failure. The intra-abdominal pressure is the steady-state pressure concealed within the abdominal cavity [7]. When this value is >12 mmHg, it is considered pathological [7]. Intra-abdominal hypertension may occur due to increased intra-abdominal or retroperitoneal volume, which probably was the prevalent mechanism in this situation [3, 6, 8]. Elevated intraabdominal pressure may affect visceral perfusion, cardiac output,

© The Author 2012. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.

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An 85-year old male was admitted with a ruptured common right IAA, with a massive haematoma measuring 2.7 cm in diameter (Fig. 1). We performed embolization with coils of the ipsilateral internal iliac artery and deployment of two iliac extensions (distal extension measuring 16 × 122 mm and proximal 20 × 88 mm)—Endurant®MetronicTM. He was transfused with 3 units of red blood cells, 2000 ml of crystalloids and 120 ml of contrast. On the first day, he developed ACS: his abdomen was distended, he had oliguria and his intra-abdominal pressure (bladder pressure) was 26 mmHg. He was given analgesia, sedation, erythromycine, metoclopramide, furosemide. A

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Figure 1: CT scan performed at admission revealing a ruptured common right iliac artery aneurysm.

Figure 2: CT scan performed after endovascular aneurysm repair revealing a retroperitoneal haematoma measuring 9.8 cm × 8.0 cm.

respiratory and renal function, and cause multi-organ failure and death [8]. An early recognition of the risk factors that contribute to the development of ACS is important to begin the intra-abdominal pressure monitoring and to optimize the treatment, which has a significant impact on survival [3, 4]. A patient with a ruptured aneurysm has multiple risk factors, such as acidosis ( pH < 7.2); polytransfusion (>10 U packed red blood/24 h), coagulopathy ( platelets < 55 000/mm3), massive fluid resuscitation (>5 L fluids/24 h) and haemoperitoneum [4, 6]. In the endovascular repair, the aortic occlusion, the conversion to the aorto-uniliac device, due to haemodynamic instability and the inability to expeditiously cannulate the contralateral gate increase the risk of ACS [3, 4, 6]. In this case, we think that the retroperitoneal haematoma, which had been present since the diagnosis and increased during the procedure, was the most important mechanism. Although we had avoided heparinization and the coagulation studies were corrected intra- and post-operatively, we believe

that the time we took to embolize the internal iliac artery and bleeding from collateral vessels contributed to the expansion of the haematoma. The endovascular repair did not allow evacuation of the retroperitoneal haematoma. However, it has not been proved that ACS is more frequent after endovascular repair [3, 9]. We believe now, that we could have used the femoral surgical approach to gain access to the retroperitoneal haematoma aspiration and evacuated it, avoiding the ACS, as some surgical centres do. Immediately after the endovascular intervention we decided to measure the intra-abdominal pressure. After recognizing intra-abdominal pressure hypertension, conservative therapy was begun. Following the guidelines of the World Society of Abdominal Compartment Syndrome, we tried to evacuate the intra-luminal contents, inserting a nasogastric and rectal tube, initiating prokinetic agents and administering enemas. We improved the abdominal wall compliance with adequate sedation and analgesia. We tried to optimize the fluid administration, avoiding crystalloids and giving colloids and furosemide. Studies have shown that resuscitation with isotonic crystalloids increases the risk of developing ACS compared with resuscitation with a solution of hypertonic crystalloids or colloids [4]. When urinary output is not sufficient to reverse the volume overload, venovenous dialysis treatment should be considered early; this could also reverse the situation and avoid a decompressive laparotomy [4]. One of the most powerful tools in the prevention of ACS in the early postoperative period is neuromuscular blockade, which was not used in this case [4]. Neuromuscular blockade is effective in lowering the intra-abdominal pressure and increasing urinary output [4]. There are important side effects of prolonged neuromuscular blockade, in particularly the risk of pneumonia [4]. However, if ACS and its treatment with open abdomen can be prevented by 12 h of neuromuscular blockade, it is worthwhile in most cases [4]. Unfortunately, none of the conservative measures implemented on the first day after surgery were effective and on the second day a CT scan was performed. We found a haematoma measuring 9.8 cm × 8.0 cm. Because of this, we decided to proceed to abdominal decompression and haematoma evacuation. In fact, abdominal decompression is recommended when the intra-abdominal pressure is >20 mmHg or ACS develops, and conservative measures described are not effective [4]. Moreover, decompression should not be delayed if an intra-abdominal pressure >30 mmHg is registered, because a life-threatening situation has developed with the risk of acute circulatory arrest [4]. It is proved that laparotomy should not be postponed: the mortality from multiple organ failure increased to 70% when the diagnosis of ACS and laparotomy were delayed; patients who underwent immediate on-table laparotomy for a presumptive diagnosis of ACS had a survival of 50% [3]. Conflict of interest: none declared.

REFERENCES [1] Hechelhammer Z, Rancic Z, Pfiffner R, Mayer D, Meir T, Lachat M et al. Midterm outcome of endovascular repair of ruptured isolated iliac artery aneurysms. J Vasc Surg 2010;52:1159–63. [2] Buckley CJ, Buckley SD. Technical tips for endovascular repair of common iliac artery aneurysms. Semin Vasc Surg 2008;21:31–4. [3] Mehta M, Darling RC, Roddy SP, Fecteau S, Ozsvath KJ, Kreienberg PB et al. Factors associated with abdominal compartment syndrome

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[7] Malbrain MLNG, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, Waele JD et al. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. Intensive Care Med 2006;32:1722–32. [8] Papavassiliou V, Anderton M, Loftus IM, Turner AD, Naylor AR, London NJM et al. The physiological effects of elevated intra-abdominal pressure following aneurysm repair. Eur J Vasc Surg 2003;26:293–8. [9] Karkos CD, Harkin DW, Giannakou A, Gerassimidis TS. Mortality after endovascular repair of ruptured abdominal aortic aneurysms. Arch Surg 2009;144:770–8.

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complicating endovascular repair of ruptured abdominal aortic aneurysm. J Vasc Surg 2005;42:1047–51. [4] Björck M, Wanhainen A, Djavani K, Acosta S. The clinical importance of monitoring intra-abdominal pressure after ruptured abdominal aortic aneurysm repair. Scand J Surg 2008;97:183–90. [5] Mayer D, Rancic Z, Meier C, Pfammatter T, Veith F, Lachat M. Open abdomen treatment following endovascular repair of ruptured abdominal aortic aneurysms. J Vasc Surg 2009;50:1–7. [6] Mehta M. Technical tips for EVAR for ruptured AAA. Semin Vasc Surg 2009;22:181–6.

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