Interact CardioVasc Thorac Surg 2008;7:285-287. doi:10.1510/icvts.2007.165134
© 2008 European Association of Cardio-Thoracic Surgery
Negative results - Aortic and aneurysmal |
Preoperative hepatic insufficiency and type III endoleak: a confirmed potential fatal association following endovascular treatment
Francis Pesteila,
Louis Labrousseb,*,
Caroline Chevreuila and
Marc Laskara
a Department of Thoracic and Cardiovascular Surgery and Angiology, Dupuytren University Hospital, Ave Martin Luther King, 87042 Limoges, France
b Department of Cardiac and Vascular Surgery, Hôpital Haut-Lévèque, Bordeaux University Hospital, 33604 Pessac, France
Received 14 August 2007;
received in revised form 19 December 2007;
accepted 21 December 2007
*Corresponding author. Department of Cardio-Vascular Surgery, Hôpital Haut Lévèque, Avenue de Magellan, 33604 Bordeaux-Pessac, France. Tel.: +33-5-57-65-64-37; fax: +33-5-57-65-81-57.
E-mail address: louis.labrousse{at}chu-bordeaux.fr (L. Labrousse).
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Abstract
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Consumptive coagulopathy is known to occur in patients with aneurysm, especially in the thoracic localization. Compared to open chest surgery, the endovascular treatment leaves in place a large thrombosed aneurysmal sac, which might induce and/or exacerbate the coagulopathy. Although exceptional, some recent reports have raised the potential disastrous issue related to this complication. We report the case of a 74-year-old patient treated for an asymptomatic thoracic aorta aneurysm by endoprosthesis who developed a fatal disseminated intravascular coagulopathy. This complication has been related to a type III endoleak associated with a preoperative hepatic insufficiency.
Key Words: Thoracic aneurysm; Coagulopathy
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1. Introduction
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Aortic aneurysms are known to be associated with disseminated intravascular coagulopathies (DICs) due to the presence of chronic thrombus [1, 2]. Similarly, following endovascular treatment (EVAR) some degree of coagulopathy is present [3, 4] but usually without clinical consequences. Recently, Higashiura et al. [5] reported a patient with liver cirrhosis who died of disseminated intravascular coagulation (DIC) induced by a type III endoleak. We present a new case of such an association (preoperative cirrhosis, EVAR and type III endoleak) complicated by a fatal symptomatic DIC.
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2. Report
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A 74-year-old man was admitted for a thoracic aneurysm involving the main part of the descending aorta (Fig. 1). Medical history included tobacco use and silicosis with consecutive chronic pulmonary insufficiency, which explains that an EVAR procedure was planned. Preoperative biological tests showed: normal hepatic enzymes, platelets at 110,000/ml, partial thromboplastin time ratio at 1.2, and the international normalized ratio (INR) of prothrombin time test at 1.4.
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Fig. 1. (a) Preoperative CT-scan (3D reconstructive picture). (b) Postoperative CT-scan with the black straight line indicating the level of the slice seen on c. (c) Type III endoleak at the overlap level between the second and the third endoprosthesis. The white arrow shows the opacification of the aorta in a non-excluded part of the aneurysm (diaphragmatic junction); the dotted line follows the posterior wall of the endoprosthesis.
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The procedure was performed under general anaesthesia and needed three endoprostheses (oversized by 10–15% relative to the normal diameter; Talent, Medtronic INC., USA), which were deployed over approximately 2 cm of healthy landing zone proximally and distally. Balloon inflation at both ends of the endoprosthesis completed the procedure. Final angiographic control seemed correct with, especially, exclusion of the aneurysm. Scopic time was 35 min, and the patient received 400 ml of contrast iodine (Iomeron®, Altana Pharma, Germany).
Initial postoperative course was uneventful with an extubation time at 2 h. From the second day and concomitantly of femoral access bleeding, lab tests showed progressive active DIC (Fig. 2), with thrombocytopenia, elevation of plasma levels of fibrin-derived products (FDP), and consumption of coagulation factors evidenced by prolongation of prothrombin time. Heparin-induced thrombocytopenia was excluded by antibody analysis. Other causes of coagulopathy, such as B12 and/or folate deficiencies and/or visceral malperfusion, were also eliminated.
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Fig. 2. (a) Preoperative and postoperative platelet measurements. Black star indicates platelet transfusion. (b) Preoperative and postoperative laboratory measurements of fibrinogen, Factor II (F II), factor VII (F VII) and factor X (F X). Black arrows indicate fibrinogen transfusion and white stars indicate plasma transfusion. Fibrinogen is expressed as g/l, FII, FV, and FX as a ratio.
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Daily blood testing showed continuously positive D-dimer latex test at more than 1/16 combined with a positive ethanol test and prolongation of prothrombin time. Treatment consisted of a low dose of non-fractionated heparin and blood replacement therapy, which was guided by the clinical and biological situation. It included red cell transfusions, fresh frozen plasma, fibrinogen, and matched platelet concentrates (Fig. 2).
The clinical and biological conditions remained stable until the 25th postoperative day when a haemoptysis led to performing a computed tomographic (CT) scan which showed a type III endoleak caused by inadequate overlapping between the second and the third stent in the curvature of the distal thoracic aorta (Fig. 1). The same day, an associated diffuse oropharyngeal bleeding with hypoxemia necessitated an endotracheal intubation. The consumptive coagulopathy gradually worsened, the patient developed renal and liver failure and died of multi-organ failure three days later. The autopsy revealed hepatic cirrhosis likely related to haemochromatosis. In total, the patient received 18 units of blood, one unit of platelets, seven units of fibrinogen and 16 units of plasma (Fig. 2).
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3. Discussion
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Aortic aneurysms are known to be associated with coagulation disorders with an increase in fibrinolytic activity and platelet activation [1, 2]. However, the presence of a true preoperative coagulopathy is rare (>4%) and usually complete resolution is obtained by aneurysm resection [1]. Most frequently aneurysm-induced DICs occur perioperatively and if laboratory DIC-like alterations are found in 40–80% of patients postoperatively, only 3% have clinical evidence of DIC [1].
EVAR has emerged as an efficient, less invasive treatment especially for high-risk patients. The main difference between endovascular repair and open surgery is that the endovascular treatment leaves in place a large thrombosed aneurysmal sac. Only few studies have focused on endovascular treatment and associated coagulopathy [3, 4]. What is known is that activation of coagulation and fibrinolysis is observed early after the procedure (FDP and D-dimer increase; platelet count, fibrinogen, antithrombin III and prothrombin activity decrease) but these disorders disappear within 2–4 weeks [3, 4] and are usually not related to clinical complications. Moreover, although blood products (such as platelets and fibrinogen) are consumed by generation of the thrombus in the aneurysmal sac [3], the thrombus is separated from the systemic blood flow by the endoprosthesis and that explains that chronic activation of coagulation and chronic fibrinolysis is not likely to occur.
To date, there have been three reports of consumptive coagulopathy following EVAR [5–7]. In two cases [6, 7], the authors highlighted technical difficulties (but without endoleak) with prolonged and repeated passage of endovascular instrumentation that might have stimulated the endothelium procoagulant activity and/or induced multiple micro-embolisations. Moreover, one of the patients had preoperative liver cirrhosis [7]. In the last recent report [5], the fatal DIC has been related to the happening of a type III endoleak four years after the EVAR procedure in a cirrhotic patient, and has been explained by an imbalance in coagulation factors due to the association of factor's consumption in the endoleak and of insufficient synthesis by the cirrhotic liver.
Indeed, there is a known close link between blood flow turbulences and intravascular coagulopathy [8], and between the degree of dilatation of a dissected aorta (correlated with thrombosed false lumen size) and the amount of coagulation disorder [4, 9]. Therefore, in our patient, a huge turbulent blood flow due to the type III endoleak has been likely created in the thrombosed aneurysmal sac and has been responsible for the induction of the DIC. This case supports Higashiura's hypothesis [5] that the type III endoleak (which mimics a large false lumen in contact with turbulent flow) might be responsible for an activation of the coagulation system that the cirrhotic liver would not be able to overcome because of its impaired coagulation factors' synthesis function.
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4. Conclusion
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The imbalance of coagulation factors induced by the turbulent flow associated to the type III endoleak is likely related to the preoperative hepatic insufficiency and its impaired synthesis function. Special attention is required in such patients with preoperative hepatic disorders, and extensive measurement of markers of coagulation and of the fibrinolytic system prior and after the procedure appears to be mandatory. Finally, endoleaks should be searched for and treated aggressively in such situations with coagulation disorders.
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References
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Abstract
1. Introduction