Disseminated Intravascular Coagulopathy Caused by Endoleak Type I: Successful Treatment by Endovascular Stent-graft Extension
Article Outline
Introduction
We present a case with acute DIC probably caused by a type I endoleak after endovascular aneurysm repair (EVAR).
Case report
An 84-year-old male underwent elective EVAR of a 7
cm sized infrarenal aortic aneurysm and developed five months later an acute DIC associated with an endoleak type I. After successful endovascular stent-graft extension the DIC resolved.
Discussion
Endoleak type I is not described to be related to DIC, however as the endovascular stent-graft extension did abolish both, endoleak and the DIC in our case. We therefore suggest that a type I endoleak can cause acute DIC.
Keywords: Abdominal aortic aneurysm, Endoleak type I, DIC
Introduction
Disseminated intravascular coagulopathy (DIC) is a known serious complication associated with abdominal aortic aneurysms (AAA), especially in cases of rupture or dissection.1 DIC has rarely been reported in association with an endovascular aneurysm repair (EVAR).
We describe the first reported case of DIC-associated type I endoleak after EVAR.
Case Report
An 84-year-old man with myelodysplastic syndrome and stable chronic thrombocytopenia of 91×109/l underwent elective endovascular repair of a 7cm sized infrarenal aortic aneurysm in May 2003. Four weeks postoperatively, follow-up computed tomography (CT) demonstrated an type I endoleak arising from the left iliac limb which was treated with endovascular stent-graft extension and coil embolization of the left internal iliac artery.
Four months later, the patient developed severe spontaneous oral mucosal bleeding, ecchymosis and petechia in the lower limbs. On admission (29th October 2003) the lowest coagulation values were as follow (Table 1): decreased platelet count of 63×109/l (normal levels: 150–400×109/l), prolonged prothrombin time (INR: 1.51), activated partial thromboplastin time of 44 sec. (normal: 26–35 sec.), severely decreased fibrinogen (0.4g/l; normal: 1.8–3.5) and increased fibrinogen degradation products (D-dimer 4517μg/l; normal: <400). Before admission, the patient's coagulation screen had been in normal range until September 2003. The current laboratory studies were consistent with an acute DIC. An underlying trauma, infection or malignancy could clinically be excluded. Inflammatory causes for DIC could be excluded as well by extended laboratory analysis. CT of the abdomen revealed an type I endoleak arising from the distal right iliac limb which was confirmed by angiography (Fig. 1). However, a retroperitoneal hematoma developed at the puncture site. Since risk of open surgical repair of the endoleak was considered to be high, a transfemoral endovascular stent-graft extension was performed after arteriotomy of the right common femoral artery. Over a guidwire a stent-graft (Talent AAA™, Medtronic AVE, USA) was inserted, advanced to the desired position under fluoroscopy and exactly deployed in the right common iliac artery in a partially overlapping fashion in order to provide secure endoleak exclusion without obstructing the ostium of the internal iliac artery. After balloon dilatation and apposition of the stent-graft to the vessel wall, final angiography showed neither endoleak nor contrast media extravasation (Fig. 2). However, due to repeated passage of endovascular instrumentation a flow-limiting dissection of the right common femoral artery occurred necessitating surgical repair at the same day. After the procedure, the patients recovered fast. Within five days after endoleak repair all of the coagulation parameters measured returned to normal range except for a slightly raised aPTT (37.5 sec). Eight days after the intervention, the patient was discharged after an uneventful postoperative recovery. Overall, a total amount of 5 units of red cell concentrate, 15 units of fresh frozen plasma and 6 units of platelets were transfused.
Table 1. Laboratory analysis outlining coagulation parameters at baseline, at one and at 30 months follow-up after stent graft placement
| Coagulation parameters | At baseline | 1 month after stent placement | 30 months after stent placement |
|---|---|---|---|
| Platelet count [150–400×109/l] | 63 | 53 | 130 |
| INR∗ | 1.51 | 1.2 | 1.2 |
| aPTT [26–35 sec.]∗ | 52 | 33 | 30 |
| Fibrinogen [1.8–3.5g/l] | 0.4 | Not available | 1.3 |
| D-dimer [<400μg/l] | 4517 | Not available | >5000 |
∗INR and aPTT denote international normalized ratio and activated partial thromboplastin time, respectively. |
Fig. 1
Retrograde transfemoral angiography confirmed an endoleak type I in the distal right iliac artery.
Fig. 2
Angiography after deployment of a Talent AAA™ stent-graft showed successful exclusion of the endoleak and preserved blood flow through covered stent-grafts.
During follow-up the patient was doing fine with no further complication. He experienced minor buttock claudication as a result of coiling of the left internal iliac artery. Coagulation parameters remained normal with stable near normal fibrinogen (1.3g/l) and platelet count (130x109/l) after 30 months of follow-up (Table 1). Fibrinogen degradation product still remained increased. CT-scan of the abdomen demonstrated sustained exclusion of the endoleak.
Discussion
Clinically overt DIC affects about 4% of patients with AAA2 and aneurysmal size correlates well with markers of blood coagulation and fibrinolysis. 3 Until recently, DIC has not been reported to be caused by an endoleak following EVAR. A fatal consumptive coagulopathy after endovascular stent-graft repair of AAA was reported by Cross and colleagues.4 They described a case in which prolonged and repeated passage of endovascular instrumentation may perturb the endothelium and stimulate procoagulant activity leading to consumptive coagulopathy.4
As coagulation parameters were normal directly after EVAR in our patient, the stent itself was not considered to be the cause for DIC. The course of the coagulation parameters showed a striking deterioration associated with the occurrence of the endoleak. After successful exclusion of the endoleak by using an iliac stent-graft extension, the DIC rapidly resolved supporting our hypothesis that the DIC was related to the endoleak. FFP is an effective way to stabilize coagulation, but we were unable to correct the coagulation after administration of overall 13 FFP to the date of graft extension, assuming that the endoleak is the promoter for DIC. A possible pathomechanism could be the liberation of coagulant material from the turbulent jet flow into the circulation or an accumulation of clotting factors at the site of the injured vessel wall as has been reported in ruptured or dissecting AAA by ten Cate and colleagues.1
Pre- and perioperative management of DIC consists of platelet transfusion and clotting factor replacement. Generally, it is agreed upon that operation provides the best hope of cure in AAA-associated DIC. However, successful treatment with endovascular stent-graft repair of DIC-associated aortic dissection is an acceptable alternative as reported by Sakamoto and colleagues.5
We conclude that a type I endoleak after EVAR can cause acute DIC, since endovascular stent-graft extension did abolish both, endoleak and DIC in our case.
Acknowledgments
The authors would like to thank J. Triller, MD, Department of Diagnostic and Interventional Radiology, University Hospital Bern, Switzerland, for all angiographic images shown herein.
References
- . Coagulopathy in ruptured or dissecting aortic aneurysms. Am J Med. 1975 Aug;59(2):171–176
- . Preoperative disseminated intravascular coagulation associated with aortic aneurysms. A prospective study of 76 cases. Arch Surg. 1983 Nov;118(11):1252–1255
- . An activated state of blood coagulation and fibrinolysis in patients with abdominal aortic aneurysm. Am J Surg. 1998 Apr;175(4):297–301
- . Consumptive coagulopathy following endovascular stent repair of abdominal aortic aneurysm. Eur J Vasc Endovasc Surg. 2000 Jan;19(1):94–95
- Chronic aortic dissection complicated by disseminated intravascular coagulation: successful treatment with endovascular stent-grafting. J Endovasc Ther. 2003 Oct;10(5):953–957
PII: S1533-3167(06)00077-X
doi:10.1016/j.ejvsextra.2006.09.003
© 2006 Published by Elsevier Inc.
Refers to article:
- Disseminated Intravascular Coagulopathy Caused by Endoleak Type I: Successful Treatment by Endovascular Stent-graft Extension , 02 November 2006
