|Year : 2017 | Volume
| Issue : 2 | Page : 99-101
An unusual case of external iliac artery thrombosis after renal transplant surgery
Vikas Dhawan1, Harshita Mehrotra2, Nitish Gupta3, Manisha Dassi4
1 Department of Urology, Army Hospital Research and Referral, New Delhi, India
2 Department of General Surgery, Andaman and Nicobar Islands Institute of Medical Sciences, Port Blair, Andaman and Nicobar Islands
3 Department of Anaesthesiology, Army Hospital Research and Referral, New Delhi, India
4 Department of Nephrology, Army Hospital Research and Referral, New Delhi, India
|Date of Web Publication||12-Sep-2017|
Department of General Surgery, Andaman and Nicobar Islands Institute of Medical Sciences, Port Blair, Andaman and Nicobar Islands - 744 101
Andaman and Nicobar Islands
Source of Support: None, Conflict of Interest: None
The rates of renal transplant for end stage renal disease are increasing worldwide. Vascular complications due to arterial thrombosis is seen only in less that 1% cases. We describe a case of 36 year old male who underwent a live-related renal transplant, whose post-operative period was complicated by juxta-anastomotic distal external iliac artery thrombosis. He was managed by thrombectomy and improved with complete recovery. Attention should be paid to anastomotic technique and prevention of formation of intimal flap. In case of arterial thrombosis, graft salvage can be attempted depending on the clinical scenario.
Keywords: End-stage renal disease, external iliac artery thrombosis, renal transplant
|How to cite this article:|
Dhawan V, Mehrotra H, Gupta N, Dassi M. An unusual case of external iliac artery thrombosis after renal transplant surgery. Indian J Transplant 2017;11:99-101
|How to cite this URL:|
Dhawan V, Mehrotra H, Gupta N, Dassi M. An unusual case of external iliac artery thrombosis after renal transplant surgery. Indian J Transplant [serial online] 2017 [cited 2019 Aug 18];11:99-101. Available from: http://www.ijtonline.in/text.asp?2017/11/2/99/214393
| Introduction|| |
Renal transplant is the treatment of choice in patients with end-stage renal disease. Despite recent advances in surgical technique, immunosuppressive therapy, and management of infections, vascular complications continue to account for 3%–15% of graft dysfunctions.,, If detected early the graft can be salvaged by prompt surgical or radiological intervention. Arterial thrombosis, the most feared vascular complication is seen in <1% of all renal transplantation cases and commonly involves the renal artery. We report an unusual case of a young patient who developed external iliac artery (EIA) thrombosis after renal transplantation. The incidence of EIA thrombosis is not reported in the literature.
| Case Report|| |
A 36-year-old male, a case of chronic kidney disease stage V (postfocal segmental glomerulosclerosis) was taken up for live-related renal transplant (mother to son) on July 3, 2013, after human leukocyte antigen matching. Pretransplant donor specific antibodies (DSA) were negative, proteinuria was 2.7 g/dl, and serum albumin was 3.8 g/dl. Basiliximab- and methylprednisolone-based induction immunosuppression was given. The vein and arterial diameter of the graft were 12 mm and 7 mm respectively with warm ischemia time of 90 s and cold ischemia time of 80 min. The vessels were healthy with no gross features of atherosclerosis or any obvious intimal flap. Both vein and artery were anastomosed to external iliac vessels using cardiovascular suture-6 and 7, respectively, in an end-to-side fashion using the continuous suturing technique. His immediate postoperative period was uneventful with a fall of creatinine from 8.1 mg/dl to 2.1 mg/dl. The patient was started on enoxaparin 40 mg subcutaneously Q24H after 6 h of the procedure.
On the 3rd postoperative day (POD), there was a drop in urine output and creatinine level rose to 3.6 mg/dl with serum potassium level of 6.0 meq/L. Distal pulses in lower limbs were equal and symmetrical. Color Doppler of the transplanted kidney revealed increased resistive index in main and segmental renal artery with no diastolic flow visualization and no obvious thrombus. Renal biopsy was done and light microscopy results were obtained within 8 h which demonstrated severe acute tubular necrosis, moderate interstitial inflammation, and no tubulitis. Immunohistochemistry for C4D (DSA) was obtained next day which revealed patchy positivity in peritubular capillaries. Initial findings raised suspicion of acute antibody-mediated rejection, and the patient was started on plasmapheresis, intravenous immunoglobulin (IVIg), and bortezomib.
A formal combined report of light microscopy and immunofluorescence was delayed as direct immunofluorescence (DIF) was outsourced and obtained after 72 h which reported DIF as C4D negative. Patient's general condition kept deteriorating with persistently decreasing urine output and worsening of renal function. Meanwhile, the patient got intermittent hemodialysis for hyperkalemia and uremic symptoms.
On the 8th POD, the patient developed abdominal distention and pain in the right leg. On examination, pulses of right limb including femoral were absent. Ankle-brachial pressure index (ABPI) of the right limb was not recordable. Color Doppler revealed a juxta-anastomotic distal right EIA thrombosis. Computed tomography (CT) angiography [Figure 1] demonstrated a free floating thrombus beginning proximal to renal artery anastomoses and continuing distally into EIA and proximal femoral artery where it completely occluded the vessel; however, good graft vascularity was noted. He was taken up for trans-femoral thrombectomy. Peroperatively, a fresh thrombus was found in EIA, and a full circumference 1 cm segment of endothelium was removed from EIA, good back-bleed seen from profunda and superficial femoral artery and pulsatile forward flow established in common femoral artery. Fluoroscopy done on table after injecting contrast confirmed patency of renal artery and ABPI of 0.73 was noted in the right limb. Postoperatively, his urine output improved and creatinine levels started falling.
|Figure 1: CT angiogram showing thrombus in right external iliac arteryno|
Click here to view
On 15th POD, the patient complained of severe abdominal distension and pain with swelling at the site of transplant wound. Clinically, he had grossly swollen wound site with blood oozing out from the suture line, otherwise, his abdomen was distended but soft. CT angiography [Figure 2] revealed normal renal perfusion with a nonflow occlusive dissection of proximal EIA extending distal to the anastomoses. Approximately, 150 ml of perigraft hematoma was seen with no leakage of contrast. He was taken up for urgent wound exploration. Hematoma found deep to the external iliac sheath was drained; other than generalized ooze, no active site of bleeding was found. The patient had a sanguineous drain of 1100 ml in first 12 h postclot evacuation. Repeat angiography and ultrasound on 16th POD confirmed normal graft vascularity with no contrast extravasation or pseudoaneurysm, and a perigraft collection of around 900 ml, the nonflow occlusive dissection flap of EIA was persistent.
|Figure 2: Perigraft hematoma with medial displacement of transplanted kidney|
Click here to view
In view of patient being hemodynamically stable with a previous history of negative exploration, it was decided to observe the patient conservatively. Patient's general condition gradually improved. Despite significant perigraft hematoma, his wound site drain stopped draining after 5 days of hematoma evacuation. He developed partial wound dehiscence with the discharge of clots and altered blood from gaped site that continued for around 2 months with spontaneous healing and complete recovery. Repeat CT angiography done 3 and 6 months after transplant did not reveal any dissection and the patient has stable graft function.
| Discussion|| |
Arterial thrombosis occurs in <1% of renal transplant patients. Technical difficulties encountered during organ retrieval and implantation constitute the majority of cases of arterial thrombosis. Creation of an intimal flap is the most common technical cause. Since postoperative CT angiography showed dissection of EIA, intimal flap creation during transplantation may have been one of the causative factors for thrombosis. In retrospect, when we tried to analyze any technical issues, we were not able to come across any definite reason other than an aged vascular clamp that could have damaged the intima. Factors such as an occlusion due to atheroma plaque in the recipient EIA or renal artery ostium, and torsion or kinking of the anastomosis can also cause thrombosis but were not evident in this case. Other causes of arterial thrombosis include hyperacute rejection, presence of antiphospholipid antibody, and cryoglobulins., IVIgs also increases the risk of thrombotic events. On 4th POD, following the suspicion of acute rejection our patient was infused IVIg that could have contributed to thrombosis.In vitro data suggest that drugs such as cyclosporine and OKT3 increase the risk of thrombosis, but it has not been borne out in clinical practice. Epidemiological data suggest increased risk of thrombosis in patients undergoing second transplant and those on peritoneal dialysis compared to those on hemodialysis, both of these factors were not there in our case.
Even though the patient was critically ill, he survived the illness, and the graft was salvaged due to timely intervention by removal of thrombus. There are case reports in which treating teams have been successful in salvaging renal graft by early thrombectomy. In such situations, salvage of the graft can be attempted depending on the clinical scenario.
| Conclusion|| |
The most common cause of thrombosis is surgical technique. Attention should be paid to the anastomosis technique and vascular dissection; in particular, the intimal layer must not be damaged. A nihilistic attitude toward acute graft thrombosis should be shunned and attempt to salvage the graft can be made depending on the clinical profile of the patient.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Jordan ML, Cook GT, Cardella CJ. Ten years of experience with vascular complications in renal transplantation. J Urol 1982;128:689-92.
Orons PD, Zajko AB. Angiography and interventional aspects of renal transplantation. Radiol Clin North Am 1995;33:461-71.
Osman Y, Shokeir A, Ali-el-Dein B, Tantawy M, Wafa EW, el-Dein AB, et al.
Vascular complications after live donor renal transplantation: Study of risk factors and effects on graft and patient survival. J Urol 2003;169:859-62.
Fervenza FC, Lafayette RA, Alfrey EJ, Petersen J. Renal artery stenosis in kidney transplants. Am J Kidney Dis 1998;31:142-8.
Irish A. Hypercoagulability in renal transplant recipients. identifying patients at risk of renal allograft thrombosis and evaluating strategies for prevention. Am J Cardiovasc Drugs 2004;4:139-49.
Vaidya S, Sellers R, Kimball P, Shanahan T, Gitomer J, Gugliuzza K, et al.
Frequency, potential risk and therapeutic intervention in end-stage renal disease patients with antiphospholipid antibody syndrome: A multicenter study. Transplantation 2000;69:1348-52.
Dalakas MC. Mechanism of action of intravenous immunoglobulin and therapeutic considerations in the treatment of autoimmune neurologic diseases. Neurology 1998;51:S2-8.
Bombeli T, Müller M, Straub PW, Haeberli A. Cyclosporine-induced detachment of vascular endothelial cells initiates the intrinsic coagulation system in plasma and whole blood. J Lab Clin Med 1996;127:621-34.
Kawano PR, Yamamoto HA, Gerra R, Garcia PD, Contti MM, Nga HS, et al.
Acase report of venous thrombosis after kidney transplantation – We can save the graft? Time is the success factor. Int J Surg Case Rep 2017;36:82-5.
[Figure 1], [Figure 2]