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Department of Radiology
Seth G.S. Medical College and K.E.M. Hospital, Mumbai , India
Interventional Case Record
Interventional Case Record
Contributed by : Aishwarya Bagde
Contributed by : Aishwarya Bagde
Endovascular salvage of renal artery stent thrombosis
Endovascular salvage of renal artery stent thrombosis
Introduction:
Introduction:
Stent thrombosis (ST) is defined as “an acute thrombotic occlusion in the stented segment of anl artery.” In spite of progress in stent technology, the safety and efficacy of patients with renal artery stenosis, ST remains serious and potentially life-threatening complication of percutaneous transluminal angioplasty with stent [1]. It usually presents with flash pulmonary edema with anuria which is associated with a high mortality rate. One of the most significant precipitating factors for stent thrombosis is the premature cessation of antiplatelet therapy.[2]
Stent thrombosis (ST) is defined as “an acute thrombotic occlusion in the stented segment of anl artery.” In spite of progress in stent technology, the safety and efficacy of patients with renal artery stenosis, ST remains serious and potentially life-threatening complication of percutaneous transluminal angioplasty with stent [1]. It usually presents with flash pulmonary edema with anuria which is associated with a high mortality rate. One of the most significant precipitating factors for stent thrombosis is the premature cessation of antiplatelet therapy.[2]
Case Presentation:
Case Presentation:
We present the case of a patient who developed acute stent thrombosis due to cessation of anti-platelet agents and his management. This 62-year-old man came with uncontrolled hypertension on three antihypertensive drugs and a diuretic. Stenting had done in July 2010.
We present the case of a patient who developed acute stent thrombosis due to cessation of anti-platelet agents and his management. This 62-year-old man came with uncontrolled hypertension on three antihypertensive drugs and a diuretic. Stenting had done in July 2010.
Investigations done were--
Investigations done were--
▪ Serum creatinine = 1.8 mg/dL
▪ Serum creatinine = 1.8 mg/dL
▪ Sonogram of the abdomen = Small sized left kidney, Bilateral renal artery stenosis
▪ Sonogram of the abdomen = Small sized left kidney, Bilateral renal artery stenosis
▪ DTPA scan - Right kidney GFR = 54 %, Left kidney GFR = 3 %
▪ DTPA scan - Right kidney GFR = 54 %, Left kidney GFR = 3 %
Initial Stenting 2010: Right renal catheter angiogram showed severe right renal ostial stenosis with mild post stenotic dilatation. (Figure 1). The stenosis was negotiated with a Cordis stabiliser wire and over this, balloon mounted stenting was done (Figure 2 to 4). Post renal stenting angiogram shows resolution of the stenosis and good nephrogram (Figure 5).
Initial Stenting 2010: Right renal catheter angiogram showed severe right renal ostial stenosis with mild post stenotic dilatation. (Figure 1). The stenosis was negotiated with a Cordis stabiliser wire and over this, balloon mounted stenting was done (Figure 2 to 4). Post renal stenting angiogram shows resolution of the stenosis and good nephrogram (Figure 5).
Fig. 1: Selective angiogram of left renal artery showing significant proximal renal artery stenosis
Fig. 2: the stabilizer wire is seen in the distal segment of right renal artery (white arrow marked).
Fig. 3: showing the balloon mounted stent placed over the stenotic region over the stabilizer-wire across stenosis
Fig. 4: showing the balloon mounted stent is deployed by inflation of balloon over the stenotic region over the stabilizer-wire across stenosis
Fig. 5: Post renal artery stenting angiogram showing resolution of stenosis
After 18 months the patient was readmitted with accelerated hypertension, paroxysmal nocturnal dyspnea with multiple episodes of flash pulmonary edema. On admission, the blood pressure was 200/100 mmHg, with history of discontinuing anti-platelets three months after procedure. The patient was on five anti-hypertensive and two diuretic medications and required dialysis twice a week. The patient developed anuria after two days of admission.
After 18 months the patient was readmitted with accelerated hypertension, paroxysmal nocturnal dyspnea with multiple episodes of flash pulmonary edema. On admission, the blood pressure was 200/100 mmHg, with history of discontinuing anti-platelets three months after procedure. The patient was on five anti-hypertensive and two diuretic medications and required dialysis twice a week. The patient developed anuria after two days of admission.
Investigations at the present admission--
Investigations at the present admission--
▪ Serum creatinine - 8.0 mg/dL
▪ Serum creatinine - 8.0 mg/dL
▪ Renal artery Doppler reveals increased velocity and acceleration time and stent stenosis in the right renal artery.
▪ Renal artery Doppler reveals increased velocity and acceleration time and stent stenosis in the right renal artery.
▪ DPTA: Right kidney GFR = 14.89 %, Left kidney GFR= 1.98 %.
▪ DPTA: Right kidney GFR = 14.89 %, Left kidney GFR= 1.98 %.
Interventional technique:
Interventional technique:
Through femoral access using 5Fr RDC catheter an angiogram was done. The right renal angiogram shows complete occlusion of the stent with non-opacification of renal artery. (Figure 6) Subsequently the stabiliser wire was negotiated through the thrombosed stent region and is seen at distal segment of renal artery. (Figure 7). A monorail balloon mounted stent was then negotiated into the original stent and deployed within it. (Figure 8 to 10). Post deployment angiogram shows resolution of thrombotic occlusion and perfusion of right kidney. (Figure 11, 12) . Post stent plasty there is improvement t into the urine output from being anuric to 1700 cc within 24 hours and subsequently 2000cc till 48 hrs of procedure. Similarly the serum creatinine levels were reduced from being 8 mg/dL to 3.6 mg/dL within 24 hours of procedure. Post re-stenting after five days the urine output was 2000- 2200 cc and serum creatinine was 1.1 mg/dL . The patient was discharged with three antihypertensive drugs - with no diuretic drug.
Through femoral access using 5Fr RDC catheter an angiogram was done. The right renal angiogram shows complete occlusion of the stent with non-opacification of renal artery. (Figure 6) Subsequently the stabiliser wire was negotiated through the thrombosed stent region and is seen at distal segment of renal artery. (Figure 7). A monorail balloon mounted stent was then negotiated into the original stent and deployed within it. (Figure 8 to 10). Post deployment angiogram shows resolution of thrombotic occlusion and perfusion of right kidney. (Figure 11, 12) . Post stent plasty there is improvement t into the urine output from being anuric to 1700 cc within 24 hours and subsequently 2000cc till 48 hrs of procedure. Similarly the serum creatinine levels were reduced from being 8 mg/dL to 3.6 mg/dL within 24 hours of procedure. Post re-stenting after five days the urine output was 2000- 2200 cc and serum creatinine was 1.1 mg/dL . The patient was discharged with three antihypertensive drugs - with no diuretic drug.
Fig. 6: Selective renal angiogram showing complete blockage of the stentdue to acute thrombosis. (white arrow)
Fig. 7: Fluoroscopic image showing crossing of guide-wire which is seen in the distal segment of right renal artery.
Fig. 8, 9 : Fluoroscopic image showing deployment of balloon mounted stent within the stent in right renal artery. (White arrow)
Fig. 10: Fluoroscopic image showing complete an angioplasty balloon completely inflated in the renal ostial region
Fig. 11, 12 : Post stenting angiogram showing resolution of stent occlusion with good filling of the renal artery.
Discussion
Discussion
Stent thrombosis (ST) is defined as “an acute thrombotic occlusion in the stented segment of a renal artery.” ST is a serious and potentially life-threatening complication after percutaneous intervention [1,2]. ST is categorised as acute (<24 hours), subacute (between 24 hours and 30 days), and late (extending past 30 days). In general, early ST is more common, accounting for 50–70% of all cases. [2-4]
Stent thrombosis (ST) is defined as “an acute thrombotic occlusion in the stented segment of a renal artery.” ST is a serious and potentially life-threatening complication after percutaneous intervention [1,2]. ST is categorised as acute (<24 hours), subacute (between 24 hours and 30 days), and late (extending past 30 days). In general, early ST is more common, accounting for 50–70% of all cases. [2-4]
The most common differential diagnosis is restenosis. While stent thrombosis is an acute occlusion that causes acute in presentation, restenosis is a slow and progressive process that involves the narrowing of the stent lumen due to the growth of biologically fibrous neointimal around the stem, resulting in renal failure. The mechanisms underlying stent thrombosis are multifactorial (Table-1) and include patient-related factors, procedural factors (including stent choice), and post-procedural factors (including type and duration of anti-platelet therapy). Numerous strategies may be employed to reduce the occurrence of stent thrombosis (Table-2) [6]
The most common differential diagnosis is restenosis. While stent thrombosis is an acute occlusion that causes acute in presentation, restenosis is a slow and progressive process that involves the narrowing of the stent lumen due to the growth of biologically fibrous neointimal around the stem, resulting in renal failure. The mechanisms underlying stent thrombosis are multifactorial (Table-1) and include patient-related factors, procedural factors (including stent choice), and post-procedural factors (including type and duration of anti-platelet therapy). Numerous strategies may be employed to reduce the occurrence of stent thrombosis (Table-2) [6]
References:
References:
1. Cutlip DE, Nakazawa G, Krucoff MW, Vorpahl M, Mehran R, Finn AV, Vranckx P, Kimmelstiel C, Berger C, Petersen JL, Palabrica T, Virmani R. Autopsy validation study of the academic research consortium stent thrombosis definition. JACC Cardiovasc Interv. 2011 May;4(5):554-9.
1. Cutlip DE, Nakazawa G, Krucoff MW, Vorpahl M, Mehran R, Finn AV, Vranckx P, Kimmelstiel C, Berger C, Petersen JL, Palabrica T, Virmani R. Autopsy validation study of the academic research consortium stent thrombosis definition. JACC Cardiovasc Interv. 2011 May;4(5):554-9.
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5. Van Werkum JW, Heestermans AA, Zomer AC, Kelder JC, Suttorp MJ, Rensing BJ, Koolen JJ, Brueren BR, Dambrink JH, Hautvast RW, Verheugt FW, ten Berg JM. Predictors of coronary stent thrombosis: the Dutch Stent Thrombosis Registry. J Am Coll Cardiol 2009; 53:1399–1409.
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6. Nakamura S, Colombo A, Gaglione A, Almagor Y, Goldberg SL, Maiello L, Finci L, Tobis JM. Intracoronary ultrasound observations during stent implantation. Circulation. 1994; 89: 2026–2034.
7. Roy P, Steinberg DH, Sushinsky SJ, Okabe T, Pinto Slottow TL, Kaneshige K, Xue Z, Satler LF, Kent KM, Suddath WO, Pichard AD, Weissman NJ, Lindsay J, Waksman R. The potential clinical utility of intravascular ultrasound guidance in patients undergoing percutaneous coronary intervention with drug-eluting stents. Eur Heart J. 2008; 29: 1851–1857.
7. Roy P, Steinberg DH, Sushinsky SJ, Okabe T, Pinto Slottow TL, Kaneshige K, Xue Z, Satler LF, Kent KM, Suddath WO, Pichard AD, Weissman NJ, Lindsay J, Waksman R. The potential clinical utility of intravascular ultrasound guidance in patients undergoing percutaneous coronary intervention with drug-eluting stents. Eur Heart J. 2008; 29: 1851–1857.
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