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1 Department of Radiology, Patrick 1, Fletcher Allen Health Care, University of Vermont College of Medicine, 111 Colchester Ave., Burlington, VT 05401.
Received April 10, 2001;
accepted after revision June 4, 2001.
Address correspondence to C. S. Morris.
Abstract
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MATERIALS AND METHODS. During a 5-year period, 212 patients (308 renal arteries) underwent percutaneous transluminal angioplasty or stent dilatation of the renal artery. Through a retrospective review of medical and radiology records, we determined that 13 of these patients suffered iatrogenic renal artery injuries.
RESULTS. The renal arterial complication rates were 4.2% per artery treated and 6.1% per patient treated. All 13 patients were successfully treated nonsurgically. Five patients with acute rupture of the renal artery were treated immediately with balloon tamponade or with placement of an additional stent or stent-graft. Six patients suffered acute thrombotic occlusion; five were successfully treated with thrombolysis, and one was successfully treated without thrombolysis by the placement of an additional stent. Presumed distal guidewire perforation caused subcapsular hematoma in one patient and a perirenal and pararenal hematoma in another; both were successfully treated with conservative management. During the clinical follow-up period (mean period, 19 months), one patient required long-term hemodialysis. No other patients required additional treatment.
CONCLUSION. The nonsurgical treatment of acute iatrogenic renal artery injuries occurring after renal artery angioplasty and stenting can be successful and may obviate additional surgery.
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Historically, the definitive treatment for traumatic renal artery rupture or pseudoaneurysm has been surgical repair [9,10,11,12]. However, in the age of PTA of the renal artery, two case reports have described the successful use of nonsurgical or percutaneous treatment strategies in the setting of iatrogenic renal artery rupture [13, 14]. More recently, other researchers have described successful treatment of an extensive iatrogenic renal artery dissection using a Wallstent (Schneider, Minneapolis, MN) [15] and successful treatment of a renal artery intimal injury using a Palmaz stent (Johnson & Johnson, Warren, NJ) [16].
We report our experience in the nonsurgical treatment of 13 patients with acute iatrogenic renal artery injuries sustained during renal artery angioplasty or stenting at a tertiary referral center.
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Patients
We identified 13 patients (8 women and 5 men; age range, 45-78 years; mean
age, 66 years) who sustained renal artery injuries serious enough to cause
acute rupture exhibiting extravasation at the angioplasty or stent site
(n = 5), acute thrombotic occlusion of the renal artery with
dissection (n = 5), acute thrombotic occlusion of an aortorenal
bypass graft (n = 1), and symptomatic subcapsular or perirenal and
pararenal hematoma requiring a blood transfusion or prolonged hospitalization
(n = 2).
All patients initially presented with ischemic nephropathy (serum
creatinine levels, 
1.4 mg/dL; range of preprocedure creatinine, 1.4-3.3
mg/dL; mean, 2.1 mg/dL) with the exception of two patients who presented only
with hypertension, and were referred for renal artery angioplasty. All
patients were hypertensive (systolic blood pressure, 160 mm Hg or
diastolic blood pressure, 90 mm Hg).
Initial Procedures
Nineteen renal arteries were treated initially with angioplasty procedures,
which were all performed using low-profile, high-pressure balloons (Ultrathin
or Ultrathin Diamond; Boston Scientific—Meditech, Watertown, MA). All
renal artery stent procedures were performed in patients in whom immediate
balloon angioplasty results were less than optimal. Balloon-expandable
metallic stents (Palmaz, Johnson & Johnson; Palmaz—Corinthian,
Cordis, Miami, FL) or balloon-expandable flexible stents (Intrastents; Sulzer
Intra Therapeutics, St. Paul, MN) hand mounted on balloon dilatation catheters
(Marshal; Boston Scientific—Meditech) were used. Seven patients
underwent bilateral renal artery dilatation. Stents were initially placed into
14 renal arteries, whereas angioplasty was the final dilatation procedure in
five renal arteries.
The diameter of the balloon used in the final angioplasty (n = 3) or stenting (n = 2) procedures for the five patients with renal artery rupture ranged between 5 and 7 mm; the mean diameter of the balloon was 6.2 mm. The balloon or stent size was estimated from the initial digital subtraction angiogram.
Six patients experienced acute thrombotic occlusion of the renal artery. One occulusion occurred after the PTA of a branch renal artery using a 4-mm diameter balloon, one after a 5-mm-diameter balloon PTA of a fibromuscular dysplastic lesion of the distal main renal artery located beyond a previously placed stent, one after PTA of a remotely placed stent in a saphenous vein aortorenal bypass graft, and the other three after placement of 5- (n = 2) and 6-mm (n = 1) stents in the proximal main renal arteries.
Four injuries resulting in thrombosis of the main renal artery were not recognized until the patients presented later. Three patients presented with anuria and flank pain (each had a single functioning kidney before the interventional procedure), and one presented with severe flank pain, diminished renal function, and CT findings indicative of renal artery thrombosis.
Three of these six patients with thrombotic occlusion showed clear evidence of medial dissection. The other three patients possibly also suffered a dissection, but mural defects on the postthrombolytic angiogram could not be definitively differentiated from residual mural thrombus. One patient was eventually diagnosed with a positive factor V Leiden hypercoagulable state.
Two patients suffered a subcapsular or perirenal and pararenal hematoma, presumably from distal guidewire perforation. Both of these were documented by a CT scan of the abdomen.
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Renal Artery Rupture Patients
Five patients suffered a rupture of the main renal artery, manifested by
acute extravasation of contrast material that was visualized on the renal
angiogram obtained immediately after dilatation. These patients were treated
with balloon tamponade (Fig.
1A,1B,1C).
The size of the angioplasty balloon chosen for tamponade was 1 mm smaller in
diameter than the size of the balloon or stent that caused the rupture, and
the balloon was fully inflated without the use of a manometer in all cases.
Two patients were treated with inflation of the balloon for a maximum of 3
min, followed by rapid deflation, and a repeat of the procedure after 2
min.
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However, one patient underwent a single 10-min balloon inflation procedure, another underwent a single 3-min balloon inflation, and the remaining patient underwent a single 1-min balloon inflation. The patient who underwent the 10-min balloon inflation also required a custom-made stent-graft that was deployed across the ruptured segment to facilitate hemostasis and repair of the renal artery. The stent-graft was made by prestretching a 4-mm-diameter thin-walled graft (ePTFE; Impra, Tempe, AZ) to 6 mm and attaching it to a Palmaz stent) with two 5-0 sutures (Prolene; Ethicon, Johnson & Johnson, Somerville, NJ), one at each end of the stent. The patient who had undergone the 3-min balloon inflation underwent angiography again 6 hr after the tamponade procedure. No extravasation was visualized. The patient who underwent the 1-min balloon inflation sustained a contained rupture through the renal artery ostium (visualized as extravasation into the subadventitial aortic wall) and was treated by placement of a second stent within the original stent followed by 2 min of balloon tamponade. After the treatment of each ruptured renal artery, a selective renal digital subtraction angiogram was obtained. No further extravasation was seen.
Renal Artery Thrombosis Patients
Six patients had acute thrombotic occlusion of the renal artery. One
occlusion occurred after 4-mm-balloon angioplasty of a branch renal artery,
one after a 5-mm-balloon angioplasty of a fibromuscular dysplastic lesion of
the distal main renal artery located beyond a previously placed stent, one
after angioplasty of a remotely placed stent within a saphenous
vein—aortorenal bypass graft, and the other three after placement of 5-
(n = 2) and 6-mm (n = 1) stents in the proximal main renal
arteries. Three of the six patients had clear evidence of medial dissection.
The other three patients possibly also had a dissection, but mural defects on
the postthrombolytic angiogram could not be definitively differentiated from
residual mural thrombus. One patient was eventually diagnosed with a positive
factor V Leiden hypercoagulable state.
Patients with acute thrombosis of the renal artery were treated with thrombolysis, except for one patient who was treated with an additional stent placed across an intimal dissection to reestablish patency. The patient was treated initially with pulse-spray thrombolysis using 250,000 IU of urokinase (Abbokinase; Abbot Laboratories, North Chicago, IL) over a 30-min period, followed by a double, coaxial drip infusion at a total rate of 120,000 IU/hr for 6 hr. An additional stent was placed to cover a dissection flap after complete thrombolysis was achieved.
The other four patients were treated with thrombolysis using tissue plasminogen activator (TPA) (Alteplase; Genentech, San Francisco, CA). The patient with the occluded aortorenal bypass graft received TPA via a double coaxial drip infusion into the thrombus at a rate of 1.0 mg/hr for 13 hr and an additional 15 mg of TPA that was injected directly into the graft over 30 min by the pulse-spray technique. Another patient with thrombotic occlusion of a renal artery stent was treated initially with TPA, using a double coaxial drip infusion at a total rate of 1.0 mg/hr for 8 hr, and with placement of an additional stent within the distal renal artery. The patient with fibromuscular dysplasia was treated with a high-dose infusion of TPA at 10 mg/hr for 1 hr after lacing of the thrombus with 15 mg of TPA. After the thrombolysis procedure, a stent was placed across an intimal dissection, several centimeters distal to the previously placed stent but located at the previous angioplasty site of an intimal web (Fig. 2A,2B,2C,2D). A third patient received 15 mg of TPA directly injected into the occluded renal artery stent by hand over 15 min. Because some thrombus persisted, an additional 15 mg of TPA was infused into the thrombus over 30 min, which resulted in complete thrombolysis. However, an intimal dissection was detected within the main renal artery at the distal end of the stent, which was treated with placement of an additional, overlapping stent.
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Perirenal, Pararenal, and Subcapsular Hematoma Patients
The patient with the subcapsular hematoma was treated conservatively with
observation and IV hydration, and the hematoma had decreased when a follow-up
CT scan was obtained 9 days after the procedure. The patient with the large
perirenal and pararenal hematoma was also successfully treated conservatively
with blood transfusions and volume IV hydration (Fig.
3A,3B).
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Clinical Follow-Up
Clinical follow-up ranged from 1 to 61 months (mean, 19 months). Five of
the nine patients with two functioning kidneys developed acute tubular
necrosis after the procedure. One patient, who had a preexisting renal
insufficiency and a preprocedure serum creatinine level of 3.3 mg/dL, did not
recover renal function and had to undergo long-term hemodialysis. The other
four patients recovered renal function, although the patient with the
subcapsular hematoma required temporary hemodialysis.
Four of the patients with a single functioning kidney recovered renal function, although one patient developed chronic renal insufficiency 61 months later associated with bilateral obstructive uropathy from bladder carcinoma. Two of the patients, both of whom had preexisting chronic renal insufficiency, required temporary hemodialysis, but all four patients are now alive and do not need dialysis. The follow-up period for this patient subgroup ranged from 3 to 61 months (mean, 26 months).
Of the two patients who presented with hypertension without renal insufficiency, one developed mild renal insufficiency with persistent hypertension, but was not dependent on dialysis when lost to follow-up 13 months after the procedure. The other patient had normal blood pressure and normal renal function 5 months after the procedure.
Three patients died during the follow-up period. In all three patients, cause of death was attributed to cardiac arrest unrelated to the angiographic procedure.
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Determining the true incidence of renal artery injury complications from renal artery angioplasty or stent dilatation procedures is difficult because reporting standards and definitions vary among studies [1,2,3,4,5]. Also, among interventional radiologists, criteria for reporting various complications are fraught with moderate rates of disagreement [18]. Another unknown is whether stent dilatation procedures in the renal artery carry a higher risk than angioplasty procedures in the same artery. In a recent prospective randomized comparison, stent dilatation patients had a slightly higher renal artery injury rate (7%) than angioplasty patients (5%) [19], although this was not a statistically significant difference.
We were able to manage each of our 13 iatrogenic renal artery injuries successfully without surgery. In each case, identifying the nature of the injury before choosing the most appropriate treatment option was important. Over the 5-year period, these treatments have evolved with the advent of new and innovative technologies.
The immediate treatment for acute iatrogenic rupture of the renal artery is balloon tamponade, which was performed in all five of our patients with documented extravasation. However, one of our patients was treated with placement of an additional stent after the failure of the initial balloon tamponade because stent placement has been used effectively in the past to treat iatrogenic venous rupture of dialysis grafts [20]. This patient was treated with additional balloon tamponade during the stent deployment, and so it is unclear whether the additional stent was effective in treating the rupture. Another patient was treated with yet another ancillary technique, the placement of a stent-graft, after the initial tamponade procedure was not successful. At the time of this patient's procedure, no stent-grafts were commercially available, so a custom-built stent-graft was placed successfully. Conceivably, a commercially manufactured stent-graft would be more readily available and easier to deploy.
All six of our patients with acute thrombotic occlusion of the renal artery were successfully treated without surgical bypass. One patient was treated with the placement of additional stents; as Morris et al. [21] have shown, patency can be quickly reestablished in acute occlusion with stenting, even in the presence of thrombus. Other researchers have also reported successful stenting of iatrogenic [15] and traumatic [16] renal artery dissections. Our other five patients with thrombotic occlusion were treated successfully with thrombolysis using urokinase or TPA. Thrombolysis with the use of streptokinase and urokinase has been shown to be very effective in the renal artery [22,23,24,25,26,27,28,29,30,31,32,33]. We have shown that successful thrombolysis of acute renal artery thrombotic occlusion with TPA is also possible.
Our two cases of presumed guidewire perforation, causing an isolated subcapsular hematoma in one patient and perirenal and pararenal hematoma in another, were both treated without surgery. We noted that the distal guide wire tip formed a looped configuration during the procedure in the patient with the perirenal and pararenal hematoma and clearly did not conform to boundaries of the vessel lumen. This guidewire tip may have been in an extravascular location, causing perforation of an intrarenal branch artery, an injury that was not recognized during the procedure. We did not perform a second angiogram on either of these patients. However, if any sign of persistent hemorrhage or hemodynamic instability had been evident, a second angiogram and a possible transcatheter embolization procedure would have been performed, if indicated.
We believe that these distal branch renal artery injuries are analogous to many injuries caused by blunt renal trauma. Over the past decade, the trauma literature has supported the conservative management of grade I, grade II, and many grade III blunt renal trauma injuries to decrease the nephrectomy rate in these patients [34]. We also believe that iatrogenic causes of subcapsular, perirenal, or pararenal hematoma can be successfully treated with conservative measures, if the patient is hemodynamically stable and shows no evidence of persistent hemorrhage.
In conclusion, we have described the successful nonsurgical treatment of 13 consecutive cases of iatrogenic renal artery injuries, which included rupture of the main renal artery; acute thrombotic occlusion and dissection of the renal artery; and subcapsular, perirenal, and pararenal hematoma. In selected patients, we believe that nonsurgical treatment techniques can be successful and, therefore, obviate further invasive surgery.
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