Endovascular Management of Renal Ischemia in a Patient with Acute Aortic Dissection and Renovascular Hypertension

Endovascular Management of Renal Ischemia in a Patient with Acute Aortic Dissection and Renovascular Hypertension

Endovascular Management of Renal Ischemia in a Patient with Acute Aortic Dissection and Renovascular Hypertension Benjamin W. Starnes, MD, Sean D. O'D...

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Endovascular Management of Renal Ischemia in a Patient with Acute Aortic Dissection and Renovascular Hypertension Benjamin W. Starnes, MD, Sean D. O'Donnell, MD, David L. Gillespie, MD, James M. Goff, MD, Patricio Rosa, MD, and Norman M. Rich, MD, Washington, D.C.

We report the endovascular management of a patient with a type B aortic dissection complicated by renal ischemia and resultant severe hypertension. A 69-year-old male presented with acute type B aortic dissection with proximal extension complicated by severe renovascular hypertension secondary to left renal ischemia. Endovascular management consisted of imaging with intravascular ultrasound and left renal artery stenting with balloon-expandable stents. His hypertension subsequently resolved and he was discharged on his baseline two-drug regimen. Management of the ischemic complications of type B aortic dissections may be primarily approached using endovascular methods in stable patients, with open surgery reserved for those patients refractory to these methods. Patients with evidence of decreased renal perfusion represent a select group with an increased risk of associated morbidity and mortality and should therefore be aggressively managed. Accurate information and assessment of anatomy can be obtained with intravascular ultrasound and is therefore an important adjunct to the armamentarium of endovascular specialists managing complications of aortic dissection.

INTRODUCTION Aortic dissection, the most frequent aortic emergency, is complicated by ischemia of peripheral vascular beds in approximately 30% of patients.1,2 Traditionally, aortic dissections have been divided into those involving the ascending aorta (Stanford type A) and those not involving the ascending aorta (Stanford type B). Indications for urgent surgical intervention include any patient with dissection involving the ascending aorta and any evidence of associated peripheral vascular com-

Walter Reed Army Medical Center, Washington, DC. Correspondence to: B.W. Starnes, MD, Vascular Surgery Service, Walter Reed Army Medical Center, Washington, DC, 20307-5001, USA, E-mail: [email protected]. Ann Vasc Surg 2001; 16: 368-374 DOI: 10.1007/s10016-001-0184-7 Ó Annals of Vascular Surgery Inc. Published online: 18 April 2002 368

promise to include mesenteric, renal, and/or lower limb ischemia. Overall operative mortality increases sharply with concurrent compromise of peripheral vascular beds.1,3 Percutaneous endovascular techniques to relieve end-organ ischemia have been championed over the past decade with variable success.3-7 We present a case of acute Stanford type B aortic dissection with proximal extension and concurrent renovascular hypertension successfully managed by percutaneous stenting of the affected renal artery. Options for management of these complex issues are discussed. The necessity for routine use of intravascular ultrasound (IVUS) in the management of complicated aortic dissections is suggested.

CASE REPORT A 69-year-old African-American male presented to the emergency department in January 2001 complaining of the acute onset of sharp abdominal pain

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Fig. 1. Preoperative contrast-enhanced CT demonstrating aortic dissection with A arch involvement, B false lumen perfusing the celiac axis, C true lumen perfusing the superior mesenteric artery, and D left renal artery perfused by false lumen.

radiating to the back 11 days earlier with progressive obstipation. Past medical history was notable for two-drug hypertension, gastroesophageal re¯ux disease, and benign prostatic hypertrophy; his only surgery was an appendectomy in 1948. Physical examination was notable for a blood pressure of 210/110, heart rate of 102, and temperature of 99.2. A systolic ejection murmur was noted on precordial auscultation and on abdominal examination he had a mildly tender abdomen with the absence of peritoneal signs. Peripheral vascular examination was normal with anklebrachial indices of >1.0 bilaterally. A contrast-enhanced CT scan of the chest, abdomen, and pelvis revealed an aortic dissection, Stanford type B. The false lumen began just beyond the origin of the left subclavian artery, continuing to the abdominal aorta and involving the celiac and left renal arteries with termination at the aortic bifurcation (Fig. 1). The patient was admitted to the intensive care unit (ICU) for strict control of heart rate and blood pressure in a monitored setting. To attain this level of control, six antihypertensive medications were required: intravenous infusion of sodium nitroprusside (100 mg/250 cc), and oral

labetolol (600 mg bid), hydralazine (100 mg qid), clonidine (0.3 mg tid), maxide (25/37.5 qd), and valsartan (160 mg qd). Blood chemistries on admission were remarkable for hematocrit of 37.9%, creatinine of 1.1 mg/dL, and a urinalysis negative for hematuria. Despite good control of hypertension and heart rate, weaning from intravenous medications was not possible over a period of 3 days. A diagnostic arteriogram with access obtained through the right common femoral artery and into the true lumen con®rmed the previous CT ®ndings (Fig. 2). An ectatic aortic arch was immediately noted and the origin of the dissection appeared to be just distal to the left subclavian artery. The true lumen perfused the superior mesenteric artery and two right renal arteries. The false lumen perfused the celiac axis. The left renal artery, perfused by the true lumen, was involved in the aortic dissection plane and was compressed by the false lumen (Fig. 3). IVUS was then performed with a Visions PV Five-648.2 Fr, 8.354 MHz probe (Jomed [formerly Endosonic], Rancho Cordova, CA) and revealed proximal extension of the dissection from the left subclavian artery to

370 Case reports

Annals of Vascular Surgery

Fig. 2. A Diagnostic arch aortogram and B post-procedural arch MRI demonstrating dissection originating at the level of the left subclavian artery.

Fig. 3. A Selective arteriogram of the left renal artery demonstrating compression of the renal artery true lumen by the false lumen. B Artist's rendition of current case.

the distal ascending aorta, with all arch vessels perfused by the true lumen (Fig. 4). The patient was then heparinized with 5,000 units of unfractionated heparin. The left renal artery was selected with a 5 Fr C2-catheter, and a 0.035 inch Glidewire (Terumo, Boston Scienti®c/ Medi-Tech, Natick, MA) passed without dif®culty. Primary stenting was accomplished ®rst with a P154 Palmaz stent (Cordis Endovascular, Warren, NJA) and then an overlapping P294 Palmaz stent (Cordis Endovascular) into the true lumen (Fig. 5). The stents were then ballooned with a 6 mm ´ 4 cm Opta-LP (Cordis Endovascular) and the more proximal stent was ¯ared into the true lumen with an 8-mm balloon (Power¯ex Plus, Cordis Endovascular). Completion angiography demonstrated a patent left renal artery without stenosis (Fig. 6).

The patient was returned to the ICU, where his requirement for antihypertensives returned to a baseline of two oral medications, and he was transferred to the ward 36 hr later. The patient was then evaluated by the cardiothoracic surgery service for proximal arch extension and a decision was made to follow up with serial MRI. The patient's blood pressure has been controlled on his baseline two-drug regimen, and repeat MRI showed no change at 9 months.

DISCUSSION The management of ischemic complications of aortic dissection has undergone a revolution in the past decade with the advent of percutaneous endovascular options. Classically, patients with type A dissections were referred for immediate surgical

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Fig. 4. Intravascular ultrasound of the proximal aortic arch demonstrating A transverse and saggital image with cursor in left subclavian artery and dissection beginning just beyond it and B same transverse image with saggital view rotated demonstrating more proximal extension of the dissection.

repair of the ascending aorta due to complications related to dissection into the aortic root that could result in valvular insuf®ciency, pericardial tamponade, or myocardial ischemia by occlusion of the origins of the coronary arteries. The management of type B dissections has consisted primarily of medical management, with surgery reserved for patients with evidence of end-organ ischemia or aneurysmal degeneration. These complications are typically manifested by mesenteric ischemic symptoms, renovascular hypertension, or lower extremity ischemia and occur in approximately 30% of all patients with aortic dissection.1,2 Open surgical repair of these ischemic complications has been associated with a mortality rate exceeding 50%.1,2 Some investigators have advocated correction of life-threatening ischemic complications

prior to de®nitive repair of an aortic dissection, and endovascular therapy has been increasingly recognized as an attractive alternative to open repair in restoring perfusion to ischemic vascular beds.2-4 The ®rst described surgery performed for complications due to aortic dissection was by Gurin in 1935 on a patient with right iliac occlusion.8 Several isolated attempts at repair were then reported, until 1954, when DeBakey et al. reported the successful repair of a type A dissection in a 58-year-old patient.9 In 1982, DeBakey reported his 28-year experience with 527 patients. Operative mortality was 20% for type I (DeBakey classi®cation), 8% for type II, and 16% for type III.10 In 1988, Cambria et al. described their 21-year experience with 325 cases of aortic dissection, with speci®c attention given to aortic branch compro-

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Fig. 5. Left renal artery after placement of a Palmaz balloon-expandable P154 stent followed by an overlapping P294 stent.

mise, which occurred in 107 patients, or 33%. The overall mortality rate was signi®cantly higher for patients with evidence of aortic branch compromise (51%) than in those without such complications (29%).2 In 1990 Fann et al. described their management of aortic dissection in 272 patients presenting with peripheral vascular complications (31%), over a 25-year span.1 The overall mortality was 25% ‹ 3% for all patients presenting with aortic dissection, but for a subset of patients with evidence of end-organ ischemia, mortality was high, with a rate of 50% ‹ 11% for those with decreased renal perfusion. Multivariate analysis revealed that impaired renal perfusion was the single-most signi®cant predictor of increased risk for operative mortality.1 Endovascular management of the ischemic complications of aortic dissection was ®rst reported in 1992 by Lacombe et al. in Boulogne-Billancourt, France, who described the endovascular management of a patient presenting with deteriorating renal function after subacute aortic dissection.11 The largest institutional experience is from Stanford, and Dake and Slonim et al. have reported their experience there from 1996 to 1999.3,4 Forty patients underwent percutaneous intervention (fenestration or stenting) for ischemic complications of acute aortic dissection. Decreased renal perfusion was noted in 30 (75%) and 22 subsequently underwent renal artery stenting. There was a 25% mortality rate throughout the entire series. Of the 30 patients with renal ischemia, 9 (30%) suffered early deaths. Of these nine patients, four had bowel resections for mesenteric ischemia and seven required dialysis. Of those with only renal involvement, there was one early mortality

Annals of Vascular Surgery

Fig. 6. Completion angiography demonstrating prompt uptake of contrast into the left kidney that was not present on initial ®lms.

(10%).3 Mesenteric ischemia was noted to signi®cantly increase mortality. Although this was a small series of patients, it represents the largest collective experience to date and demonstrated considerably less mortality (25% vs. >50%) than that with open surgical repair for ischemic complications of aortic dissection. From a review of recent series and case reports, overall mortality for patients undergoing endovascular management of renal ischemia in conjunction with aortic dissection was 22.2% (Table I). Peripheral vascular complications of aortic dissection therefore remain a morbid condition, yet mortality is markedly improved when compared with traditional surgical repair of ischemic vascular beds. Two alternatives exist for the endovascular management of ischemic complications of aortic dissection. Endovascular aortic fenestration is a process in which an opening is created in the aortic septum with the use of a needle and subsequent wire access to the contralateral lumen, followed by balloon angioplasty.3,4,12 This allows for equalization of pressures between true and false lumens and subsequent ¯ow of blood from the true lumen into the isolated ischemic arterial branch within the false lumen. This procedure is often accompanied by aortic stenting in an attempt to obliterate the false lumen in the region of ischemia. This technique has had variable results and those most experienced with endovascular fenestration have recently reserved it for patients presenting with lower limb ischemia and dissection involving the aortic bifurcation.3 The other endovascular technique for relief of ischemic complications is stenting of compromised vascular beds with either balloon-expandable or

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Table I. Review of endovascular management (fenestration ‹ stenting) of patients with aortic dissection and renal ischemia

Reference

With renal ischemia (n)

Stent s (n)

Mortality [n = (%)]

Initial success (%)

Average follow-up (months)

Lacombe et al. (1992)1 Walker et al. (1993)5 Hata et al. (1997)13 Park et al. (1997)12 Slonim et al. (1999)3 Manke et al. (1999)7 Behrendt et al. (2000)6 Starnes et al. (2001) Total

1 5 1 1 30 4 2 1 45

1 7 1 0 22 5 2 1 37

0 1 (20) 0 0 9 (30) 0 0 0 10 (22.2)

100 100 100 100 93 100 100 100 99.13

5 9 12 0.2 29 5.8 19.5 9 11.19

self-expanding stents.3,5-7,11,13 This is accomplished by ®rst gaining wire access to the vessel in question. Wire access can at times be dif®cult if the origin of the involved artery has been avulsed from the aortic septum. Percutaneous balloon angioplasty alone is usually unsuccessful because of vessel recoil.5,13 Stenting into the true lumen allows for perfusion without compression by the surrounding false lumen. If true lumen obliteration has occurred, stent deployment within the true lumen combined with either fenestration and/or branch vessel stenting has been advocated.4 Renovascular hypertension can be a devastating disease process in this subgroup of patients. Renal artery compromise causes rennin-dependent hypertension, which is notoriously dif®cult to control and may further exacerbate the aortic dissection. All reports of primary stenting for renal ischemia associated with aortic dissection have demonstrated complete resolution of hypertensive symptoms or at least a return to baseline antihypertensive regimens. In all studies reviewed, hypertension resolved after intervention.3,5-7,12,13 IVUS is capable of displaying real-time crosssectional imaging of arterial vasculature and the technology supporting IVUS has progressed substantially since its introduction into clinical use in the early 1990s. Image resolution is superior and probes with improved resolution provide for accurate assessment of vascular anatomy. Software is now available for three-dimensional and rotational imaging which allows for a single pass of the probe and storing of images for later viewing.14 IVUS can be used to differentiate the true from the false lumen in aortic dissections, and in cases where conventional aortography cannot de®ne the distal extent of the dissection, IVUS can.15 In our case report, IVUS was used to de®ne the level of the dissection and involved branch arteries. IVUS is superior to two-

dimensional arteriography with respect to volume of information and absence of contrast risk. In our case, IVUS actually demonstrated proximal extension of an aortic dissection that was not determined on either CT or follow-up MRI.

CONCLUSIONS Management of the ischemic complications of type B aortic dissections may be primarily approached using endovascular methods in stable patients, with open surgery reserved for those patients refractory to these methods. Patients with evidence of decreased renal perfusion represent a select group with an increased risk of associated morbidity and mortality and should therefore be aggressively managed. An endovascular approach to aortic dissection has been increasingly recognized as an attractive alternative to open repair in restoring perfusion to ischemic vascular beds. It seems intuitive that any patient with a diagnosis of acute aortic dissection presenting with renovascular hypertension should be approached with every intention to expeditiously correct the malperfusion with an endovascular approach. This approach carries the highest chance of success and is associated with markedly lower morbidity than that with open surgical repair. IVUS can provide accurate information and assessment of anatomy and represents an important adjunct to the armamentarium of endovascular specialists managing complications of aortic dissection. REFERENCES 1. Fann JI, Sarris GE, Mitchell RS, et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990;212:705-713. 2. Cambria RP, Brewster DC, Gertler J, et al. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988;7:199-209.

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3. Slonim SM, Miller DC, Mitchell RS, Semba CP, Razavi MK, Dake MD. Percutaneous balloon fenestration and stenting for life-threatening ischemic complications in patients with acute aortic dissection. J Thorac Cardiovasc Surg 1999;117:1118-1126. 4. Slonim SM, Nyman UR, Semba CP, Miller DC, Mitchell RS, Dake MD. True lumen obliteration in complicated aortic dissection: endovascular treatment. Radiology 1996;201: 161-166. 5. Walker PJ, Dake MD, Mitchell RS, Miller DC. The use of endovascular techniques for the treatment of complications of aortic dissection. J Vasc Surg 1993;18:10421051. 6. Behrendt P, Do D, Baumgartner I, Triller J, Kniemeyer H, Mahler F. Renal artery stenting following acute aortic dissection: implantation and follow-up. Vasa 2000;29:138-140. 7. Manke C, Strotzer M, Seitz J, et al. Ischemic complications in aortic dissectionÐpercutaneous treatment with balloon fenestration and stent implantation [in German]. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1999;170:198-204. 8. Gurin D. Dissecting aneurysm of the aorta. NY State J Med 1935;35:1200-1202.

Annals of Vascular Surgery

9. DeBakey ME. Surgical considerations of dissecting aneurysm of the aorta. Ann Surg 1955;142:586-612. 10. DeBakey ME, McCollum CH, Crawford ES, et al. Dissection and dissecting aneuryms of the aorta: twenty-year followup of ®ve hundred twenty-seven patients treated surgically. Surgery 1982;92:1118-1134. 11. Lacombe P, Mulot R, Labedan F, et al. Percutaneous recanalization of a renal artery in aortic dissection. Radiology 1992;185:829-831. 12. Park JH, Chung JW, Cho YK, Kim SH, Ahn H, Oh BH. Percutaneous fenestration of aortic dissection: salvage of an ischemic solitary left kidney. Cardiovasc Intervent Radiol 1997;20:146-148. 13. Hata M, Zuguchi M, Saito H, Tabayashi K. Stent angioplasty for renovascular disease associated with acute aortic dissection. Ann Thorac Surg 1997;63:244-246. 14. Cavaye DM, White RA, Kopchok GE, Mueller MP, Maselly MJ, Tabbara MR. Three-dimensional intravascular ultrasound imaging of normal and diseased canine and human arteries. J Vasc Surg 1992;16:509-517. 15. Pande A, Meier B, Fleisch M, Kammerlander R, Simonet F, Lerch R. Intravascular ultrasound for diagnosis of aortic dissection. Am J Cardiol 1991;67:662-663.