Heart, renal, hepatic, and pancreatic transplantations are being performed with increasing frequency, leading to a greater demand for knowledgeable evaluation of vascular complications involving these grafts. Arterial anomalies associated with implantation of these grafts and arterial complications following transplantation, both present unique anatomic and physiologic problems. Arterial and venous stenoses and occlusions, pseudoaneurysms, and arteriovenous fistulas may occur in this patient population. Here, we summarize the most common arterial complications that take place in transplant recipients with a discussion of how to approach these complications.

There is a wide spectrum of vascular complications that can occur with renal transplantation. Fortunately renal artery complications are not very common. The most frequent arterial problems seen are renal artery stenosis, renal artery thrombosis, dissection of the external, internal iliac or common iliac arteries, renal artery pseudoaneurysm, and renal transplant arteriovenous fistula.

While postrenal transplant hypertension is a common problem, renal artery stenosis should be considered in patients presenting with severe or intractable hypertension after renal transplantation. Transplant renal artery stenosis (TRAS) is important to identify because it is a correctable form of hypertension. Although it can present at any time, renal artery stenosis usually becomes evident between 3 months and 2 years posttransplant.¹

Diagnosis of hemodynamically significant renal artery stenosis rests on a radiologic demonstration of ≥50% reduction in renal artery diameter.² The rationale for this assumption is derived from experimental evidence that the stenosis needs to occlude at least 50% of the lumen before renal blood flow and perfusion pressure start to decrease and systemic blood pressure increase.² The risk factors for renal transplant artery stenosis include atherosclerotic disease of donor or recipient vessels, cytomegalovirus (CMV) infection, delayed allograft function, and rejection.^3,4,5,6 In a recent retrospective study of 29 recipients with stenosis and a case-control group of 58 patients, an increased risk of stenosis was significantly associated with CMV infection (41% versus 12%) and delayed graft function (48% versus 16%).³

Renal artery stenosis can present with short segment, long segment, unifocal, and multifocal involvement. The prevalence of anastomotic renal transplant artery stenosis can be difficult to assess because of discrepancy in the definition of hemodynamically significant lesions and the use of different diagnostic modalities. Renal artery stenosis occurs in 1% to 12% of the patients after transplantation.⁷

Persistent, uncontrolled hypertension, flash pulmonary edema, and an acute elevation in blood pressure are other common features of this disorder and should alert the clinician.^8,9

Multiple techniques have been used to diagnose renal artery stenosis. Arteriography remains the procedure of choice for establishing the definitive diagnosis of renal artery stenosis after transplantation, but other noninvasive techniques such as duplex ultrasound (US), magnetic resonance (MR) angiography, and computed tomography (CT) angiography are increasingly utilized techniques to screen and/or diagnose transplant recipients for the presence of renovascular disease. It is essential to rule out renal parenchymal disease and usually a kidney biopsy is performed prior to angiography, since the presence of chronic renal allograft disease will decrease the likelihood of a successful response to correction of the stenosis and could be taken as a relative contraindication to intervention.^10,11

Doppler ultrasonography is the preferred screening modality for stenosis of the transplanted renal artery in many centers. The presence of a peak systolic velocity of ≥2.5 m/s has a sensitivity and specificity of 100% and 95% respectively.¹² However, Doppler US has the caveat of being highly operator-dependent. Recently, other noninvasive procedures such as MR angiogram or CT angiogram are increasingly being used for screening in some centers.

In a small series, combined analysis using gadolinium-enhanced MRA and three-dimensional phase contrast postgadolinium had shown sensitivities and specificities close to 100% in detecting stenosis.¹³ Spiral CT angiography has also been used as a noninvasive alternative to arteriography.^6,9

Most interventional radiologist or cardiologist taking care of these problems use measurement of pressures during the diagnostic angiography and try to demonstrate a gradient through a kink or stricture.¹⁴ In some instances, the diagnosis of TRAS even with angiography could be difficult, and some experts believe that kinks and strictures are significant if they create a gradient that ultimately will cause hypoperfusion of the graft, hypertension, and elevation of creatinine. In 2004, Chua et al. from St. George’s Hospital in London described that kinks of the transplant artery cause velocity gradients on Doppler US, but some will have no intraarterial pressure gradient across the kink. This particular subgroup of patients may not benefit from any intervention. They concluded that kinks of the renal transplant artery with normal intraarterial pressures do not appear to progress and threaten renal graft function. In this study, satisfactory graft outcomes were seen after 5-year follow-up with conservative therapy alone.¹⁴

The management options available to correct stenosis of the transplant renal artery include angioplasty, with or without stenting, and surgery. The utilization of medical treatment will result sometimes in resolution of the hypertension episode but will not treat the perfusion problem to the transplanted kidney.

For many years, surgical correction had been the only treatment option for TRAS, with reported correction rates ranging from 63% to 92%.¹⁵ The procedure, however, carries a significant risk of graft loss, uretheral injury, reoperation, and mortality.¹⁵

In the last few years, percutaneous transluminal revascularization has gained large popularity as a relatively noninvasive approach to improve both blood pressure control and kidney perfusion and is now considered the treatment of choice for patients with renal artery stenosis. Initial technical success of Percutaneous Transluminal Angioplasty (PTA) in the treatment of TRAS has been reported to be greater than 80% although effectiveness is strongly depended on center experience and on the type of the lesion.^11,16,17,18 Long-term clinical success defined as either improvement in blood pressure control or stabilization/improvement in renal function is reported to be 63% to 82% at 1 year,^11,17 with the restenosis rate after PTA to be in the range of 10% to 36%.^11,19,20 Endovascular stents have been used for the treatment of recurrent and/or ostial stenosis and in cases of suboptimal results with PTA. In addition, serious complications of PTA can be salvaged with stents. We found very few studies to date to assess the benefits of stent placement (TRAS). Stents have been used usually in the clinical scenario of recurrent or resistant TRAS,²¹ but may be necessary after the initial angioplasty if the problem is at the level of the ostium (Figure 52-1A,52-1B,52-1C).

The extensive fibrosis and scarring around the transplanted kidney makes surgical correction of a transplant artery stenosis difficult. Surgery should therefore be considered in few cases where severe arteriosclerotic disease is present and percutaneous approach has failed. A risk of graft loss after surgical vascular reconstruction has been reported in as many as 20% of cases and recurrence rates ranging from 7% to 15% after surgical intervention.²²

Thrombosis of the transplanted renal artery is a rare complication usually occurring immediately after transplantation. Posttransplant acute tubular necrosis (ATN) is responsible for approximately 90% of acute renal failure episodes occurring within the first few weeks following renal transplantation.²³ Most patients with ATN will eventually recover. ATN has to be distinguished from other causes of acute renal failure early after transplantation such as the renal artery thrombosis, hyperacute rejection, and obstruction of the urinary tract.²³ In the setting of renal artery thrombosis, conventional color Doppler US usually shows the absence of flow within the renal artery and graft. This can usually be confirmed by angiography. In some instances, hyperacute or severe acute rejection are associated with thrombosis of intrarenal branches and subsequent thrombosis of the main artery. Renal artery thrombosis can also be associated with technical problems, hypotension, hypercoagulable states, and atherosclerotic embolism. Renal infarction appears as a nonenhancing kidney with an enhancing capsule in the radioisotope renal scan. Thrombosis has been treated with percutaneous techniques using fibrinolytic agents or with surgical intervention with the intent of declotting the main renal artery, but the success rate is low and renal artery thrombosis usually results in loss of the renal allograft.

Iliac artery dissection can happen during dissection prior to actual implantation of the kidney or after reperfusion of the transplant kidney. Also dissection of the transplanted renal artery has been described.²⁴ Kidney transplant recipients have relatively higher incidence of peripheral vascular disease. Diabetes mellitus is the leading single cause of end-stage renal disease (ESRD). According to the 2002 Annual Data Report of the United States Renal Data System (USRDS), 42% of non-Hispanic dialysis patients in the United States have ESRD caused by diabetes.²⁵ Hypertension is the second leading cause of ESRD in adults, accounting for 25% of the cases. These two diseases are common risk factors for peripheral vascular disease.^26,27 The presence of calcified and partially occlusive atheromatous plaque in these vessels makes intima fragile and prone to separate if not handle appropriately. Careful dissection of iliac vessels as well as appropriate selection of site for vascular clamps and the anastomosis is cructial (Figure 52-2A and 52-2B). In several cases, utilization of special atraumatic vascular clamps are necessary in order to avoid intimal injury. The consequences of dissection of the iliac vessel or the renal artery can be diverse and include ischemia to the transplanted kidney and/or to the ipsilateral lower extremity. Isolated dissection of the renal artery can also occur specially in the presence of extensive renal artery atherosclerosis and calcified plaques that are more often present in older and extended criteria donors.

Intrarenal arteriovenous fistulas and pseudoaneurysms are usually caused by trauma during percutaneous needle biopsy. They occur in 1% to 18% of renal biopsies.²⁸ Pseudoaneurysms can occur at the vascular anastomosis, biopsy sites, or in association with infection.²⁹ This diagnosis of pseudoaneurysm should be considered when a hypoechoic or complex mass is near the vascular anastomoses or within a graft after biopsy. Usually duplex shows a disorganized, pulsatile flow within a hypoechoic, or variably complex perivascular mass. Arteriovenous fistulas may form when an artery and vein are lacerated; pseudoaneurysms result when only the artery is lacerated. Small pseudoaneurysms may resolve spontaneously; if they do not, they can be successfully treated with percutaneous transcatheter embolization. Seventy percent of all intrarenal arteriovenous fistulas and pseudoaneurysms close spontaneously with in 1 to 18 months.²⁸ They are usually asymptomatic but can manifest with hypertension and deterioration of renal function. Doppler US is the modality of choice for screening. Helical CT scan is a good alternative when US cannot define the nature of the lesion.

In order to be able to understand and treat arterial complications that occur in liver transplant recipients, one should have adequate knowledge of hepatic artery anatomy and its variants. The anatomy of the hepatic artery, and its anatomic variants, has been described in the literature starting with Haller in the eighteenth century, Tidemann in the nineteenth century and more recently by Flint and Michels in the twentieth century, 1930s, and 50s repetitively. An understanding of arterial anatomy is of importance in planning and performance of all surgical and radiologic procedures in the upper abdomen. Approximately 80% of the cases have the conventional anatomic configuration where the left and right hepatic arteries are the terminal branches of the main hepatic artery originating form the celiac axis^30,31,32 (Figure 52-3).

The left hepatic artery has its origin from the common hepatic artery trunk in most cases around 80% to 85% of cases, from the left gastric artery in approximately 15%, the splenic artery in aproximately 1%, from the gastroduodenal artery in 1% and rarely directly from the aorta or the celiac axis or the superior mesenteric artery. The aberrant left hepatic artery runs in the lesser omentum, traversing forward and medially. The right hepatic artery has its origin from the main trunk of the common hepatic artery in approximately 75% of the cases, from the superior mesenteric in approximately 18%, gastroduodenal artery in 4% to 6%, and rarely from the right gastric artery or the aorta. The anomalous right hepatic artery arising from the superior mesenteric or gastroduodenal artery runs a course to the right of the portal vein.^30,31

These are the most common variations but other less common variants have been described such as celiac axis and the superior mesenteric artery with common origin and a completely replaced system with the absence of celiac axis and hepatic artery arising from the superior mesenteric artery.

Advances in the care of recipients of liver transplantation in conjunction with refinements in surgical technique have contributed to a current 1-year survival of 90% or better after transplantation.^33,34 Recently, the utilization of living donor liver transplantation and split livers has revolutionized the field of liver transplantation.^35,36 Living donor liver transplants are performed routinely in pediatric population.^37,38 The ethics and outcome of living donor liver transplants in the adult population is under extensive scrutiny.^39,40 The utilization of partial grafts have made the arterial reconstruction during transplantation even more challenging because of the utilization of smaller vessels such as segmental left or right hepatic arteries for reconstruction.

Hepatic artery thrombosis (HAT) is the most common vascular complication following liver transplantation, seen in 5% of adult and 9% to 18% of pediatric liver transplantation.^41,42 HAT is associated with a significant mortality of 20% to 60% and is the second leading cause of graft failure in the early postoperative period. This may present clinically in different ways: massive hepatic necrosis; biliary leak as a result of bile duct ischaemia and necrosis, or recurrent sepsis. In some patients, HAT can be asymptomatic and that is the rationale for the utilization of routine Doppler US after liver transplantation in some centers.⁴³ Associated risk factors include increased, cold, ischemic time of the donor liver, ABO blood type incompatibility, small donor or recipient vessels, complex arterial reconstructions, and acute rejection.^44,45 Delayed HAT, which may occur years after transplantation, is associated with chronic rejection and sepsis. US will enable detection of approximately 95% of patent hepatic arteries.⁴⁶ The absence of color or spectral Doppler flow, often with a “wall thump” in the US, necessitates further investigation. Advances in the CT and MR angiography now provide further noninvasive techniques for imaging of the hepatic artery.^47,48 However, arteriography remains the definitive investigation, particularly if surgery is being considered (Figure 52-4). Hepatic artery stenosis (HAS) occurs in 3% to 5% of transplant recipients,⁴⁹ most commonly developing at the site of the anastamosis and early in the postoperative period, although late development is well recognized. HAS is usually attributed to surgical technique, graft rejection, or microvascular injury. Causes include clamp injury, intimal trauma caused by perfusion catheters at the time of surgery, or disrupted vasa-vasorum leading to ischemia of the arterial ends. In duplex US, HAS produces an intrahepatic tardus et parvus waveform, defined as prolonged systolic acceleration time with an RI <0.5.^50,51 In the setting of markedly diminished hepatic artery flow, such as in severe hepatic edema, systemic hypotension, or high-grade HAS, or in a suboptimal duplex US study, perhaps limited by patient obesity or gross ascites, interpretation of intrahepatic tardus-parvus waveforms should be performed with caution. In combination, these parameters have 85% to 97% sensitivity for detecting HAS.⁵⁰ Dodd et al.⁵⁰ found a sensitivity of 97% for significant hepatic artery complications (including thrombosis and stenosis) if one or more of the following Doppler US criteria were demonstrated: resistive index less than 0.5, acceleration time greater than 0.08 seconds, no flow in the main hepatic artery, or a peak hepatic artery velocity greater than 2 m/s. Spectral Doppler waveforms should be interpreted with caution in the intraoperative and immediate postoperative stage, as they may return to normal spontaneously. Clinically, it may lead to biliary ischemia, causing hepatic dysfunction and eventual hepatic failure. Treatment includes balloon angioplasty or retransplantation.