Indian Journal of Radiology and Imaging Indian Journal of Radiology and Imaging

TRANSPLANT IMAGING
Year
: 2014  |  Volume : 24  |  Issue : 4  |  Page : 339--349

Imaging in pancreatic transplants


Matthew T Heller1, Puneet Bhargava2,  
1 Department of Radiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
2 Department of Radiology, University of Washington Harborview Medical Center, Seattle, Washington, USA

Correspondence Address:
Matthew T Heller
University of Pittsburgh Medical Center, 200 Lothrop Street, Suite 3950 PST, Pittsburgh, Pennsylvania - 15213
USA

Abstract

Pancreatic transplantation, performed alone or in conjunction with kidney transplantation, is an effective treatment for advanced type I diabetes mellitus and select patients with type II diabetes mellitus. Following advancements in surgical technique, postoperative management, and immunosuppression, pancreatic transplantation has significantly improved the length and quality of life for patients suffering from pancreatic dysfunction. While computed tomography (CT) and magnetic resonance imaging (MRI) have more limited utility, ultrasound is the preferred initial imaging modality to evaluate the transplanted pancreas; gray-scale assesses the parenchyma and fluid collections, while Doppler interrogation assesses vascular flow and viability. Ultrasound is also useful to guide percutaneous interventions for the transplanted pancreas. With knowledge of the surgical anatomy and common complications, the abdominal radiologist plays a central role in the perioperative and postoperative evaluation of the transplanted pancreas.



How to cite this article:
Heller MT, Bhargava P. Imaging in pancreatic transplants .Indian J Radiol Imaging 2014;24:339-349


How to cite this URL:
Heller MT, Bhargava P. Imaging in pancreatic transplants . Indian J Radiol Imaging [serial online] 2014 [cited 2020 Jul 4 ];24:339-349
Available from: http://www.ijri.org/text.asp?2014/24/4/339/143896


Full Text

 Introduction



Pancreatic transplantation is effective for achieving normoglycemia in patients with insulin-dependent diabetes mellitus (type I) and in select patients with type II diabetes mellitus. [1],[2],[3] Additionally, pancreatic transplantation counteracts the complications of diabetes mellitus, including diabetic neuropathy and retinopathy. [4],[5] The increasing success of the procedure is largely due to refinements of surgical technique, postoperative management, and immunosuppression. [6],[7],[8] Pancreatic transplantation typically utilizes a cadaveric allograft and is most commonly performed in conjunction with a kidney transplant; [4] this combined transplantation procedure has been shown to increase the survival of the patients and the transplanted organs. [9],[10] While ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MRI) can all be effectively used to image the pancreatic transplant, US is the preferred initial imaging modality. [11]

Indications and work-up for pancreatic transplant

Pancreatic transplantation is limited by the number of available organs. The large majority of available pancreata go to patients with advanced type I diabetes mellitus who have, or are at risk of developing secondary complications of the disease, such as retinopathy, neuropathies, and nephropathy. [12] Preoperative evaluation typically considers the potential recipient's age and ability to survive the operation. Key components of the assessment include determining the presence of renal, cardiac, peripheral vascular, cerebrovascular, and psychiatric diseases. The pre-transplant work-up consists of extensive laboratory, infectious, and physiologic testing. [13] Of note, the only imaging examination that is typically required by most centers is chest radiography.

It has been shown that the simultaneous pancreas and kidney transplant is associated with 50% lower mortality and decreased morbidity compared to kidney transplant alone for patients with advanced type I diabetes with co-existing end-stage renal disease. [10] Therefore, simultaneous transplant is the treatment of choice in this setting; patients experience decreased morbidity since insulin and dialysis are no longer required after successful pancreas transplant. [7],[14] For patients with labile serum glucose who are not yet uremic, pancreas transplant alone (PTA) may be considered.

Types of pancreatic transplants

There are four general types of pancreatic transplants that depend on the presence and timing of a co-existing kidney transplant: PTA, pancreas after kidney (PAK), simultaneous pancreas-kidney transplant (SPK) from a cadaveric donor, and simultaneous cadaveric donor pancreas and live donor kidney (SPLK) transplant. According to data from the International Pancreas Transplant Registry, the recent unadjusted 5-year patient survival rates following pancreatic transplant are 87% for SPK, 83% for PAK, and 89% for PTA. [1],[15] The organs used for SPK transplant are harvested from a single cadaveric donor and transplanted during the same operation. PAK transplant recipients receive a kidney from a cadaveric or living donor, followed by the subsequent pancreas transplant from an unrelated, cadaveric donor in a separate operation; the timing between the kidney and pancreas transplants is variable and based upon the patient's symptoms and clinical course. During the SPLK procedure, the transplant recipient receives the kidney from a live donor and the pancreas from a cadaveric donor within the same operation. SPK has traditionally been the most commonly performed procedure of the four types, accounting for approximately 70-80% of all pancreas transplants over the past 15 years. [9],[15],[16] Conversely, PTA has historically been the least common method, accounting for approximately 12%. [9] The PAK procedure is performed less commonly than SPK transplants due to lower long-term pancreatic graft survival in PAK transplants. [6] However, there is still a role for the PAK procedure; its advantages include significantly reduced transplant waiting times for uremic patients, the opportunity for a potential living kidney donor, and increased kidney graft survival compared to kidney transplant alone. [17],[18] The SPKL transplant is also associated with shorter waiting times and has been proven to have a lower rate of delayed graft dysfunction compared to SPK transplants. [19]

Regardless, the presence or absence of a kidney transplant does not significantly influence the pancreatic surgical anatomy. The cadaveric pancreas is harvested with a short segment of duodenum that contains the ampulla of Vater. The splenic and proximal superior mesenteric arteries are also harvested. In addition, a segment of the donor's common iliac artery through its bifurcation into the internal/external iliac arteries is removed and fashioned into a Y-graft that is connected to the donor's splenic and mesenteric arteries to craft a single arterial conduit [Figure 1]; the end of this conduit is connected to the recipient's common or external iliac artery in a single end-to-side arterial anastomosis. The venous drainage of the pancreatic transplant is most commonly fashioned after distal ligation of the donor's splenic and superior mesenteric veins and anastomosis between a segment of the donor's portal vein and the recipient's common or external iliac vein in an end-to-side manner [Figure 2]. [16],[20] Alternatively, some surgeons may choose to create the anastomosis between the donor's portal or superior mesenteric vein and the recipient's superior mesenteric vein, thereby ultimately creating a portal venous route of drainage in the recipient that is thought to slow the development of insulin resistance and atherosclerosis. [21],[22] However, no significant difference of glycemic control has been shown to exist based on whether the transplant's venous drainage is into the recipient's iliac vein or superior mesenteric vein.{Figure 1}{Figure 2}

For many years, the duodenal cuff was anastomosed to the urinary bladder intraperitoneally in the right iliac fossa. The constant drainage of pancreatic exocrine secretions into the bladder often resulted in numerous urinary complications for transplant recipients, such as cystitis, urethritis, recurrent infections, dehydration, calculi, hematuria, and reflux into the pancreatic transplant that resulted in episodes of pancreatitis. Therefore, an enteric anastomosis between the oversewn duodenal cuff and the recipient's jejunum has become the preferred route for drainage of exocrine secretions [Figure 3]. [16],[23] The success of the enteric anastomosis is based on the physiologic delivery of bicarbonate and enzymes into the bowel and was corroborated by studies that showed no difference in perioperative morbidity or long-term graft failure compared to pancreatic transplant patients who had bladder anastomoses. [24],[25] {Figure 3}

Normal post-transplant evaluation

US is the most commonly used imaging modality in the postoperative setting and includes both gray-scale and Doppler interrogation. Performance of a proper Doppler interrogation is of paramount importance in the early postoperative setting to confirm vessel patency and adequate perfusion of the allograft; application of color or power Doppler should reveal flow throughout the allograft while spectral Doppler analysis should elucidate arterial and venous waveforms in the intrapancreatic vessels [Table 1]. A thorough gray-scale investigation is needed to check for the development of fluid collections. Unlike kidney transplants that are positioned in the extraperitoneal space of the iliac fossa, pancreatic transplants are located in the intraperitoneal space and may be more readily obscured by overlying bowel gas. Re-positioning of the patient (in the oblique or lateral decubitus position) or application of gentle pressure with the US transducer can be performed in an attempt to displace overlying bowel and allow visualization of the pancreatic transplant. Although the lack of an organ capsule generally results in an ill-defined appearance, the pancreatic transplant can be identified by its relatively cylindrical shape and its normally homogeneous echotexture that lies immediately anterior to the transplanted splenic vein. [26],[27] Compared to the surrounding mesenteric fat, the pancreatic transplant is hypoechoic [Figure 4]. [11] The pancreatic transplant can be differentiated from the adjacent fluid-filled bowel due to its lack of peristalsis during real-time imaging and its slightly higher echogenicity. With respect to the native pancreas, the transplanted pancreas is typically less echogenic due to parenchymal edema in the postoperative setting. [26] If the pancreatic transplant is not apparent upon initial gray-scale evaluation, it can usually be found by applying color Doppler analysis and scanning the length of the patient's iliac vessels [Figure 5]. After the anastomosed vessels are identified, they should be interrogated with spectral Doppler to evaluate the velocities and waveforms [Figure 6]. The arterial velocities can be quite variable, but should be normalized to the ipsilateral iliac artery by determining the velocity ratio of the vessels. However, arterial anastomotic velocities can be much higher in the immediate postoperative setting, presumably due to transient postoperative edema or vessel kinking. An intrapancreatic artery waveform with a brisk systolic upstroke should be identified [Figure 7]; the normal venous waveform will be mildly undulating and will show continuous flow [Figure 8].{Table 1}{Figure 4}{Figure 5}{Figure 6}{Figure 7}{Figure 8}

On non-contrast CT, the pancreatic transplant appears as an elongated, homogeneous structure in the iliac fossa [Figure 9], but may  be difficult to distinguish from the adjacent bowel. [26],[28],[29] On MRI, the normal pancreatic transplant is isointense to renal cortex on T1W images and has intermediate signal on T2W images. The normal pancreatic transplant should enhance homogenously after infusion of intravenous contrast material on CT or MRI [Figure 10]; however, it should be noted that iodinated intravenous contrast material may place the transplanted kidney at risk for contrast-induced nephropathy, while gadolinium-based contrast agents may pose the risk of nephrogenic systemic fibrosis in select patients with advanced renal dysfunction. [26],[27] However, with MRI, non-contrast time-of-flight images can be used to assess the vasculature. With both CT and MRI, post-contrast images should clearly depict the exocrine drainage anastomosis (duodenocystostomy or duodenojejunostomy), vascular anastomoses, and vascular structures of the allograft. The normal pancreatic duct is generally not visible with US or CT, but may be observed as a thin (≤3 mm) smooth line on T2W MRI.{Figure 9}{Figure 10}

Imaging of complications of pancreatic transplants

Complications of pancreatic transplants can generally be divided into vascular and non-vascular categories. The non-vascular category can be further subdivided into complications that affect the parenchyma and bowel. The most common complications leading to early transplant failure are acute rejection and vascular thrombosis. [30] Although the imaging findings and clinical signs and symptoms of transplant dysfunction are often nonspecific when considered alone, their integration often permits diagnosis and facilitates treatment.

Vascular complications

Vascular complications of pancreatic transplants consist of venous and arterial thrombosis, pseudoaneurysms, arteriovenous fistulas, and anastomotic strictures. The most feared complication is complete vascular thrombosis since it can quickly lead to infarction of the allograft. [31] Complete arterial thrombosis is shown as absence of arterial Doppler signal within the graft despite parameter optimization [Figure 11]. The parenchyma becomes heterogeneous at gray scale US, CT, or MRI; angiographic images can reveal the site of vascular occlusion within the donor artery. [32] Venous thrombosis is more common than arterial thrombosis and can result in enlargement of the pancreatic transplant and parenchymal edema due to the venous outlet obstruction. [31] Gray-scale US findings include increased hypoechogenicity or heterogeneity of the pancreatic parenchyma and perigraft fluid; occasionally, echogenic clot can be identified within the splenic vein. Spectral Doppler findings include the absence of a venous waveform and reversal of diastolic flow on the arterial waveform [Figure 12]. In rare cases, extrinsic compression or kinking of the veins can masquerade as venous thrombosis at Doppler interrogation. [33] Venous thrombosis generally affects pancreatic allografts within the first few weeks after surgery and complicates approximately 5% of allografts. [34] Treatment options include anticoagulation, mechanical thrombectomy, or pancreatectomy.{Figure 11}{Figure 12}

Pseudoaneurysms associated with pancreatic transplants result from damage to the arterial wall and should be considered in the differential diagnosis for any perigraft fluid collection. [27],[35] While most pseudoaneurysms occur at, or near, the arterial anastomosis, they can occur elsewhere secondary to biopsy sites, pancreatitis, and infections. [27],[35] At gray-scale US, pseudoaneurysms appear as anechoic, round, or ovoid structures of variable size. Application of color Doppler reveals internal flow with a typical swirling or "yin-yang" appearance. [11] When the neck of the pseudoaneurysm is interrogated with spectral Doppler US, the waveform consists of a classic "to-and-fro" pattern characterized by biphasic flow. [11],[36] Post-contrast CT and MRI show a round or ovoid focus of enhancement adjacent to the transplant. Treatment options include percutaneous stent placement or surgical repair.

An additional uncommon vascular complication is formation of an arteriovenous fistula. The fistula typically has an iatrogenic etiology, resulting from previous biopsy or during surgery. There are generally no gray-scale imaging findings, but color Doppler can show a focus of color aliasing at the abnormal connection between an artery and the adjacent vein; the associated waveform is notable for a high-velocity, low-resistance pattern with increased diastolic flow in the artery and pulsatile flow in the draining vein [Figure 13]. Post-contrast CT and MRI may reveal early opacification of the draining vein during arterial phase images. [32] The majority of small arteriovenous fistulas will spontaneously resolve, while large, hemodynamically significant fistulas may require surgical repair.{Figure 13}

The arterial and venous anastomoses should ideally be identified each time the pancreatic transplant is evaluated with US. The most reliable landmark that can be used to identify the anastomosis is the patient's iliac vessels. The anastomoses can then be found as branch points that project laterally. The anastomotic region should be interrogated with color and spectral Doppler analysis. Color interrogation is important initially to show turbulent flow that is identified as a focus of aliasing [Figure 14]. If focal color aliasing is identified, the spectral Doppler box should be placed on that site so that the velocity and waveforms can be studied; elevated velocities and turbulent flow are findings that suggest stricture, but can be transient in the immediate postoperative setting. [37] The velocities at the anastomoses should be compared to the velocities in the ipsilateral iliac vessels. For an arterial anastomotic stricture to be considered hemodynamically significant, the ratio of the velocities recorded at the anastomosis to iliac artery should be greater than ≥ 2.5; [38] for the venous anastomoses, the ratio should be should be ≥ 3.5. While it is not uncommon for arterial anastomotic velocities to be elevated (300-400 cm/s or greater) in the immediate postoperative period, these velocities should normalize over the next 5-7 days as the perianastomotic edema resolves. Persistent velocity gradients after this time are suggestive of stenosis [Figure 15]. Persistently elevated anastomotic velocities should be further investigated by CT angiography or MR angiography to confirm the presence of anastomotic stricture prior to a catheter-based angiogram.{Figure 14}{Figure 15}

Fluid collections

Postoperative fluid collections are the most common complication affecting pancreatic transplants. Clinically significant fluid collections can be identified by US, CT, or MRI. The development of intra-abdominal fluid collections can be variable, occurring anywhere from the immediate to late postoperative periods. The presence of postoperative fluid collections may herald intra-abdominal infection; however, not all fluid collections are abscesses. One of the most common postoperative fluid collections is a hematoma. If imaged within the first few days after surgery, hematomas appear typically well-marginated and are shown to be echogenic and devoid of color Doppler flow on US; CT shows the hematoma as a non-enhancing, hyperattenuating collection. In the subacute and chronic phases, hematomas evolve and may develop internal complexity consisting of heterogeneous contents, septations, and fluid hematocrit levels. Eventually hematomas liquefy, becoming more homogeneously hypoechoic and hypoattenuating with US and CT evaluations, respectively. The MRI signal of hematomas varies with the age of the hematoma; when a larger concentration of extracellular methemoglobin is present, there is high intensity signal on both T1- and T2-W images. [37] The complex internal contents of hematomas can make differentiation from abscess difficult, although the presence of clinical findings of infection facilitates the diagnosis.

Abscesses can occur within any portion of the surgical field due to contamination during surgery or can be associated with anastomotic dehiscence and leakage of enteric contents. [27],[39] Compared to most other types of fluid collections, abscesses are generally more complex: They typically contain internal debris, have thicker, more irregular walls, and are associated with adjacent inflammation or infiltration of the surrounding tissue planes [Figure 16]. Relative hyperemia within the abscess wall manifests as increased color flow on Doppler US and as rim enhancement on contrast-enhanced CT. Gas within a fluid collection is typically readily apparent at CT and appears as echogenic foci with reverberation artifact, also known as "dirty shadowing" on US; the presence of gas within a fluid collection near the pancreatic transplant is suggestive of abscess. [26]{Figure 16}

Abscesses can also arise from infected pseudocysts. However, majority of the pseudocysts are not infected and have a relatively simple imaging characteristic; they appear as well-circumscribed collections with relatively thin walls. In most cases, the pseudocysts are anechoic and show strong through transmission, but occasionally, a small amount of layering debris can be observed as internal low-level echoes. CT or MRI can show a mild degree of adjacent inflammation. Pseudocysts are associated with prior bouts of allograft pancreatitis and may form within the pancreatic transplant or in the perigraft tissues. [28]

Although a pseudocyst may be suggested based on the clinical context, several other types of postoperative fluid collections are often indistinguishable from them. Pseudocysts, seromas, lymphoceles, and urinomas can all appear as well-marginated, anechoic fluid collections [Figure 17]. Due to the lack of specificity of imaging characteristics, percutaneous sampling is needed if definitive diagnosis is required.{Figure 17}

Bowel-related complications

Although most cases of allograft dysfunction are readily assessed by US, bowel complications are better evaluated by CT. As with any bowel surgery, there are risks of anastomotic leak and obstruction. Anastomotic leak is relatively easy to diagnose when ingested oral contrast extravasates from the anastomotic site into the peritoneum [Figure 18]. If oral contrast has not been ingested, CT findings that suggest leak include the presence of new or persistent extraluminal gas or fluid near the anastomosis. In most cases, bowel leaks must be repaired surgically. Common causes of small bowel obstruction include internal hernias and adhesions, which have been reported to occur in 3% and 5% of patients, respectively. [27]{Figure 18}

Allograft dysfunction

Severe pancreatitis affects only approximately 10% of pancreatic transplants and can be confirmed by elevation of the serum amylase level. [27],[40] In mild pancreatitis, the US findings are often normal. With more severe disease, the pancreatic transplant becomes heterogeneous and more hypoechoic due to parenchymal edema [Figure 19]. As edema and inflammation progress, the transplant can develop a more globular appearance with associated loss of the normal mild surface undulation as the acini become blunted; this gray-scale appearance can be indistinguishable from acute rejection. Variable amounts of perigraft fluid may develop. Application of color Doppler reveals a varying degree of parenchymal hyperemia in cases of more advanced pancreatitis. On CT and MRI, perigraft fluid, infiltration of the adjacent fat, and heterogeneous parenchymal enhancement can all be observed [Figure 20]. Management of allograft pancreatitis consists of conservative medical management unless parenchymal necrosis is present. On US, the hallmark of necrosis is lack of arterial and venous flow within segments of the parenchyma or throughout the entire gland; on CT or MRI, there is regional or diffuse lack of parenchymal enhancement. Regions of necrosis may liquefy and lead to intraparenchymal fluid collections. Additionally, necrosis may be complicated by superinfection with development of intraparenchymal gas which manifests as echogenic foci with associated incomplete or "dirty" shadowing. If necessary, follow-up evaluation with non-contrast CT can confirm the presence of intraparenchymal gas.{Figure 19}{Figure 20}

Rejection of the pancreatic transplant can be acute, subacute, or chronic depending on the timing of onset relative to the transplant operation. Rejection is a common reason for patient morbidity and failure of the allograft; it has been shown that acute and chronic rejection affect approximately 15% and 25% of pancreatic transplants, respectively. [41] Despite the frequency at which pancreatic allografts are affected, renal transplants are more commonly subjected to bouts of acute rejection. Unfortunately, there are no specific imaging findings of acute rejection in a pancreatic transplant. The possibility of rejection can be suggested based on changes in the size of the allograft [Figure 21]; acute rejection generally results in enlargement due to parenchymal edema while chronic rejection eventually leads to volume loss and atrophy. Although some studies have previously suggested that elevated arterial resistive indices coincided with episodes of acute rejection, others have failed to show a correlation. [11],[29],[42] One previous study showed that the resistive index was typically elevated in chronic rejection, but neither the absolute value nor an increase of the resistive index correlated with episodes of acute rejection [Figure 22]. [43] On CT and MRI evaluation, abnormal size, degree of enhancement, and increased T2 signal of the allograft have been associated with rejection, but are also nonspecific. [26],[44] Due to the inaccuracy of imaging and serum biochemical markers, acute rejection is usually suspected by clinical signs and symptoms and confirmed by US-guided biopsy of the pancreatic transplant. [11],[45]{Figure 21}{Figure 22}

Post-transplant lymphoproliferative disorder (PTLD) is an uncommon complication that has been reported to affect approximately 3-12% of pancreatic transplant patients. [10],[26],[46] The onset of PTLD is typically several months to even years after pancreatic transplantation; while the precise etiology has not been fully elucidated, the development is likely related to the interaction of the Epstein-Barr virus and chronic immunosuppression. PTLD can range from a relatively benign polyclonal lymphoid hyperplasia to overt lymphoma. [47] Imaging findings include lymphadenopathy, potential hepatic masses, and diffuse enlargement of the allograft, a nonspecific finding which can also be found in pancreatitis and acute rejection. [28],[48]

Complications of the lower urinary tract

Complications of the lower urinary tract are rare and generally limited to patients who have an anastomosis between the pancreatic transplant and the urinary bladder. When the lower urinary tract is bathed in pancreatic exocrine secretions, the urothelial mucosa is repeatedly exposed to chemical irritation and subjected to injury. The chronic irritation can lead to cystitis, urethritis, or balanitis; cystitis results in bladder wall thickening and inflammation during imaging examinations. In males, the urethral mucosa is also subject to chronic inflammation and injury. In severe cases, urethral perforation can occur; perforation most commonly affects the bulbous segment of the anterior segment or the bulbomembranous junction. Urethral perforation is often associated with recent instrumentation and predisposes the patient for future strictures. [49] The pertinent imaging finding is extravasation of injected contrast material during retrograde urethrography.

Percutaneous interventions for pancreatic transplants

Percutaneous biopsy of the pancreatic transplant can be facilitated by US guidance and has been shown to be a safe and effective means of further evaluating the pancreatic parenchyma when allograft dysfunction is detected clinically. [45],[50] The biopsy procedure is typically performed with an 18-guage core biopsy needle after Power Doppler analysis has been applied to exclude the intervening vessels [Figure 23]. Power Doppler is also applied after the biopsy to evaluate for complications such as hemorrhage and pseudoaneurysm formation. US-guided percutaneous biopsy yields diagnostic tissue in most cases, having been reported to be as high as 100% in one study. [51] In addition to its use during biopsy, imaging guidance is often used to allow percutaneous drainage of postoperative fluid collections. Drainage of fluid collections can be performed as either needle aspiration or placement of an indwelling catheter via Seldinger or direct trocar technique. US permits continuous visualization of the needle or catheter as it enters the fluid collection, allowing for optimal positioning and more efficient drainage.{Figure 23}

When extensive bowel gas obscures US identification of the pancreatic transplant, CT can often be used to facilitate the percutaneous intervention. Placing the patient in supine or slightly oblique position generally allows the maximum access to the allograft. If differentiation of the pancreatic transplant from adjacent bowel is still problematic, it is suggested that the patient ingest oral contrast material and return to the CT suite after the contrast has traversed the adjacent bowel.

 Conclusion



Pancreatic transplantation is an effective treatment for patients with advanced type I diabetes. Pancreatic transplantation can be performed alone or combined with renal transplantation. In order to provide clinically relevant interpretation of imaging examinations involving the transplanted pancreas, the radiologist should have knowledge of the types of pancreatic transplantation, the typical surgical anatomy of the transplanted pancreas, and the appearance of various associated complications. US is the preferred initial imaging modality to evaluate the pancreatic transplant. US provides an effective, non-invasive method for determining the presence of various complications that can affect the parenchyma, vascular supply, and adjacent tissues. CT is the preferred imaging modality to evaluate potential bowel complications associated with pancreatic transplants. Image guidance also plays a central role in facilitating percutaneous therapeutic intervention.

References

1Boggi U, Vistoli F, Egidi FM, Marchetti P, De Lio N, Perrone V, et al. Transplantation of the pancreas. Curr Diab Rep 2012;12:568-79.
2Orlando G, Stratta RJ, Light J. Pancreas transplantation for type 2 diabetes mellitus. Curr Opin Organ Transplant 2011;16:110-5.
3Sampaio MS, Kuo HT, Bunnapradist S. Outcomes of simultaneous pancreas-kidney transplantation in type 2 diabetic recipients. Clin J Am Soc Nephrol 2011;6:1198-206.
4Robertson RP, Davis C, Larsen J, Stratta R, Sutherland DE. Pancreas and islet transplantation for patients with diabetes. Diabetes Care 2000;23:112-6.
5Robertson RP, Davis C, Larsen J, Stratta R, Sutherland DE; American Diabetes Association. Pancreas and islet transplantation in type 1 diabetes. Diabetes Care 2006;29:935.
6Sutherland DE, Gruessner RW, Gruessner AC. Pancreas transplantation for treatment of diabetes mellitus. World J Surg 2001;25:487-96.
7Sutherland DE, Gruessner RW, Dunn DL, Matas AJ, Humar A, Kandaswamy R, et al. Lessons learned from more than 1,000 pancreas transplants at a single institution. Ann Surg 2001;233:463-501.
8Gruessner AC, Sutherland DE. Pancreas transplant outcomes for United States (US) cases as reported to the United Network for Organ Sharing (UNOS) and the International Pancreas Transplant Registry (IPTR). Clin Transpl 2008:45-56.
9Leichtman AB, Cohen D, Keith D, O'Connor K, Goldstein M, McBride V, et al. Kidney and pancreas transplantation in the United States, 1997-2006: The HRSA Breakthrough Collaboratives and the 58 DSA Challenge. Am J Transplant 2008;8:946-57.
10Smets YF, Westendorp RG, van der Pijl JW, de Charro FT, Ringers J, de Fijter JW, et al. Effect of simultaneous pancreas-kidney transplantation on mortality of patients with type-1 diabetes mellitus and end-stage renal failure. Lancet 1999;353:1915-9.
11Nikolaidis P, Amin RS, Hwang CM, McCarthy RM, Clark JH, Gruber SA, et al. Role of sonography in pancreatic transplantation. Radiographics 2003;23:939-49.
12White SA, Shaw JA, Sutherland DE. Pancreas transplantation. Lancet 2009;373:1808-17.
13Tavakoli A, Liong S. Pancreatic transplant in diabetes. Adv Exp Med Biol 2012;771:420-37.
14Sollinger HW, Odorico JS, Knechtle SJ, D'Alessandro AM, Kalayoglu M, Pirsch JD. Experience with 500 simultaneous pancreas-kidney transplants. Ann Surg 1998;228:284-96.
15Gruessner AC. 2011 update on pancreas transplantation: Comprehensive trend analysis of 25,000 cases followed up over the course of twenty-four years at the International Pancreas Transplant Registry (IPTR). Rev Diabet Stud 2011;8:6-16.
16Gruessner AC, Sutherland DE. Pancreas transplant outcomes for United States (US) and non-US cases as reported to the United Network for Organ Sharing (UNOS) and the International Pancreas Transplant Registry (IPTR) as of June 2004. Clin Transplant 2005;19:433-55.
17Kleinclauss F, Fauda M, Sutherland DE, Kleinclauss C, Gruessner RW, Matas AJ, et al. Pancreas after living donor kidney transplants in diabetic patients: Impact on long-term kidney graft function. Clin Transplant 2009;23:437-46.
18Humar A, Ramcharan T, Kandaswamy R, Matas A, Gruessner RW, Gruessner AC, et al. Pancreas after kidney transplants. Am J Surg 2001;182:155-61.
19Farney AC, Cho E, Schweitzer EJ, Dunkin B, Philosophe B, Colonna J, et al. Simultaneous cadaver pancreas living-donor kidney transplantation: A new approach for the type 1 diabetic uremic patient. Ann Surg 2000;232:696-703.
20Chandra J, Phillips RR, Boardman P, Gleeson FV, Anderson EM. Pancreas transplants. Clin Radiol 2009;64:714-23.
21Gaber AO, Shokouh-Amiri MH, Hathaway DK, Hammontree L, Kitabchi AE, Gaber LW, et al. Results of pancreas transplantation with portal venous and enteric drainage. Ann Surg 1995;221:613-24.
22Stratta RJ, Gaber AO, Shokouh-Amiri MH, Reddy KS, Alloway RR, Egidi MF, et al. Evolution in pancreas transplantation techniques: Simultaneous kidney-pancreas transplantation using portal-enteric drainage without antilymphocyte induction. Ann Surg 1999;229:701-12.
23Gruessner AC, Sutherland DE. Analyses of pancreas transplant outcomes for United States cases reported to the United Network for Organ Sharing (UNOS) and non-US cases reported to the International Pancreas Transplant Registry (IPTR). Clin Transpl 1999:51-69.
24Monroy-Cuadros M, Salazar A, Yilmaz S, McLaughlin K. Bladder vs enteric drainage in simultaneous pancreas-kidney transplantation. Nephrol Dial Transplant 2006;21:483-7.
25Aideyan OA, Foshager MC, Benedetti E, Troppmann C, Gruessner RW. Correlation of the arterial resistive index in pancreas transplants of patients with transplant rejection. AJR Am J Roentgenol 1997;168:1445-7.
26Pozniak MA, Propeck PA, Kelcz F, Sollinger H. Imaging of pancreas transplants. Radiol Clin North Am 1995;33:581-94.
27Sandrasegaran K, Lall C, Berry WA, Hameed T, Maglinte DD. Enteric drainage pancreatic transplantation. Abdom Imaging 2006;31:588-95.
28Freund MC, Steurer W, Gassner EM, Unsinn KM, Rieger M, Koenigsrainer A, et al. Spectrum of imaging findings after pancreas transplantation with enteric exocrine drainage: Part 2, posttransplantation complications. AJR Am J Roentgenol 2004;182:919-25.
29Vandermeer FQ, Manning MA, Frazier AA, Wong-You-Cheong JJ. Imaging of whole-organ pancreas transplants. Radiographics 2012;32:411-35.
30Holalkere NS, Soto J. Imaging of miscellaneous pancreatic pathology (trauma, transplant, infections, and deposition). Radiol Clin North Am 2012;50:515-28.
31Eubank WB, Schmiedl UP, Levy AE, Marsh CL. Venous thrombosis and occlusion after pancreas transplantation: Evaluation with breath-hold gadolinium-enhanced three-dimensional MR imaging. AJR Am J Roentgenol 2000;175:381-5.
32Hagspiel KD, Nandalur K, Pruett TL, Leung DA, Angle JF, Spinosa DJ, et al. Evaluation of vascular complications of pancreas transplantation with high-spatial-resolution contrast-enhanced MR angiography. Radiology 2007;242:590-9.
33Dillman JR, Elsayes KM, Bude RO, Platt JF, Francis IR. Imaging of pancreas transplants: Postoperative findings with clinical correlation. J Comput Assist Tomogr 2009;33:609-17.
34Foshager MC, Hedlund LJ, Troppmann C, Benedetti E, Gruessner RW. Venous thrombosis of pancreatic transplants: Diagnosis by duplex sonography. AJR Am J Roentgenol 1997;169:1269-73.
35Madan AK, Allmon JC, Harding M, Cheng SS, Slakey DP. Extrapancreatic pseudoaneurysm after pancreas transplantation. Transplantation 2001;71:1853-6.
36Tobben PJ, Zajko AB, Sumkin JH, Bowen A, Fuhrman CR, Skolnick ML, et al. Pseudoaneurysms complicating organ transplantation: Roles of CT, duplex sonography, and angiography. Radiology 1988;169:65-70.
37Low RA, Kuni CC, Letourneau JG. Pancreas transplant imaging: An overview. AJR Am J Roentgenol 1990;155:13-21.
38Norton PT, DeAngelis GA, Ogur T, Saad WE, Hagspiel KD. Noninvasive vascular imaging in abdominal solid organ transplantation. AJR Am J Roentgenol 2013;201:W544-53.
39Troppmann C. Complications after pancreas transplantation. Curr Opin Organ Transplant 2010;15:112-8.
40Cattral MS, Hemming AW, Greig PD, Rowsell C, Chari R, Cole E, et al. Outcome of kidney transplantation alone versus synchronous pancreas-kidney transplantation in type 1 diabetics. Transplant Proc 1998;30:1938-9.
41Waki K, Kadowaki T. An analysis of long-term survival from the OPTN/UNOS pancreas transplant registry. Clin Transpl 2007:9-17.
42Gilabert R, Bru C, Ricart MJ, Astudillo E, Saenz A, Llovera JM, et al. Pancreatic transplant rejection: Evaluation by duplex-Doppler ultrasound with urinary amylase monitoring correlation. Transplant Proc 1992;24:11.
43Nelson NL, Largen PS, Stratta RJ, Astudillo E, Saenz A, Llovera JM, et al. Pancreas allograft rejection: Correlation of transduodenal core biopsy with Doppler resistive index. Radiology 1996;200:91-4.
44Krebs TL, Daly B, Wong-You-Cheong JJ, Carroll K, Bartlett ST. Acute pancreatic transplant rejection: Evaluation with dynamic contrast-enhanced MR imaging compared with histopathologic analysis. Radiology 1999;210:437-42.
45Atwell TD, Gorman B, Larson TS, Charboneau JW, Ingalls Hanson BM, Stegall MD. Pancreas transplants: Experience with 232 percutaneous US-guided biopsy procedures in 88 patients. Radiology 2004;231:845-9.
46Kuo PC, Johnson LB, Schweitzer EJ, Bartlett ST. Simultaneous pancreas/kidney transplantation--a comparison of enteric and bladder drainage of exocrine pancreatic secretions. Transplantation 1997;63:238-43.
47Meador TL, Krebs TL, Cheong JJ, Daly B, Keay S, Bartlett S. Imaging features of posttransplantation lymphoproliferative disorder in pancreas transplant recipients. AJR Am J Roentgenol 2000;174:121-4.
48Sudan D, Sudan R, Stratta R. Long-term outcome of simultaneous kidney-pancreas transplantation: Analysis of 61 patients with more than 5 years follow-up. Transplantation 2000;69:550-5.
49Dumas MD, Bude RO, Sonda PL 3 rd , Cohan RH, Merion RM. Urethral disruption with urinary extravasation: A delayed complication of pancreatic transplantation. Radiology 1996;201:761-5.
50Gaber AO, Gaber LW, Shokouh-Amiri MH, Hathaway D. Percutaneous biopsy of pancreas transplants. Transplantation 1992;54:548-50.
51Kuhr CS, Davis CL, Barr D, McVicar JP, Perkins JD, Bachi CE, et al. Use of ultrasound and cystoscopically guided pancreatic allograft biopsies and transabdominal renal allograft biopsies: Safety and efficacy in kidney-pancreas transplant recipients. J Urol 1995;153:316-21.