Rejection is a common cause of pancreatic graft failure [17]. For the period 2000-2004, the IPTR reported acute rejection to be the cause of graft failure in 7-25% of cases. Chronic rejection was reported to be the cause of graft failure in 2-33% of cases [18]. Rejection has no specific imaging features. The cause of early graft failure is often difficult to determine clinically. Imaging therefore has a vital role in the exclusion of other causes of pancreatic graft failure and in guiding biopsy (Fig. 5).
The potential complications of pancreas transplant may be divided into three categories: those related to the vessels, those related to the graft parenchyma and those related to the enteric anastomoses.
Pancreas graft vascular complications
Graft thrombosis is the most common non-immunological cause of early graft failure. The incidence of graft thrombosis has been reported to range from 2 to 19% [19–26]. Venous thrombosis is more common than arterial thrombosis [27–29].
In venous thrombosis, US Doppler imaging demonstrates absent venous flow, and a high resistance arterial waveform, with reversed diastolic flow, may also be seen occasionally. Unenhanced CT may show thrombus as a high attenuation portal vein or splenic vein (Fig. 6a). A filling defect may be seen following the adminstration of intravenous contrast medium (Fig. 6b); but subtle thromboses may be obscured following parenchymal enhancement. Side-branch venous thromboses may be seen where small venous side branches have been ligated during retrieval. These are commonly of no clinical significance but are monitored to exclude the presence of thrombus propagation. Venous-graft thrombosis may result in pancreatic necrosis or duodenal stump breakdown, which usually necessitates graft pancreatectomy. Prompt diagnosis and immediate thrombectomy may be successful.
Graft arterial thrombosis is much less common than venous thrombosis, and can occur in the early or late phase post-transplantation. The thrombosis may also be seen as a hyperdense vessel on unenhanced CT, with subsequent non-enhancement following intravenous contrast medium (Fig. 7). Early arterial thrombosis may occur spontaneously at any of the anastomotic sites, or as a consequence of vascular rejection, and results in non-enhancement and subsequent necrosis of the pancreatic graft. Late arterial occlusion may represent the end point of graft rejection. This initially involves the smaller vessels and progresses to involve the larger ones [30].
Emphysematous transformation may occur within a necrotic graft. This is demonstrated on CT as gas locules within the pancreatic graft [31]. It is impossible to differentiate between emphysematous transformation and gas-forming infection on CT. Scintigraphy with radioisotope-labelled white blood cells may be used as a suitable non invasive alternative, where there is clinical uncertainty regarding the presence of graft associated infection (Fig. 8). However, in this situation, surgical graft exploration is usually indicated.
Haemorrhage may result from failure of the arterial anastomoses, but more commonly occurs where the superior mesenteric vessels or splenic vessels have been ligated. A haematoma may be demonstrated as a high attenuation collection on an initial unenhanced CT series. Contrast extravasation may then be detected in the arterial and/or venous phases. While significant intra–abdominal bleeding after pancreas transplantation remains one of the most common reasons for relaparotomy, less than 0.3% of all pancreas grafts are lost as a result of haemorrhage [32].
Pseudoaneurysms, arteriovenous fistulae, arterial dissection and arterial stenosis represent some rarer vascular complications. Pseudoaneurysms may be the result of surgical technique (particularly if the mesenteric pedicle has been divided with a linear stapling device), infection, severe pancreatitis, or allograft biopsy. Arteriovenous fistulae may be the result of vascular injury, either at surgery or post-biopsy; they are common in the stapled edge of the mesentery where the superior mesenteric vessels have been divided. Arterial stenosis can arise at any anastomosis and may ultimately lead to reduced graft perfusion (Fig. 9). Occasionally, the arterial “Y graft” conduit may kink; this can result in significant haemodynamic compromise and graft dysfunction. Furthermore, the donor portal vein may appear kinked proximal to the anastomosis with the recipient IVC. It is yet to be determined whether this is clinically significant. Our experience suggests that this does not cause graft dysfunction.
CT angiography is the best tool in the initial assessment of these vascular complications. Conventional angiography is used to confirm vascular abnormalities which may then be amenable to endovascular therapy.
Parenchymal complications
Pancreatic parenchymal graft complications are an important cause of morbidity in the early post-operative period. These complications include acute rejection, pancreatitis, pseudocyst formation, and infection with abscess formation.
The exact incidence of post-transplant pancreatitis is very difficult to determine because of the lack of a universally accepted definition [33–35]. Prolonged hyperamylasaemia is seen early post transplant in up to 35% of all recipients [33]. Unfortunately amylase and lipase levels correlate poorly with the severity of graft pancreatitis [33], making evaluation of the true incidence of graft pancreatitis near impossible.
Early graft pancreatitis is often due to reperfusion injury and usually involves the whole graft (Fig. 10). In the early post-operative period, ill-defined fat planes around the pancreatic graft are commonly seen. The graft may appear as an enhancing ‘mass’ surrounded by an omental wrap in the right iliac fossa. At an early stage it may be difficult to distinguish radiologically between the appearance of the normal post operative pancreatic graft and early graft pancreatitis. Furthermore, focal oedema of the donor’s mesenteric fat attached to the SMA stump, presumably the result of donor lymphatic vessel ligation, should not be misinterpreted as focal oedematous pancreatitis [36]. MDCT is valuable in evaluating the complications of pancreatitis, such as parenchymal necrosis and abscess formation. Collections may be amenable to image-guided drainage to alleviate the pressure effect on the vascular supply and drainage of the pancreatic graft.
Repeated episodes of pancreatitis may be secondary to ampullary or duodenal anastomotic stricture or mucus plugging. MRCP may be of diagnostic use in this situation. Mucus plugging may cause focal or generalised duct dilatation, whereas an ampullary or anastomotic stricture will result in generalised duct dilatation in the absence of a pancreatic duct stricture. US can show a bulky pancreas, possibly with associated fluid collections. However, interpretation may be hampered by poorly defined pancreatic margins. Both CT and US may be used to guide percutaneous abscess drainage.
Pseudocysts form at a later stage as a result of graft pancreatitis. They may occur inside or outside the graft and have the potential to become infected. This may result in vascular pseudoaneurysm formation. The diagnosis should be considered in patients with a pulsatile abdominal mass, unexplained anaemia and/or haemodynamic instability, and when there is rapid enlargement of a pseudocyst. CT angiography is used to evaluate this possibility. Formal angiography is subsequently used to confirm the presence of a pseudoaneurysm (Fig. 11) and permit embolisation.
Another potential complication of pancreatitis is fistula formation. Fistulae may form between the pancreatic graft and the skin or the peritoneal cavity (Fig. 12). Sinus tracts may also develop. Fistulae connecting to the skin are best assessed with CT fistulograms. Internal fistulae are best assessed with MRI.
Enteric complications
Thickening of the bowel loops surrounding the pancreas graft frequently occurs in the post-operative period, often due to manipulation during the surgical procedure, the formation of a Roux loop and aggressive rehydration. This usually resolves within 3–4 weeks. The donor duodenum may also appear thick-walled [37].
Duodenal segment leaks may occur at the duodenojejunostomy, but are more common at the staple line of the duodenal stump (Fig. 13). These occur early due to ischaemia, or late (>4 weeks) secondary to infection or rejection. Free air around the graft is common in the early post-operative period, but seen late may indicate an anastomotic leak. Free fluid may also be seen and collections may form adjacent to the leaking point.
Small bowel obstruction is most commonly secondary to adhesions, a generic risk of abdominal surgery (Fig. 14). Another potential cause is internal herniation of jejunal loops posterior to the pancreatic graft, through a mesenteric defect related to the Roux loop formation [37].
Complications of immunosuppressive therapy may manifest in the bowel. Rarely, a neutropenic typhlitis may develop. Alternatively, opportunistic infections with organisms such as cytomegalovirus, or antibiotic-associated Clostridium difficile may cause colitis.
Complications secondary to immunosuppression
The common complications secondary to immunosuppression seen in solid organ transplantation are generally categorised as related to either infection or tumour. We would like to highlight the specific complication of post-transplant lymphoproliferative disorder (PTLD) that can be diagnosed using cross-sectional imaging. PTLD is a serious but rare complication of pancreas transplantation. It has a reported incidence after pancreatic transplantation of 3-12% [38, 39]. It is associated with the higher levels of immunosuppression needed in SPK transplants compared with other solid organ transplants. It is associated with a donor acquired EBV infection and is therefore commoner in younger previously EBV-naive transplant recipients, for example, type I DM recipients of SPK grafts. Diffuse enlargement of the pancreatic graft is a common manifestation, which is indistinguishable from oedematous pancreatitis or transplant rejection. Less commonly focal intra- or extra-allograft masses may develop (Fig. 15), and lymphadenopathy and other organomegaly may also occur [40]. A tissue diagnosis is essential as the treatment modalities include a reduction in immunosuppression and consideration of chemotherapy.