COMPLICATIONS

In the past, technical failures and graft rejection were the main reasons for pancreas graft loss. 

Venous thrombosis can be partial or total occlusive and can involve the superior mesenteric, splenic vein or both [11, 12, 13].

Sometimes, the donor portal vein may appear kinked proximal to the anastomosis with the recipient inferior vena cava. It is yet to be determined whether this is clinically significant [14].

Graft thrombosis after the early postoperative period may be the result of acute or chronic graft rejection. Extensive thrombosis may cause parenchymal necrosis, requiring urgent pancreatectomy [15].

US findings depend on the degree and location of thrombus and may highlight the presence of the obstruction which is seen as an echogenic intraluminal thrombus on grey scale; moreover venous flow is absent and high resistance arterial waveform with reversed diastolic flow may also be seen. If there is associated graft infarction it may appear hypoechoic and enlarged.

Prompt diagnosis and immediate thrombectomy may prevent graft loss.

Graft arterial thrombosis can occur in the early or late phase post-transplantation and may be a result of technical complications. It usually involves the superior mesenteric artery or splenic artery, however it may be compensated by intrapancreatic arterial collateral flow.

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. This initially involves the smaller vessels and progresses to involve the larger ones [14]. 

On US Doppler arterial flow is absent. It may be possible to identify the thrombus inside the vessel but this depends on the degree and location of thrombosis [16, 17].

CT scan with contrast medium administration is useful to demonstrate lack of enhancement of the parenchymal graft, indicating graft necrosis.

Moreover, in the later course, graft loss due to arterial occlusion represents the end-point of graft rejection due to alloimmune vasculitis, resulting in occlusion of small vessels, progressing to larger vessels, and finally involving the donor's anastomosed greater vessels.

Graft thrombosis both of vein or artery after the early postoperative period may be the result of acute or chronic graft rejection, in which autoimmune vasculitis and fibrosis cause the gradual occlusion of small and large vessels.

The treatment for most cases of severe venous thrombosis is graft pancreatectomy [15].

Arterial pseudoaneurysm may occur as a complication of pancreatitis, infection, abscess or at the anastomotic site.  It may also be secondary to biopsy or surgical trauma, sometimes associated with arterio-venous fistula formation [15].

On color Doppler US, a pseudoaneurysm shows internal swirling blood flow with a characteristic to-and-fro waveform in the feeding vessel [5, 17].

Endovascular intervention includes coil embolization and covered stent insertion, with appropriate pre- and post-intervention antibiotic therapy [19].

Arteriovenous fistulae may be the result of vascular injury, either at surgery or post-biopsy. At Color-Doppler US aliasing and a characteristic high-velocity low resistance Doppler waveform with pulsatile flow are shown in the draining vein if the fistula is large [17].

Small fistulas are self-limiting while those of bigger dimensions require endovascular or surgical intervention [19, 20].

Arterial stenosis may occur at the site of anastomosis and may reduce the perfusion of the graft. Occasionally, the arterial “Y graft” conduit may kink [14].

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.

US demonstrates free fluid, fluid collections with internal echoes and fluid–fluid levels. On unenhanced CT studies high-attenuation intraperitoneal free fluid or collections, with a fluid–fluid level can be seen. Performing contrast enhanced CT may reveal extravasation of contrast if there is active bleeding [21].

In the early postoperative period, a mild pancreatitis is common (about 35% of patients) as reperfusion injury after transplantation, which may lead to impaired microcirculation, but is often self-limiting [22].

On US the pancreas can appear enlarged and heterogeneous; moreover surrounding fluid or mural thickening of the adiacent bowel loops may be noted. Necrosis, fluid collection, pseudocyst, pancreatic infarction and necrosis can also be detected on US.

CT and MR are more sensitive than US at detecting complications [16].

MR imaging can better demonstrate graft oedema and related complications such as vascular thrombosis.

Rejection continues to be the primary cause of graft loss, with rates between 5% and 25%, depending on the immunosuppressive regimen [1].

Although the rate of acute rejection has decreased significantly in recent years, chronic rejection remains the major long-term cause of graft failure after the first 6 months, with little long-term improvement in pancreas survivability [23]. 

On US non-specific findings such as graft enlargement and increased parenchymal heterogeneity are seen. These findings may however also be visualised in acute pancreatitis and ischemia [24].

MR imaging demonstrates allograft edema as increased T2 signal intensity which is also seen in ischemia and pancreatitis.

In chronic rejection clinical findings include loss of exocrine and endocrine function of the organ.

On US the graft is no longer recognisable.

CT findings are non-specific: loss of volume, decreased post contrast enhancement and calcification may be seen.

MR angiography demonstrates homogenously decreased or heterogenous enhancement of the graft. Infarction, necrosis and occlusion of the small-vessels are also seen [1].

Graft duodenal leakage complication can be associated with pancreatic graft loss and requires surgical repair (suture of duodenal defect, jejuno-jejunal Roux-en-Y exclusion, or jejunal patch over the duodenal defect).

CT with oral and intravenous contrast administration is useful for evaluating and directly demonstrating duodenal leaks, perforation or peritoneal inflammation, intra-abdominal abscess or collection, small bowel obstruction, infectious colitis due to immunosuppression, pancreatic leakage and pancreatic fistula. Pancreatic leakage is rarely encountered, as most procedures are performed with enteric drainage for exocrine secretions. However, the complication might occur when the graft is biopsied. A pancreatic fistula usually appears as peri-pancreatic graft collection containing high amylase levels on biochemical examination of fluid following aspiration. It tends to resolve with conservative treatment. It may result from anastomotic leakage at the duodeno-enterostomy site or small bowel obstruction.

Small bowel obstruction is more often due to intestinal adhesions.

An internally drained pancreas with intraperitoneal placement is an additional risk for internal hernia which increases the risk for strangulation more than bowel adhesion. At CT scan it is seen as dilatation of loops of distal small bowel posterior to the graft [9].

Post-Transplant Lymphoproliferative Disease (PTLD) is a rare late complication and has been reported with an incidence of 3–12% after pancreatic transplantation.

Focal masses, inside or outside the graft, lymphadenopathy and/or organomegaly may also be seen on US, CT and MR imaging.

CT and MR may demonstrate the presence of focal masses, wall thickening and dilatation of involved bowel.