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Current Opinion in Organ Transplantation:
doi: 10.1097/MOT.0b013e32835c6f0f
PANCREAS TRANSPLANTATION: Edited by Walter mark

Risk factors for and management of graft pancreatitis

Nadalin, Silvio; Girotti, Paolo; Königsrainer, Alfred

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Department of General, Visceral and Transplant Surgery, Tuebingen University Hospital, Germany

Correspondence to Silvio Nadalin, MD, FEBS, Department of General, Visceral and Transplant Surgery, Tuebingen University Hospital, Hoppe Seyler Str 3, 72076 Tübingen, Germany. Tel: +49 7071 2986600; fax: +49 7071 294934; e-mail: silvio.nadalin@med.uni-tuebingen.de

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Abstract

Purpose of review: Systematic and detailed analysis of risk factors, pathophysiology, clinical manifestation, diagnosis and management of graft pancreatitis in its different forms, that is acute and chronic graft pancreatitis (A-GP and C-GP), and A-GP being further distinguished into: physiological (P-AGP), early (E-AGP) and late AP (L-AGP).

Recent findings: Graft pancreatitis is the second most-frequent complication following pancreas transplantation. P-AGP is an unavoidable entity related to ischemic reperfusion injury. It is usually clinically silent. It is a timely and prognostically self-limited process. E-AGP occurs within 3 months after pancreas transplantation (PTx) in 35% of cases and is associated with high rates of graft loss (78–91%). Clinical signs are pain, systemic inflammatory response (SIRS) and haematuria. Therapy can be medical, interventional and surgical. L-AGP occurs 3 months following PTx in 14–25% of cases and represents an uncommon cause of graft loss. Typical clinical signs are pain, abdominal tenderness and fever. Typical laboratory signs are hyperamylasaemia, hyperglycaemia and hypercreatininaemia. Therapy is usually conservative. C-GP is difficult to be distinguished from chronic rejection and is associated to graft loss in 4–10% of cases. Recurrent A-GPs and infections are the main risk factors. Specific symptoms are chronic abdominal malaise, constipation and recurrence of DM. Isolated hyperglycaemia is typical of C-GP. The therapy is usually conservative.

Summary: This systematic analysis of different manifestations of graft pancreatitis provides the basis for a clinical approach to tackling this complex entity.

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INTRODUCTION

After vascular thrombosis, graft pancreatitis is the second most-frequent complication following pancreas transplantation in its various techniques.

To date there is no standard definition for graft pancreatitis. Most definitions conform with the ones usually used for classical acute and chronic pancreatitis.

For didactic reasons two major entities of graft pancreatitis are distinguished: acute and chronic graft pancreatitis (A-GP and C-GP). A-GP has been further distinguished in three subtypes: physiological (P-AGP), early (E-AGP) and late A-GP (L-AGP).

We here describe the above-mentioned different forms of graft pancreatitis in detail.

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PHYSIOLOGICAL ACUTE GRAFT PANCREATITIS

Physiological acute graft pancreatitis occurs in 100% of pancreas transplantation (PTx) secondarily to an acute inflammatory response related to ischaemic reperfusion injury (IRI). It may occur between 30 min and 72 h after reperfusion.

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Risk factors

Per se there is not a single particular risk factor for P-AGP apart from IRI, which is intrinsically related to the procedure itself. Moreover, various factors like cold ischaemia time (CIT), donor age and microvascular disease of the graft may influence P-AGP entity [1–3].

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Pathophysiology
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The pathophysiological mechanism of P-AGP was recently described in detail by Busing et al.[1]. Induced by ischaemia (hypoxia) and reperfusion-related damage to the graft, capillary endothelial cells undergo a displacement of energy involving acidosis and the production of oxygen-free radicals (usually within the endoplasmic reticulum). This causes necrosis of endothelial cells with consequent endotheliitis and arteritis, thus leading to microvascular thrombosis and an increase in hypoxic damage and consequently in lymphocytic infiltration. This has been reported in the context of acinar necrosis and may trigger an immunological reaction (so-called innate immunity).

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Pathology

As a pancreas graft biopsy is usually not performed immediately after reperfusion or at the end of the operation, the pathological findings of P-AGP have been derived from animal studies, in which the following pathological patterns were described [1]:

1. Endothelialitis

2. Arteritis

3. Granulocytic infiltration

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Clinical manifestation

Although P-AGP appears clinically silent, it is usually associated with high levels of amylase or lipase in drain fluids and systemically increased C-reactive protein (CRP).

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Complications and prognosis

Due to its nature and perioperative administration of steroids and anticoagulant medication acting at different inflammatory phases, P-AGP is a timely and prognostically limited process.

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Diagnosis

Apart from histological patterns associated with P-AGP, no reports on diagnostic procedures have been available in the literature concerning this particular form of graft pancreatitis.

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Therapy and prophylaxis

As P-AGP is an unavoidable entity, the only possibility is to limit this acute inflammatory process at different stages of pancreas transplantation [1]:

1. The pancreas is already at risk for severe oedema upon brain death when the donor undergoes aggressive fluid resuscitation and later after revascularization upon reperfusion in the recipient. In this context, steroids administered along the retrieval procedure as well as the recipient operation may counteract the damage.

2. Calcium channel blockers may improve organ function by inducing better perfusion and reducing a high intracellular calcium concentration, which usually leads to cell death after IRI.

3. Hypotension, hypovolaemia and high doses of catecholamines at reperfusion (here, anaesthesiological management plays a pivotal role) should be avoided.

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EARLY ACUTE GRAFT PANCREATITIS

Occurring with an incidence of 35–38% mainly within 3 months after PTx, E-AGP is an acute form of pancreatitis. It develops either spontaneously or as a consequence of surgical complications [4▪▪,5–7].

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Risk factors

1. Donor [4▪▪,7,8,9▪]:

a. age above 50

b. cardio-cerebro-vascular cause of death

c. significant haemodynamic instability

d. massive volume resuscitation

2. Graft procurement [10]:

a. Procurement technique [4▪▪,7] not in accordance with the standard guidelines and the technical pitfalls reported in the literature [11]. that is:

i. careful ‘no-touch’ technique [12,13]

ii. identification of and respect for the inferior pancreaticoduodenal artery [14]

iii. ’en-bloc’ multivisceral procurement and ex-situ preparation of pancreas graft with consequent reduction of in-situ warm ischemia and careful preparation of vascular structures [10,15,16].

b. The procurement surgeon plays a key role in this context. In fact, as recently reported by Stratta et al.[17], there is no difference in transplant outcome between local and imported pancreas allografts when the graft is retrieved by an experienced PTx surgeon.

c. Preservation solution: the literature contains controversial data on preservation solutions [18]. Various authors reported a higher incidence of allograft pancreatitis and graft loss in cases of pancreata flushed with histidine-tryptophan-ketoglutarate (HTK) as compared with University of Wisconsin solution [19–21]Conversely, a recent randomized, controlled study failed to show any significant difference between HTK and University of Wisconsin solution for pancreas allograft preservation [22]. Similar results have been reported by Fridell et al.[23,24] and Becker et al.[25].

d. The back table phase: preparation of the pancreas graft at the back table requires good surgical skills and should therefore be performed by an experienced pancreas transplant surgeon. Additionally, particular technical pitfalls such as meticulous reconstruction of the superior mesenteric and splenic arterial inflow, avoidance of extension grafts of the portal vein or even revascularization of the gastroduodenal artery and the right gastroepiploic vein [4▪▪,26] require the surgeon's cautious attention [27–30].

3. Recipient operation

a. Endocrine drainage: portal versus systemic. Although theoretically, portal drainage is more physiological and should improve postoperative control of glucose metabolism [31], several studies have definitively demonstrated that portal vein drainage is at least equivalent to systemic drainage with regard to patient and short-term graft survival rates and technical complication rates [32,33]. For this reason, most PTx centres have abandoned portal vein drainage because of technical difficulties and increased morbidity as a result of venous thrombosis and enteric leaks [10].

b. Exocrine drainage.Stratta et al.[34] reported a slight increase in E-AGP in patients with exocrine drainage into the bladder (see also pathophysiology).For patients with intestinal drainage Grochowiecki et al.[35] considered the fact that the postoperative swelling of the papilla Vateri may create an obstacle to pancreatic juice outflow with consequent oedema of the pancreas graft and graft pancreatitis. The authors thus suggest that an open sphincterectomy should be performed to decompress the pancreatic graft [35].

4. RecipientRecipients who underwent peritoneal dialysis prior to transplantation [26] and those with hypercoagulability status [36] showed a higher frequency of E-AGP.

5. Infection [4▪▪,26,37]

a. Cytomegalovirus (CMV)Due to the current prophylaxis policy, CMV infection is rarely associated with acute graft loss as the result of early acute graft pancreatitis [38–40].

b. Fungal infectionCandida (albicans and glabrata) and other fungal infections are infrequent, but possible agents of acute necrotizing pancreatitis. Consequently, proper antifungal prophylaxis is essential [41].

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Immunosuppression

An immunosuppressive regimen with cyclosporin A may increase the risk for E-AGP [42–45].

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Pathophysiology

With regard to pathophysiology, two different kinds of E-AGP are distinguished.

1. E-AGP pure

a. postinfective (i.e. CMV and fungal) 10%

b. immunological (i.e. acute rejection) 30%

2. E-AGP related to surgical procedure:

a. Vascular thrombosisVascular thrombosis is responsible for 60–70% of E-AGP cases and is secondary to technical problems in 59% of patients with E-AGP or can be associated with immunological endothelial damage (e.g. hyperacute rejection) in 33% of cases [46]

b. Exocrine bladder drainageReflux of bladder-duodenal content with active trypsin and infected urine may damage the ductal mucosal barrier, resulting in intrapancreatic activation of enzymes [47–49].

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Pathology

Typical signs of post-thrombotic pancreatitis are focal or diffuse ischaemic (coagulative) or haemorrhagic necrosis [46].

Fibrinoid necrosis of arteries and veins associated with massive vascular thrombosis and parenchymal necrosis (IgG and C3 positive in the wall of blood vessels) has been shown to be typical of E-AGP secondary to hyperacute allograft rejection [50,51].

Endotheliitis and various degrees of necrotizing arteritis are the typical histological signs (acute rejection grades IV and V) of acute allograft rejection [50,51].

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Clinical manifestation

Typical clinical signs of E-AGP are pain (due to graft tenderness and enlargement), systemic inflammatory response (SIRS) (in the case of complications) and haematuria (in the case of exocrine bladder drainage) [4▪▪,6,7].

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Complications and prognosis

Early acute graft pancreatitis is associated with 1-year graft loss rates of 78–91% and with suprainfection rates with consequent SIRS in 10–20% of cases [4▪▪,7,52].

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Diagnosis

1. Laboratory

a. Hyperglycaemia

b. Hyperamylasemia (not present in case of rejection alone)

2. Imaging

a. Sonography can detect heterogeneous parenchymal echotexture, pancreatic duct dilatation and change in blood flow, but cannot assess vessel contour abnormality. Sonography is thus not a reliable means of identifying acute organ rejection or pancreatitis and, moreover, is operator-dependent [53].

b. Computed tomography (CT) scan is the gold standard for the diagnosis of complications following PTx. It is widely available and relatively low in cost. Moreover, rapid image acquisition multidetector CT (MDCT) is a quick noninvasive means of identifying the cause of pancreatic graft dysfunction when renal function is not markedly impaired. CT scan is useful for demonstrating the extent and severity of graft pancreatitis. CT findings are similar to those for native pancreatitis, that is peripancreatic fat stranding and peripancreatic collections [53–56]. Additionally, a CT-guided biopsy of the graft can also be performed.

c. Contrast-enhanced magnetic resonance (MR) angiography has been shown to reliably assess the vascular anatomy in cases of impaired graft function or suspected vascular complications. However, the following two possible complications should be kept in mind: the risk for nephrogenic systemic fibrosis from gadolinium administration in the setting of severe renal impairment and the possible induction of movement of surgical clips during the early postoperative period [57,58].

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Therapy

1. Medical (depending on cause) [4▪▪,7].

a. Antithrombotic therapy

b. Bowel rest and temporary administration of total parenteral nutrition

c. Treatment of concurrent infections

2. Radiological interventionalIn the case of vascular thrombosis transarterial or transvenous graft salvage procedures with long-term graft survival rates of 50% have been reported [59–61].

3. SurgicalTo date the literature contains no clear standardized guidelines for timing or type of surgical procedure like necrosectomy or graft explantation. These procedures depend on intraoperative findings, clinical course and the surgeon's experience. If a pancreas graft is removed, a pancreas re-transplantation should not be performed before 2–4 weeks [5,8,62–64].

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LATE ACUTE GRAFT PANCREATITIS

Graft pancreatitis occurring 3 months following PTx may be termed L-AGP and has been observed in 14–25% of cases [65,66].

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Risk factors and pathophysiology [38,66]

1. Exocrine bladder drainage: most cases of L-AGP are attributed to urinary reflux, urinary tract infection or bladder outflow obstruction. In this last case a bladder pressure above 20 cmH2O2 may induce a vascular disorder such as a decrease in differential venous pressure, resulting in acute ischaemia.

2. Mechanical stricture and trauma or direct mechanical pressure to the graft.

3. Direct traumatic injury of the graft.

4. Intraparenchymal microvascular thrombosis due to a chronic immunological disturbance that does not induce acute rejection, but may chronically influence venous outflow from the pancreas graft and consequently cause ischemic damage.

5. Recurrent infection surrounding the graft like in the case of a late microleak of exocrine drainage.

6. Occlusion of Oddi's sphincter secondary to rejection.

7. CMV infection: as reported above, CMV infection is rarely associated with acute graft loss due to the development of early acute graft pancreatitis, but CMV reactivation seems to be associated with delayed graft function and the risk for late acute pancreatitis and chronic recurrence of diabetes mellitus (DM) [38,40].

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Pathology

Typical signs of L-AGP are lymphocytic infiltrates involving the pancreatic duct and its branches. It should be differentiated from acute late rejection, which presents with the pathognomonic vascular changes of endothelialitis or vasculitis [46,50]

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Clinical manifestation

The most frequently reported symptoms of L-AGP are pain in 100%, abdominal tenderness in 87% and fever in 64% of cases. In 48% of cases associated symptoms are also reported: vomiting, diarrhoea and bloating [47,66–71].

Rare manifestations of L-AGP are:

1. acute urinary retention [67],

2. erythema nodosum in the pretibial areas (pancreatic panniculitis) [68,72],

3. haemorrhagic cystitis in patients with bladder drainage [70].

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Prognosis

Late acute graft pancreatitis is an uncommon cause of graft loss.

In patients with L-AGP overall graft survival at 1, 3 and 5 years has been reported to be 95, 93 and 89%, respectively [66,73].

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Diagnosis

1. LaboratoryThe typical laboratory sign of L-AGP is the triad hyperamylasemia + hyperglycaemia + hypercreatininaemia or an increase of inflammatory parameters.Graft pancreatitis can be differentiated from acute rejection on the basis of marked hyperamylasemia and significant local findings adjacent to the allograft, both of which are not characteristic of acute rejection (usually characterized by isolated hyperglycaemia) [66,74,75].It is important to mention that in patients with bladder drainage urinary amylase does not correlate with L-AGP [47].

2. Imaging.

a. Sonography: detection of peripancreatic fluid collections and presence or absence of blood flow [76].

b. Computed tomography: this is the gold standard radiological investigation for diagnosis of L-AGP. It demonstrates pancreatic infiltration, oedema, and peripancreatic fluid [47,66,71].

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Therapy

Most authors [47,66–71] who have reported on L-AGP suggest the following therapeutic principles:

1. Bowel rest (100%)

2. Hydration (100%)

3. Close monitoring (100%)

4. Antibiotics (50–73%)

In patients with complicated L-AGP a percutaneous or operative drainage is suggested in 12% and relaparotomy without pancreatectomy in 12%.

In case of L-AGP associated to complicated course after bladder drainage, the enteric conversion of the exocrine drainage may result in excellent long-term graft function and significant resolution of symptoms even years after SPK. Notwithstanding, postoperative morbidity after enteric conversion including early reoperation and graft loss has to be considered [77]. No clear data about indication and timing of pancreatectomy have been reported.

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CHRONIC GRAFT PANCREATITIS

No clear definition of chronic graft pancreatitis (C-GP) has been established to date because its nature is characteristically an overlapping of chronic rejection and chronic pancreatitis. Similarly, no data have been reported on its incidence [46,50,51]

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Risk factors and pathophysiology

The literature also contains very few data on these two aspects. The main pathogenic factors can be considered to be:

1. Inflammatory: recurrent acute pancreatitis of different cause

2. Immunological: chronic rejection

3. Infective: CMV and fungal

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Pathology

Typical histological features of C-GP are isleitis (i.e. disruption of beta cells), extensive interstitial fibrosis, acinar atrophy and obliterative arthritis [51].

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Clinical manifestation

Specific symptoms of C-GP are [46,50,51]:

1. Chronic abdominal malaise

2. Chronic obstipation

3. Recurrence of DM

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Prognosis

Chronic graft pancreatitis can be complicated by suprainfections.

It is a cause of late graft loss in 4–10% of cases [46,50,51].

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Diagnosis

1. LaboratoryThe typical sign of C-GP is isolated hyperglycaemia with no changes in amylasemia.

2. ImagingComputed tomography and MRI usually show a retracted fibrotic graft.

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Therapy

No clear data/guidelines have been established to date.

In patients with C-GP but without complications we suggest a conservative therapy. A graft pancreatectomy should be performed for local and systemic complications and to halt immunosuppression in cases of pancreas transplantation alone.

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CONCLUSION

In this study we have reviewed the concept of graft pancreatitis in its different forms, i.e. physiological, early acute, late acute and chronic graft pancreatitis.

This systematic analysis of different manifestations of graft pancreatitis provides better understanding and therefore the basis for a clinical approach to tackling this complex entity.

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Acknowledgements

We would like to express our immense gratitude to Ms Mary Margreiter for her essential support in improving the English grammar and syntax of the text.

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Conflicts of interest

There are no conflicts of interest to declare.

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REFERENCES AND RECOMMENDED READING

Papers of particular interest, published within the annual period of review, have been highlighted as:

▪ of special interest

▪▪ of outstanding interest

Additional references related to this topic can also be found in the Current World Literature section in this issue (pp. 124–125).

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REFERENCES

1. Busing M, Hopt UT, Quacken M, et al. Morphological studies of graft pancreatitis following pancreas transplantation. Br J Surg 1993; 80:1170–1173.

2. Benz S, Bergt S, Obermaier R, et al. Impairment of microcirculation in the early reperfusion period predicts the degree of graft pancreatitis in clinical pancreas transplantation. Transplantation 2001; 71:759–763.

3. Grewal HP, Garland L, Novak K, et al. Risk factors for postimplantation pancreatitis and pancreatic thrombosis in pancreas transplant recipients. Transplantation 1993; 56:609–612.

4▪▪. Troppmann C. Complications after pancreas transplantation. Curr Opin Organ Transplant 2010; 15:112–118.

Excellent systematic review of complications after pancreas transplantation focused mainly on donor and recipient selection as well on preservation and surgical factors affecting the short- and long-term outcome.

5. Manrique A, Jimenez C, Lopez RM, et al. Relaparotomy after pancreas transplantation: causes and outcomes. Transplant Proc 2009; 41:2472–2474.

6. Ozaki CF, Stratta RJ, Taylor RJ, et al. Surgical complications in solitary pancreas and combined pancreas-kidney transplantations. Am J Surg 1992; 164:546–551.

7. Goodman J, Becker YT. Pancreas surgical complications. Curr Opin Organ Transplant 2009; 14:85–89.

8. Troppmann CPJ, Perez RV, Gruessner RW. The unrecognized posterior gastric artery: a potential cause of surgical complications in pancreas transplantation. Am J Transplant 2004; 4:544–553.

9▪. Fellmer PT, Pascher A, Kahl A, et al. Influence of donor- and recipient-specific factors on the postoperative course after combined pancreas-kidney transplantation. Langenbecks Arch Surg 2010; 395:19–25.

Excellent single-centre analysis of 210 SPKs aimed to identify donor- and recipient-specific factors related to postoperative complications.

10. Lam VW, Pleass HC, Hawthorne W, et al. Evolution of pancreas transplant surgery. ANZ J Surg 2010; 80:411–418.

11. Schulz T, Flecken M, Schenker P, et al. Pancreas removal by external teams. Chirurg 2005; 76:581–586.discussion 586–587.

12. D’Alessandro AM, Stratta RJ, Sollinger HW, et al. Use of UW solution in pancreas transplantation. Diabetes 1989; 38 (Suppl 1):7–9.

13. Stratta RJ, Taylor RJ, Spees EK, et al. Refinements in cadaveric pancreas-kidney procurement and preservation. Transplant Proc 1991; 23:2320–2322.

14. Abu-Elmagd K, Fung J, Bueno J, et al. Logistics and technique for procurement of intestinal, pancreatic, and hepatic grafts from the same donor. Ann Surg 2000; 232:680–687.

15. Brockmann JG, Vaidya A, Reddy S, et al. Retrieval of abdominal organs for transplantation. Br J Surg 2006; 93:133–146.

16. Boggi U, Vistoli F, Del Chiaro M, et al. A simplified technique for the en bloc procurement of abdominal organs that is suitable for pancreas and small-bowel transplantation. Surgery 2004; 135:629–641.

17. Stratta RJ, Farney AC, Rogers J. Import pancreas allografts: good from far or far from good? Transplantation 2009; 88:622–623.

18. Ridgway D, Manas D, Shaw J, et al. Preservation of the donor pancreas for whole pancreas and islet transplantation. Clin Transplant 24:1–19.

19. Alonso D, Dunn TB, Rigley T, et al. Increased pancreatitis in allografts flushed with histidine-tryptophan-ketoglutarate solution: a cautionary tale. Am J Transplant 2008; 8:1942–1945.

20. Stewart ZA, Cameron AM, Singer AL, et al. Histidine-tryptophan-ketoglutarate (HTK) is associated with reduced graft survival in pancreas transplantation. Am J Transplant 2009; 9:217–221.

21. Englesbe MJ, Moyer A, Kim DY, et al. Early pancreas transplant outcomes with histidine-tryptophan-ketoglutarate preservation: a multicenter study. Transplantation 2006; 82:136–139.

22. Schneeberger S, Biebl M, Steurer W, et al. A prospective randomized multicenter trial comparing histidine-tryptophane-ketoglutarate versus University of Wisconsin perfusion solution in clinical pancreas transplantation. Transpl Int 2009; 22:217–224.

23. Fridell JA, Mangus RS, Powelson JA. Histidine-tryptophan-ketoglutarate for pancreas allograft preservation: the Indiana University experience. Am J Transplant 2010; 10:1284–1289.

24. Fridell JA, Mangus RS, Powelson JA. Organ preservation solutions for whole organ pancreas transplantation. Curr Opin Organ Transplant 2011; 16:116–122.

25. Becker T, Ringe B, Nyibata M, et al. Pancreas transplantation with histidine-tryptophan-ketoglutarate (HTK) solution and University of Wisconsin (UW) solution: is there a difference? JOP 2007; 8:304–311.

26. Troppmann C, Gruessner AC, Dunn DL, et al. Surgical complications requiring early relaparotomy after pancreas transplantation: a multivariate risk factor and economic impact analysis of the cyclosporine era. Ann Surg 1998; 227:255–268.

27. Thai N, Khan A, Tom K, et al. Revascularization of the gastroduodenal artery in a pancreas allograft from a donor with a replaced right hepatic artery. Transplantation 2005; 79:503.

28. Socci C, Orsenigo E, Zuber V, et al. Triple arterial reconstruction improves vascularization of whole pancreas for transplantation. Transplant Proc 2006; 38:1158–1159.

29. Nghiem DD. Ipsilateral portal enteric drained pancreas-kidney transplantation: a novel technique. Transplant Proc 2008; 40:1555–1556.

30. Muthusamy AS, Elker DE, Roy D, et al. Complex arterial reconstruction for pancreas transplantation in recipients with advanced arteriosclerosis. Transplantation 2008; 85:161–162.

31. Calne RY. Paratopic segmental pancreas grafting: a technique with portal venous drainage. Lancet 1984; 1:595–597.

32. Stratta RJ, Shokouh-Amiri MH, Egidi MF, et al. A prospective comparison of simultaneous kidney-pancreas transplantation with systemic-enteric versus portal-enteric drainage. Ann Surg 2001; 233:740–751.

33. Quintela J, Aguirrezabalaga J, Alonso A, et al. Portal and systemic venous drainage in pancreas and kidney-pancreas transplantation: early surgical complications and outcomes. Transplant Proc 2009; 41:2460–2462.

34. Stratta RJ, Gaber AO, Shokouh-Amiri MH, et al. Allograft pancreatectomy after pancreas transplantation with systemic-bladder versus portal-enteric drainage. Clin Transplant 1999; 13:465–472.

35. Grochowiecki T, Szmidt J, Galazka Z, et al. Duodenal patch and sphincterotomy: modification of an old technique to prevent graft pancreatitis. Transplant Proc 2006; 38:269–272.

36. Adrogue HE, Matas AJ, McGlennon RC, et al. Do inherited hypercoagulable states play a role in thrombotic events affecting kidney/pancreas transplant recipients? Clin Transplant 2007; 21:32–37.

37. Berger N, Wirmsberger R, Kafka R, et al. Infectious complications following 72 consecutive enteric-drained pancreas transplants. Transpl Int 2006; 19:549–557.

38. Margreiter R, Schmid T, Dunser M, et al. Cytomegalovirus (CMV)--pancreatitis: a rare complication after pancreas transplantation. Transplant Proc 1991; 23:1619–1622.

39. Maglione M, Biebl MO, Bonatti H, et al. Cytomegalovirus mismatch as major risk factor for delayed graft function after pancreas transplantation. Transplantation 90:666–671.

40. Parsaik AK, Bhalla T, Dong M, et al. Epidemiology of cytomegalovirus infection after pancreas transplantation. Transplantation 92:1044–1050.

41. Rossetto A, Baccarani U, Lorenzin D, et al. Disseminate fungal infection after acute pancreatitis in a simultaneous pancreas-kidney recipient. J Transplant 2010; 2010:898245.

42. Steurer W, Malaise J, Mark W, et al. Spectrum of surgical complications after simultaneous pancreas-kidney transplantation in a prospectively randomized study of two immunosuppressive protocols. Nephrol Dial Transplant 2005; 20 (Suppl 2):ii54–62.

43. Kandaswamy R, Humar A, Gruessner AC, et al. Vascular graft thrombosis after pancreas transplantation: comparison of the FK 506 and cyclosporine eras. Transplant Proc 1999; 31:602–603.

44. Humar A, Ramcharan T, Kandaswamy R, et al. Technical failures after pancreas transplants: why grafts fail and the risk factors: a multivariate analysis. Transplantation 2004; 78:1188–1192.

45. Vinkers MT, Rahmel AO, Slot MC, et al. How to recognize a suitable pancreas donor: a Eurotransplant study of preprocurement factors. Transplant Proc 2008; 40:1275–1278.

46. Drachenberg CB, Papadimitriou JC, Farney A, et al. Pancreas transplantation: the histologic morphology of graft loss and clinical correlations. Transplantation 2001; 71:1784–1791.

47. Fernandez-Cruz L, Sabater L, Gilabert R, et al. Native and graft pancreatitis following combined pancreas-renal transplantation. Br J Surg 1993; 80:1429–1432.

48. Kallen R, Borgstrom A. Characterization of immunoreactive trypsin as a means of differentiating graft pancreatitis and allograft rejection after porcine pancreatic transplantation. Transplantation 1992; 53:25–29.

49. See WA, Smith JL. Urinary levels of activated trypsin in whole-organ pancreas transplant patients with duodenocystostomies. Transplantation 1991; 52:630–633.

50. Sibley RK, Sutherland DE. Pancreas transplantation. An immunohistologic and histopathologic examination of 100 grafts. Am J Pathol 1987; 128:151–170.

51. Nakhleh RE, Gruessner RW, Swanson PE, et al. Pancreas transplant pathology. A morphologic, immunohistochemical, and electron microscopic comparison of allogeneic grafts with rejection, syngeneic grafts, and chronic pancreatitis. Am J Surg Pathol 1991; 15:246–256.

52. Malaise J, Secchi A, Caldara R, et al. Metabolic assessment after simultaneous pancreas-kidney transplantation. Transplant Proc 2005; 37:2851–2852.

53. Tan ZY, Lau KK. Multidetector CT/CT angiogram assessment of acute pancreatic graft dysfunction. J Med Imaging Radiat Oncol 2011; 55:571–576.

54. Low RA, Kuni CC, Letourneau JG. Pancreas transplant imaging: an overview. Am J Roentgenol 1990; 155:13–21.

55. Ciancio G, Montalvo B, Roth D, et al. Allograft pancreatic duct dilatation following bladder drained simultaneous pancreas-kidney transplantation: clinical significance. JOP 2000; 1:4–12.

56. Dachman AH, Newmark GM, Thistlethwaite JR Jr, et al. Imaging of pancreatic transplantation using portal venous and enteric exocrine drainage. Am J Roentgenol 1998; 171:157–163.

57. Krebs TL, Daly B, Wong JJ, et al. Vascular complications of pancreatic transplantation: MR evaluation. Radiology 1995; 196:793–798.

58. Boeve WJ, Kok T, Tegzess AM, et al. Comparison of contrast enhanced MR-angiography-MRI and digital subtraction angiography in the evaluation of pancreas and/or kidney transplantation patients: initial experience. Magn Reson Imaging 2001; 19:595–607.

59. Stockland AH, Willingham DL, Paz-Fumagalli R, et al. Pancreas transplant venous thrombosis: role of endovascular interventions for graft salvage. Cardiovasc Intervent Radiol 2009; 32:279–283.

60. Douzdjian V, Abecassis MM, Cooper JL, et al. Pancreas transplant salvage after acute venous thrombosis. Transplantation 1993; 56:222–223.

61. Gilabert R, Fernandez-Cruz L, Real MI, et al. Treatment and outcome of pancreatic venous graft thrombosis after kidney: pancreas transplantation. Br J Surg 2002; 89:355–360.

62. MacMillan N, Fernandez-Cruz L, Ricart MJ, et al. Venous graft thrombosis in clinical pancreas transplantation: options for a rescue treatment. Transplant Proc 1998; 30:425–426.

63. Sansalone CV, Maione G, Rossetti O, et al. Pancreas retransplantation: ideal timing and early and late results. Transplant Proc 2006; 38:1153–1155.

64. Hollinger EF, Powelson JA, Mangus RS, et al. Immediate retransplantation for pancreas allograft thrombosis. Am J Transplant 2009; 9:740–745.

65. Linder R, Tyden G, Tibell A, et al. Late graft pancreatitis. Transplantation 1990; 50:257–261.

66. Small RM, Shetzigovski I, Blachar A, et al. Redefining late acute graft pancreatitis: clinical presentation, radiologic findings, principles of management, and prognosis. Ann Surg 2008; 247:1058–1063.

67. Laven BA, Rapp DE, Avila D, et al. Necrotic pancreatic graft causing acute urinary retention. Urol Int 2005; 74:278–279.

68. Pike JL, Rice JC, Sanchez RL, et al. Pancreatic panniculitis associated with allograft pancreatitis and rejection in a simultaneous pancreas-kidney transplant recipient. Am J Transplant 2006; 6:2502–2505.

69. Sharma AK, Sinha S, Smith D, et al. Recurrent graft pancreatitis in a pancreatic-renal allograft recipient does not affect endocrine function. Transpl Int 2002; 15:521–522.

70. Roxvall LI, Frisk B, Hedman L, et al. Graft pancreatitis and hemorrhagic cystitis. Treatment with bladder irrigation and protease inhibition. Transpl Int 1988; 1:228–229.

71. Jayawardene SA, Taylor JD, Koffman CG, et al. Acute allograft pancreatitis associated with renal allograft rejection. Nephrol Dial Transplant 2002; 17:288–290.

72. Langeveld-Wildschut EG, Toonstra J, Oldenburg B, et al. Pancreatogenic panniculitis. Ned Tijdschr Geneeskd 1996; 140:28–31.

73. Gruessner 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; 19:433–455.

74. Stratta RJ, Sollinger HW, Groshek M, et al. Differential diagnosis of hyperamylasemia in pancreas allograft recipients. Transplant Proc 1990; 22:675–677.

75. Papadimitriou JC, Drachenberg CB, Wiland A, et al. Histologic grading of acute allograft rejection in pancreas needle biopsy: correlation to serum enzymes, glycemia, and response to immunosuppressive treatment. Transplantation 1998; 66:1741–1745.

76. Nikolaidis P, Amin RS, Hwang CM, et al. Role of sonography in pancreatic transplantation. Radiographics 2003; 23:939–949.

77. Kleespies A, Mikhailov M, Khalil PN, et al. Enteric conversion after pancreatic transplantation: resolution of symptoms and long-term results. Clin Transplant 2011; 25:549–560.

Keywords:

complications; graft pancreatitis; pancreas transplantation

© 2013 Lippincott Williams & Wilkins, Inc.

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