Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Pancreas Transplantation Follow-up

  • Author: Dixon B Kaufman, MD, PhD; Chief Editor: Ron Shapiro, MD  more...
 
Updated: Dec 02, 2015
 

Further Outpatient Care

Transplantation outpatient follow-up care

Typical visit schedule following discharge from the hospital is as follows:

  • Two or 3 visits in week 1
  • Two visits in week 2
  • One visit in week 3
  • Monthly thereafter, until 6 months posttransplantation
  • Every 3 months through the first year
  • Every 6 months through the second year
  • Annually thereafter

Laboratory follow-up studies occur in the transplantation clinic and at a local laboratory near the patient's home. A typical schedule is as follows:

  • Every Monday, Wednesday, and Friday in month 1
  • Every Monday and Thursday in month 2
  • Every Monday in months 3-6
  • Every other week in months 7-24
  • Every month after 24 months

Typical laboratory evaluation includes complete blood count, electrolytes, BUN, creatine, glucose, serum amylase, and immunosuppression blood levels (if transplantation recipient is receiving cyclosporine, tacrolimus, or sirolimus).

Next

Inpatient & Outpatient Medications

See the list below:

  • Immunosuppression medications: Immunosuppression must be taken for as long as the patient's transplanted organs are functioning. Immunosuppression cannot be stopped, or rejection of the organs will ensue.
Previous
Next

Complications

Rejection

The first criteria for the diagnosis of acute cell-mediated allograft rejection (ACMR) were established in 2008.[11] At the time, only tentative criteria for the diagnosis of antibody-mediated rejection (AMR) were characterized. In 2011 comprehensive guidelines were presented for the diagnosis of AMR.[12]

Surgical and nonimmunological complications of pancreas transplantation

Surgical complications are more common after pancreas transplantation as compared to kidney transplantation. Nonimmunological complications of pancreas transplantation account for graft losses in 5-10% of cases. These occur commonly within 6 months of transplantation and are as important an etiology of pancreas graft loss in SPK transplantation as acute rejection is.

Thrombosis

Vascular thrombosis is a very early complication, typically occurring within 48 hours and usually within 24 hours of the transplantation.[5] This generally is due to venous thrombosis of the pancreas portal vein. The etiology is not defined entirely but is believed to be associated with reperfusion pancreatitis and the relatively low-flow state of the pancreas graft. Prudent selection of donor pancreas grafts, short cold-ischemia times, and meticulous surgical technique are all necessary to minimize graft thrombosis.

Transplantation pancreatitis

Pancreatitis of the allograft occurs to some degree in all patients postoperatively. Temporary elevation in serum amylase levels for 48-96 hours after transplantation is common. These episodes are transient and mild, without significant clinical consequence. Interestingly, patients undergoing simultaneous kidney-pancreas transplantation commonly have a greater degree of fluid retention for several days after transplantation, as compared to a recipient of a kidney transplant alone. Though not proven, this may be related to the graft pancreatitis that ensues in the perioperative period. The retained fluid is mobilized early postoperatively. It is important to minimize the risk of delayed kidney graft function by shortening cold-ischemia time so that the retained third-spaced fluid may be eliminated rapidly to avoid an episode of heart failure or pulmonary edema.

Complications of bladder-drained pancreas transplantation

Bladder-drained pancreas transplantation is a safer procedure than enteric-drained pancreas transplantation with respect to the possibility of intra-abdominal abscess. However, it is hampered by numerous less morbid complications. The pancreas transplantation eliminates approximately 500 mL of richly bicarbonate fluid with pancreatic enzymes into the bladder each day. Change in pH level of the bladder accounts, in part, for a greater increase in urinary tract infections. In some cases, a foreign body, such as an exposed suture from the duodenocystostomy, acts as a nidus for urinary tract infections or stone formation.

Acute postoperative hematuria of the bladder-drained pancreas usually is due to ischemia/reperfusion injury to the duodenal mucosa or to a bleeding vessel on the suture line that is aggravated by the antiplatelet or anticoagulation protocols to minimize vascular thrombosis. These cases are self-limited but may require change in bladder irrigations and, if severe, cystoscopy to evacuate the clots. Occasionally, performing a formal open cystotomy and suture ligation of the bleeding vessel is necessary intraoperatively. If relatively late chronic hematuria occurs, transcystoscopic or formal operative techniques may be necessary treatments.

Sterile cystitis, urethritis, and balanitis may occur after bladder-drained pancreas transplantation. This is due to the effect of the pancreatic enzymes on the urinary tract mucosa and is experienced more commonly in male recipients. Urethritis can progress to urethral perforation and perineal pain. Conservative treatment with Foley catheterization and operative enteric conversion represent the extremes of the continuum of treatment.

Metabolic acidosis routinely develops as a consequence of bladder excretion of large quantities of alkaline pancreatic secretions. Patients must receive oral bicarbonate supplements to minimize the degree of acidosis. Because of the relatively large volume losses, patients also are at risk of episodes of dehydration exacerbated by significant orthostatic hypotension.

Reflux pancreatitis can result in acute inflammation of the pancreas graft, mimicking acute rejection. It is associated with pain and hyperamylasemia and is believed to be secondary to reflux of urine through the ampulla and into the pancreatic ducts. Often, the urine is found to be infected with bacteria. This frequently occurs in a patient with neurogenic bladder dysfunction. This complication is managed by Foley catheterization. Reflux pancreatitis will resolve quickly. The patient may require a complete workup of the cause of bladder dysfunction, including a pressure-flow study and voiding cystourethrogram. Interestingly, in older male patients, even mild hypertrophy of the prostate has been described as a cause of reflux pancreatitis. If recurrent graft pancreatitis occurs, enteric conversion may be indicated.

Urine leak from breakdown of the duodenal segment can occur and is usually encountered within the first 2-3 months following transplantation but can occur years following transplantation. This is the most serious postoperative complication of the bladder-drained pancreas. The onset of abdominal pain with elevated serum amylase, which can mimic reflux pancreatitis or acute rejection, is a typical presentation. A high index of suspicion for urinary leak is necessary to make the diagnosis accurately and swiftly. Supporting imaging studies using a cystogram or CT scan are necessary to confirm the diagnosis. Operative repair is usually required with exploration. The degree of leakage can be determined best intraoperatively, and proper judgment can be made whether direct repair is possible or more aggressive surgery involving enteric diversion or even graft pancreatectomy is indicated.

Complications of enteric-drained pancreas transplantation

The most serious complication of the enteric-drained pancreas transplantation is leak and intra-abdominal abscess. This serious problem usually occurs 1-6 months after transplantation. Patients present with fever, abdominal discomfort, and leukocytosis. A high index of suspicion is required to make a swift and accurate diagnosis. Imaging studies involving CT scan are very helpful.

Percutaneous access of intra-abdominal fluid collection for Gram stain and culture is essential. The flora typically is mixed with bacteria and often fungus, particularly Candida. Broad-spectrum antibiosis is essential. Surgical exploration and repair of the enteric leak is necessary. A decision must be made on whether the infection can be eradicated without removing the pancreas allograft. Incomplete eradication of the infection will result in progression to sepsis and multiple organ system failure. Peripancreatic infections can result in development of a mycotic aneurysm at the arterial anastomosis that could cause arterial rupture. Transplantation pancreatectomy is indicated if mycotic aneurysm is diagnosed.

Occurrence of intra-abdominal abscess has been reduced greatly with greater recognition of the criteria for suitable cadaveric pancreas grafts for transplantation. Improved perioperative antibiosis, including antifungal agents, has contributed to the decreased incidence of intra-abdominal infection, as well. No convincing evidence exists that a Roux-en-Y intestinal reconstruction decreases its incidence. Perhaps the most significant contribution to reducing the incidence of intra-abdominal abscess is the efficacy of the immunosuppressive agents in reducing the incidence of acute rejection and thereby minimizing the need for intensive antirejection immunotherapy.

GI bleeding occurs in the enteric-drained pancreas from a combination of perioperative anticoagulation and bleeding from the suture line of the duodenoenteric anastomosis. This is self-limited and will manifest as diminished hemoglobin level associated with heme-positive or melanotic stool. Conservative management will suffice; the necessity for reoperative exploration is extremely unusual.

Previous
Next

Prognosis

The 2007 survival rates of kidney and pancreas grafts and for patients (the most recent era analyzed by the Scientific Registry of Transplant Recipients and International Pancreas Transplant Registry) were the best outcomes reported to date. One-year survival rates were 95-98% for patients, 92% for kidney grafts, and 86% for pancreas grafts. Statistically and clinically, the outcome of kidney transplantation is significantly superior in patients receiving SPK transplantation versus patients with type I diabetes receiving kidney transplantation alone.

For pancreas-after-kidney transplantation, patient survival rates have steadily improved over the interval from 1998-2007, with a current 1-year patient survival rate of 95.7%. Similarly, pancreas graft functional survival rates have greatly improved over this interval, from a nadir of 65% to a high of 77% at 1 year after transplantation. The immunologic risk for graft loss for the technically successful cases has been reduced from a high of 28% to only 9% at 1 year. The relative risks for pancreas graft loss in the pancreas after kidney recipient include increasing donor and recipient age, increasing HLA mismatches, and retransplantation. Positive effects are shown with the use of tacrolimus maintenance immunosuppression.

One analysis of 2,776 PAK recipients in the US between 1989 and 2007 compared their risk of kidney failure to young adult diabetic kidney-only transplant recipients during the same time period. Results showed an increased risk of mortality early after pancreas transplantation, but a lowered risk of kidney allograft failure in PAK recipients compared to kidney-only recipients.[13]

For patients receiving pancreas transplantation alone, patient survival rates have been increasing over the period from 1998-2007; the current rate is 97.6% at 1 year posttransplantation. Pancreas graft functional survival rates have improved significantly to the current rate of 81% at 1 year posttransplantation. The immunological risk for graft loss for the technically successful cases is approximately 10% at 1 year. The relative risks for pancreas graft loss for pancreas transplantation alone recipients are increasing donor age and HLA mismatches, and a positive affect can be observed with the use of anti–T-cell induction immunotherapy and use of tacrolimus maintenance immunotherapy.

Effect of pancreas transplantation on secondary complications of diabetes

Recipients of successful pancreas transplantation maintain normal plasma glucose levels without the need of exogenous insulin therapy. This results in normalization of glycosylated hemoglobin levels and a beneficial effect on many secondary complications of diabetes. The durability of the transplanted endocrine pancreas has been established with the demonstration that normalization of glycosylated hemoglobin is maintained as long as the allograft functions. The potential lifespan of the transplanted pancreas is not known precisely because, at present, survivors with functioning pancreas transplantations still are doing well more than 16 years after transplantation. The implications of prolonged normalization of glycemia and glycosylated hemoglobin levels are significant with respect to patients' quality of life, kidney structure, and motor-sensory and nerve function.

One long-term follow-up study of 15 years showed that pancreas transplantation in patients with type 1 diabetes mellitus and end-stage renal failure has long-term functional viability. However, some deterioration in pancreas function should be expected, as shown in oral glucose tolerance test results.[14]

The quality of life of pancreas transplantation recipients has been well studied. Patients with a functioning pancreas graft describe their quality of life and rate their health significantly more favorably than those with nonfunctioning pancreas grafts. Satisfaction encompasses not only the physical capacities but also relates to psychosocial and vocational aspects. The functioning pancreas graft leads to even better quality of life when compared to recipients of kidney transplantation alone.[8, 15] Virtually all patients with a successful pancreas transplantation report that managing their life, including immunosuppression, is much easier since the transplantation. Successful pancreas transplantation will not elevate all patients with diabetes to the level of health and functioning of the general population, but transplant recipients consistently report a significantly better quality of life than do patients who remain diabetic.

The development of diabetic nephropathy in transplanted kidneys residing in patients with type I diabetes has been well established. Marked variability is observed in the rate of renal pathology, including mesangial expansion and a widening of the glomerular basement membrane, in patients with type I diabetes and kidney transplantation alone. The onset of pathological lesions can be detected within a few years of kidney transplantation. Clinical deterioration of renal allograft function can lead to loss 10-15 years after transplantation.

A successful pancreas transplantation prevents glomerular structure changes of kidney allografts in patients with type I diabetes. This has been observed in transplanted kidneys of patients undergoing SPK transplantation, as well as in kidneys of recipients undergoing pancreas after kidney transplantation. These studies provide evidence of the efficacy of normalizing blood glucose and glycosylated hemoglobin levels to prevent the progression of diabetic glomerulopathy in renal allografts.

Furthermore, successful pancreas transplantation will halt or reverse the pathology in the native kidneys of patients with type I diabetes and very early proteinuria. Pancreas transplantation recipients all had persistently normal glycosylated hemoglobin values after transplantation for 5-10 years. The thickness of the glomerular and tubular basement membranes and mesangial volume steadily decrease over a 10-year interval. These early studies have important implications for the role of pancreas transplantation alone in patients with type I diabetes and very early changes in native renal function.

Successful pancreas transplantation has been shown to halt, and in many cases, reverse motor-sensory and autonomic neuropathy 12-24 months after transplantation. This has been studied most extensively in recipients of SPK transplantations. This raises the possibility that improvement of diabetic neuropathy occurs, in part, because of improvement of uremic neuropathy. However, pancreas transplantation alone in preuremic patients also has been shown to result in improvement in diabetic neuropathy. Many patients express subjective improvements of peripheral sensation 6-12 months after pancreas transplantation. Very interestingly, the effect of reversal of autonomic neuropathy in patients with type I diabetes with pancreas transplantation has been associated with better patient survival rates than patients with failed or no transplantation.

Pancreas transplantation does not have an immediate dramatic beneficial effect on preestablished diabetic retinopathy. Retinopathy appears to progress for at least 2 years following transplantation of the pancreas, but it begins to stabilize in 3-4 years compared to diabetic recipients of kidney transplantation only. Longer-term studies of 5-10 years, similar to those described above, have not been reported.

Previous
Next

Patient Education

During hospitalization, transplant recipients are prepared for discharge with respect to expectations of medical compliance, education about the pharmacology of their new immunosuppression medications, and lifestyle issues. Patients usually are provided a booklet that delves into the above-mentioned topics.

Compliance with medical therapy may be one of the most important variables affecting transplant outcome. Transplant recipients must take immunosuppressive medications daily for the rest of their lives.

Previous
 
Contributor Information and Disclosures
Author

Dixon B Kaufman, MD, PhD Ray D Owen Professor and Chief, Division of Transplantation, Department of Surgery, University of Wisconsin School of Medicine and Public Health

Dixon B Kaufman, MD, PhD is a member of the following medical societies: American Surgical Association, American College of Surgeons, American Society of Transplant Surgeons, Association for Academic Surgery, Central Surgical Association, Society of University Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, American Gastroenterological Association

Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other; Received grant/research funds from MannKind for other.

Chief Editor

Ron Shapiro, MD Professor of Surgery, Robert J Corry Chair in Transplantation Surgery, Associate Clinical Director, Thomas E Starzl Transplantation Institute, University of Pittsburgh Medical Center

Ron Shapiro, MD is a member of the following medical societies: American Society of Transplantation, American Surgical Association, American College of Surgeons, Transplantation Society, International Pediatric Transplant Association, American Society of Transplant Surgeons, Association for Academic Surgery, Central Surgical Association, Society of University Surgeons

Disclosure: Nothing to disclose.

References
  1. Demartines N, Schiesser M, Clavien PA. An evidence-based analysis of simultaneous pancreas-kidney and pancreas transplantation alone. Am J Transplant. 2005 Nov. 5(11):2688-97. [Medline].

  2. Burke GW 3rd, Vendrame F, Virdi SK, Ciancio G, Chen L, Ruiz P, et al. Lessons From Pancreas Transplantation in Type 1 Diabetes: Recurrence of Islet Autoimmunity. Curr Diab Rep. 2015 Dec. 15 (12):121. [Medline].

  3. Kerr HR, Hatipoglu B, Krishnamurthi V. Pancreas transplant for diabetes mellitus. Cleve Clin J Med. 2015 Nov. 82 (11):738-44. [Medline].

  4. Ziaja J, Bozek-Pajak D, Kowalik A, Krol R, Cierpka L. Impact of pancreas transplantation on the quality of life of diabetic renal transplant recipients. Transplant Proc. 2009 Oct. 41(8):3156-8. [Medline].

  5. Decker E, Coimbra C, Weekers L, et al. A retrospective monocenter review of simultaneous pancreas-kidney transplantation. Transplant Proc. 2009 Oct. 41(8):3389-92. [Medline].

  6. Becker LE, Hallscheidt P, Schaefer SM, Klein K, Grenacher L, Waldherr R, et al. A Single-center Experience on the Value of Pancreas Graft Biopsies and HLA Antibody Monitoring After Simultaneous Pancreas-Kidney Transplantation. Transplant Proc. 2015 Oct. 47 (8):2504-12. [Medline].

  7. Redfield RR, Scalea JR, Odorico JS. Simultaneous pancreas and kidney transplantation: current trends and future directions. Curr Opin Organ Transplant. 2015 Feb. 20 (1):94-102. [Medline].

  8. McCullough KP, Keith DS, Meyer KH, Stock PG, Brayman KL, Leichtman AB. Kidney and pancreas transplantation in the United States, 1998-2007: access for patients with diabetes and end-stage renal disease. Am J Transplant. 2009 Apr. 9(4 Pt 2):894-906. [Medline].

  9. Sampaio MS, Poommipanit N, Cho YW, Shah T, Bunnapradist S. Transplantation with pancreas after living donor kidney vs. living donor kidney alone in type 1 diabetes mellitus recipients. Clin Transplant. 2010 Nov. 24(6):812-20. [Medline].

  10. Schenker P, Vonend O, Krüger B, Klein T, Michalski S, Wunsch A, et al. Long-term results of pancreas transplantation in patients older than 50 years. Transpl Int. 2011 Feb. 24(2):136-42. [Medline].

  11. Drachenberg CB, Odorico J, Demetris AJ, Arend L, Bajema IM, Bruijn JA, et al. Banff schema for grading pancreas allograft rejection: working proposal by a multi-disciplinary international consensus panel. Am J Transplant. 2008 Jun. 8(6):1237-49. [Medline].

  12. Drachenberg CB, Torrealba JR, Nankivell BJ, Rangel EB, Bajema IM, Kim DU, et al. Guidelines for the Diagnosis of Antibody-Mediated Rejection in Pancreas Allografts-Updated Banff Grading Schema. Am J Transplant. 2011 Aug 3. [Medline].

  13. Browne S, Gill J, Dong J, Rose C, Johnston O, Zhang P, et al. The Impact of Pancreas Transplantation on Kidney Allograft Survival. Am J Transplant. 2011 Jul 12. [Medline].

  14. Mora M, Ricart MJ, Casamitjana R, Astudillo E, López I, Jiménez A, et al. Pancreas and kidney transplantation: long-term endocrine function. Clin Transplant. 2010 Nov. 24(6):E236-40. [Medline].

  15. Ojo AO, Meier-Kriesche HU, Hanson JA, et al. The impact of simultaneous pancreas-kidney transplantation on long-term patient survival. Transplantation. 2001 Jan 15. 71(1):82-90. [Medline].

  16. 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 Aug. 19(4):433-55. [Medline].

  17. United Network for Organ Sharing (UNOS). United Network for Organ Sharing (UNOS). [Full Text].

 
Previous
Next
 
Simultaneous pancreas-kidney transplantation with enteric drainage. Illustrated by Simon Kimm, MD. Image courtesy of Landes Bioscience.
Solitary pancreas transplantation with enteric drainage. Illustrated by Simon Kimm, MD. Image courtesy of Landes Bioscience.
Solitary pancreas transplantation with bladder drainage. Illustrated by Simon Kimm, MD. Image courtesy of Landes Bioscience.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.