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Volume: 17 Issue: 5 October 2019

FULL TEXT

CASE REPORT
Simultaneous Pancreas-Kidney Transplant After Bricker Loop Urinary Diversion: A Case Report

Simultaneous pancreas-kidney transplant is the ultimate therapy for patients who have uncontrolled and complicated type 1 diabetes mellitus with end-stage renal disease. The combined pancreas transplant provides a euglycemic milieu for the kidney and protects it from recurrence of diabetic complications. Our patient, a 41-year-old woman with end-stage diabetic nephro-pathy and history of multiple abdo-minal surgeries (ovarian cyst fenestration, adnexal extirpation, abdomi-nal wall reconstruction), including urinary diversion (Bricker loop, above double J stent), underwent simul-taneous pancreas-kidney transplant. After reperfusion, the kidney had immediate function and creatinine levels dropped to normal levels during the early postoperative period (creatinine of 102 µmol/L, estimated glomerular filtration rate of 52 mL/min/1.73 m2) and remained stable during follow-up. Serum glucose levels dropped to within normal ranges postoperatively and remained so during follow-up. The postoperative course was complicated by hydro-nephrosis due to transient edema of the anastomosis of the ureter to the Bricker loop, after early incidental removal of the double J catheter. This was successfully treated with a temporary percu-taneous nephrostomy. Multiple previous surgeries, including a Bricker devia-tion, may not be a definitive contra-indication for simul-taneous pancreas-kidney transplant. In selected cases, special considerations may lead to a successful proce-dure providing better quality of life and life expectancy, even for patients with multiple comorbidities.


Key words : Diabetes mellitus, Diabetic nephropathy, End-stage renal disease

Introduction

Growing numbers of diabetic patients have posed new challenges in surgical treatment and complication management.1 Simultaneous pancreas-kidney (SPK) transplant remains the best long-term therapy for patients with type 1 diabetes mellitus (T1DM), including end-stage renal disease (ESRD).2 Pancreas transplant provides a euglycemic milieu for the kidney, which can increase graft survival of both organs.3 In patients with multiple previous surgeries and several comorbidities, a multidisciplinary consultation is required to select a personalized therapeutic modality. Neurogenic bladder dysfunction or other urinary bladder diseases may be treated with urinary diversion, such as Bricker loop ileostomy.4,5 However, multiple previous abdominal surgeries may interfere with transplant, although for selected cases SPK transplant remains a possible option.

Case Report

A 41-year-old female patient with type 1 diabetes mellitus and diabetic nephropathy, for which she started hemodialysis 3 years previously, presented to our clinic. She also presented with hypertensive cardiomyopathy and severe diabetic proliferative retinopathy (which required right eye bulb enucleation in 1996). In 2000, a subcutaneous insulin pump had been removed because of infection and subcutaneous abscess. Repeated gynecologic (right ovarian cyst fenestration, right adnexal extirpation due to large fibroid tumor in 2005) and abdominal wall reconstruction due to incisional herniation (2003) were also in her previous medical history. In 2010, she had a diastolic heart failure episode due to hypertension and insufficiency. Moreover, as a consequence of demyelinating polyneuropathy, she used a wheelchair. Since 1996, she has been self-catheterization-dependent due to neurogenic urinary dysfunction, which resulted in a cystectomy and Bricker loop ileostomy in 2012. Urinary production had been reduced to under daily 100 mL at the time of transplant. A SPK transplant was performed from a brain-dead donor (mismatch of 1-1-1, 0% panel reactive antibodies).

During back-table preparation, the pancreas was found to be well-perfused with normal aspect of the parenchyma. The pancreatica dorsalis artery was detected from the splenic artery. The patient was prepared for implantation with a Y-graft (iliac) between the splenic artery and superior mesenteric artery. The left kidney was chosen, which showed normal anatomy, good perfusion, and normal parenchyma. After the kidney was prepared, a protocol biopsy was taken.

Alemtuzumab induction therapy was administered just before transplant. The transplant procedure was performed through a median laparotomy. To provide sufficient space for the pancreas graft, the Bricker-ileum loop was mobilized from the abdominal wall with special care to preserve vascularization. The bilateral, native ureters draining into the ileum loop were ligated and resected, since there was no remaining diuresis and to provide enough space for the pancreas graft. The kidney was implanted intraperitoneally to the left iliac fossa with end-to-side anastomosis between the renal and iliac vessels. Warm ischemic time (WIT) was 28 minutes. Diuresis started right after reperfusion.

After the ileocecal corner was mobilized, an appendectomy was performed, and the pancreas graft was placed into the right lateral side of the abdomen. An arterial reconstruction was performed on the back-table with a Y-graft from the donor iliac arteries on the superior mesenteric artery and the splenic artery. The portal vein of the pancreas graft was implanted end-to-side to the inferior vena cava, and the Y-graft was implanted end-to-side to the internal iliac artery. Warm ischemia time was 23 minutes. After pancreas reperfusion, glucose serum levels dropped to within normal range. The pancreas graft was bowel drained by anastomosis of the graft from duodenum to the terminal ileum. Extensive hemostasis control and lavage procedures were performed. The ureter of the kidney graft was then anastomosed to the Bricker loop with running sutures (polydioxanone 5/0), over a double J-stent connected to a urinary catheter directed through the ileostomy. The graft ureter was then placed between the greater omentum and the abdominal wall. Cholecystectomy was performed due to cholelithiasis. After meticulous hemostasis control, lavage, and placement of silicone drains (Douglas space and right paracolic), the abdominal wall was closed. About 300 cm3 of antibiotic fluid (cefazolin) and amph-otericin B were injected through both drains into the abdominal cavity. Injection drains were then closed, left for 1 hour, and subsequently reopened.

There was remarkable urine production through the urine catheter during the early postoperative period. After incidental removal of the urine catheter, and subsequently the double J-stent that was con-nected to it, urine production decreased significantly. This was accompanied by body weight gain of 3 kg and left lower abdominal distension. Abdominal ultrasonography revealed hydronephrosis, which was again verified by urography. The urography also showed a slight stenosis at the site of the uretero-ileostostomy (on the Bricker loop), most probably caused by postoperative edema. A percutaneous nephrostomy was inserted for 7 days to the kidney graft, and anastomotic stenosis/edema resolved spontaneously, as shown by control urography. The kidney graft function further normalized to creatinine level of 102 μmol/L and estimated glomerular filtration rate of 52 mL/min/1.73 m2.

As an unexpected event, our patient incidentally had a pertrochanteric fracture with minimal dislo-cation as a result of a fall due to orthostatic hypotension. This fracture was treated conserva-tively in agreement with trauma surgeons and physicians. Our patient was discharged after 18 days with well-functioning grafts and with normal blood glucose and creatinine levels (creatinine = 102 μmol/L, estimated glomerular filtration rate = 52 mL/min/1.73 m2, glucose = 6.3 mmol/L). At 3 months after surgery, the patient had no need for external insulin medication.

Discussion

For patients with benign disease (such as T1DM) and serious lower urinary tract symptoms, cystectomy and urinary diversion are usually the last treatment options for patients who do not respond to less invasive forms of treatment.6 This circumstance happens because of a neurogenic bladder as a consequence of serious T1DM, as in our patient. The major goal of surgery for these patients is to reduce urologic symptoms and improve quality of life.7 Nevertheless, SPK transplant is currently the standard therapy to achieve long-term insulin-independent normoglycemia in patients with T1DM and end-stage kidney failure. However, medical treatment, including techniques and care after SPK transplant for patients with diabetes mellitus, despite significant recent developments, may still be challenging.

Simultaneous pancreas-kidney transplant is a complicated procedure that requires meticulous preparation. The growing number of patients with multiple complications has raised new challenges for even experienced medical staff.8 However, multiple previous surgeries may not signify a definitive contraindication. In selective cases, special con-siderations may lead to a successful surgery, allowing a better quality of life and life expectancy for patients with multiple complications.9 According to our knowledge, we have recorded the first case in the literature of a patient receiving a SPK transplant after a Bricker deviation. Her successful operation and posto-perative course may indicate that this option should be considered for patients with similar complex medical histories and previous operations.

Despite multiple comorbidities in our patient, we were able to perform a SPK transplant without major complications, which resulted in excellent graft function. This improved her quality of live drama-tically and reduced the progression of potentially fatal conditions, including cardiovascular events.


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Volume : 17
Issue : 5
Pages : 685 - 687
DOI : 10.6002/ect.2018.0100


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From the Leiden University Medical Centre, Department of Surgery, Division of Transplantation, Leiden, The Netherlands
Acknowledgements: The authors have no sources of funding for this study and have no conflicts of interest to declare.
Corresponding author: Dávid Ágoston Kovács, Móricz Zsigmond krt 22, 4032 Debrecen, Hungary
Phone: +36 303131469
E-mail: drkovacsdavid@gmail.com