Renal Paratransplant Hernia. An Uncommon Variant of Internal Hernia. Are We Aware of It?

Paratransplant hernia (PH) consists of an unusual variant of internal hernia, which was first reported by Kyriakides et al. (1) as entrapment of bowel through a defect in the peritoneum covering the transplanted kidney. It is an uncommon but potentially fatal complication of renal transplantation. To our knowledge, nine cases have been previously reported (2, 3). We presented the very first case of Richter hernia as a variant of renal PH. A 53-year-old man presented to our department with 48-hr symptoms of abdominal pain, distension, and nausea. Three months ago, he underwent kidney transplantation from a deceased donor because of a 6-year history of uremia. His body temperature was normal and no signs of peritonitis were present. Plain abdominal x-ray demonstrated widespread small bowel obstruction (SBO) and multiple air-fluid levels. A nasogastric tube was inserted and an enema administered to release the distension. However, over the next 2 days, the patient’s condition did not improve. Abdominal computed tomography (CT) scan revealed that most small bowel loops were dilated and filled with fluid, without being able to identify cause of the obstruction. An exploratory laparotomy was performed. A necrotic segment of partially obstructed small bowel approximately 8 cm long was found herniated within a peritoneal defect at the site of allograft implantation (Fig. 1). The so-called Richter hernia was diagnosed. Viable bowel was anastomosed by side-to-side fashion. The peritoneal defect was closed with nonabsorbable sutures. The patient had a sound postoperative course and was discharged at the eighth postoperative day.FIGURE 1: A necrotic segment of small bowel and the peritoneal defect at the site of allograft implantation.DISCUSSION Richter hernia is the protrusion or strangulation, or both, of only part of the circumference of the intestine’s antimesenteric border through a rigid small defect of the abdominal wall (4). To our knowledge, we presented the very first case of Richter hernia as a variant of renal PH. In a review by Martin et al. (5), internal hernias were found to account for 0.5% to 5.8% of all intestinal obstruction and associated with a mortality rate greater than 50%. This incidence is comparable to the reported incidence of ureteric stones (0.16%) and renal venous thrombosis (1%) as post-renal transplantation complications (2, 3). Because of its rarity, it is difficult to define predisposing factors and indicative clinical characteristics. Symptoms and signs of SBO including abdominal pain, distention, and nausea are the initial clinical manifestation of PH, presenting from 4 days to months after transplantation (2), as in our case. However, these symptoms are nonspecific because ileus secondary to adhesions or even anesthesia are possible causes (1). Moreover, the large dosage of corticosteroids administered to renal transplant recipients, especially in early-posttransplant period, can mask early signs of peritonitis. Consequently, radiographic examination is usually required for establishing a diagnosis of SBO and determining possible causes. Although plain abdominal x-ray is useful for diagnosing SBO, abdominal CT scan is believed to be the most useful for the preoperative diagnosis of PH (2, 4), despite the fact that in our case, CT failed to lead us to the diagnosis. However, we suggest the early use of CT scan to determine the presence of a PH in cases when signs and symptoms of SBO develop after transplantation. Conservative treatment is not recommended because this complication is very dangerous; once the intestine herniates into the narrow space around the transplanted kidney, intestinal necrosis is likely. Early exploratory surgery should be planned because a single septic nidus can lead to a life-threatening infection. Prompt surgical intervention is essential to improve the prognosis of PH. During surgery, it is crucial to avoid damage to the allograft, as the herniated bowel loop may emerge in the iliac fossa over the transplant or in the paravesical space, depending on the location of the peritoneal defect. If necrosis of the herniated bowel is evident, resection of the bowel segment is required. Once the hernia had been reduced, the peritoneal defect should be closed with nonabsorbable sutures to prevent recurrence (2). Peritoneal defects result from careless maneuvers during the transplantation, such as in cases of excessive dissection of the extraperitoneal space to obtain enough room for graft implantation or during closing the incision when one improper stitch can tear the peritoneum leading to a defect. Careful dissection should be performed in all cases, and if a peritoneal defect is found, it should be closed regardless of its size to avoid the occurrence of a PH. All in all, PH is a relatively uncommon but potentially fatal complication after renal transplantation, and its nonspecific symptoms may lead to misdiagnosis. Physician awareness, prompt diagnosis, and early surgical intervention are crucial. Additionally, meticulous surgical technique during transplantation may help avoid this complication. Demetrios Moris, MD 1 Spiridon Vernadakis, MD, PhD, MSc, FEBS2 1 1st Department of Surgery Athens University School of Medicine “Laikon”, General Hospital Athens, Greece 2 Department of General, Visceral and Transplantation Surgery University Hospital Essen, Germany