Abstract

Primary closure of the abdominal wall in children following renal transplantation may be challenging, especially if the transplanted kidney restricts the abdominal domain. Pressure on the graft can be further exacerbated by bowel edema leading to abdominal compartment syndrome (ACS) and graft compromise (1). The subject of this report is an 11-year-old female patient whose past medical history was significant for a previous living-related renal transplant lost because of noncompliance and acute rejection, and several laparotomies for intestinal intussusception and adhesive intestinal obstruction. A kidney from a 16-year-old donor was accepted for her second transplant. The transplant was performed through a midline laparotomy. At exploration, a “frozen abdomen” was found. The first kidney graft was found in the right lower abdomen. A decision was made to sew the new graft to the left iliac vessels and urinary bladder. The transplant was straightforward and followed by a primary abdominal closure. Brisk diuresis continued for the first six hours but gradually decreased to a plateau of 10 mL/min. A Doppler ultrasound exam of the kidney found a decreased flow in the iliac vein while the arterial flow to the graft was normal. An urgent contrast venogram showed external compression of the iliac vein. An emergency exploration found that the kidney was edematous and cyanotic, but it rapidly improved as the abdominal domain was increased. A decision was made to avoid a prosthetic abdominal closure and perform a component separation instead. The external oblique muscles were exposed and transected bilaterally from the costal arch to the iliac crests (2), allowing a tension-free fascial closure. On-table venogram showed no further compression of the iliac vein. The urine output increased to 100 mL/hour within 24 hours; the serum creatinine reached a reference range in 48 hours. The patient was free of complaints six months after the procedure and had an intact abdominal closure and normal kidney function. Prolonged increase of the intra-abdominal venous pressure reduces the perfusion pressure and results in ACS, a vicious circle of reduced venous outflow, tissue ischemia, and edema (3), which impairs all systems including the renal system (4). ACS has infrequently been reported in renal transplant. Four previous studies describing seven patients (1996–2003) were quoted by a recently published report of 11 ACS patients (4). ACS typically presented with renal disfunction (4, 5), similar to our observation. Our recognition of ACS was based on clinical criteria such as urine output and observation of the graft perfusion. Ultrasound Doppler of the interlobar and segmental renal arteries showing absent or reversed diastolic blood flow (4, 5) was not observed in our patient. Treatment of ACS consists of intraperitonealization (3, 4) with or without fasciotomy (4), or prosthetic bridging (6–8) if the kidney is extraperitoneal. There is one previous report of a pediatric intra-abdominal renal transplant treated with decompressive fasciotomy (5) and another report describing a prosthetic fascial bridge, which prevented ACS (9). Our report is the third in the pediatric setting. We propose component separation as a definitive solution to obtain a tension-free abdominal closure. Julian E. Losanoff Department of Surgery Wayne State University and John D. Dingell VAMC Detroit, MI Trevor W. Reichman Marc R. Garfinkel Giuliano Testa J. Michael Millis Department of Surgery University of Chicago Chicago, IL

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