In the early postoperative period, the pediatric recipient can experience any complication associated with operation (bleeding, infection, wound complications, etc.). Those unique to renal transplant recipients usually revolve around graft dysfunction. Signs and symptoms of graft dysfunction include anorexia, malaise, weight gain, fever, abdominal pain, allograft tenderness, decreased urine output (< 1 cc/kg/hour), and elevated creatinine. The differential diagnosis includes vascular occlusion, urinary obstruction, urine leak, prerenal azotemia, rejection, CsA toxicity, and acute tubular necrosis. The diagnostic approach to this common scenario is systematic.2 The recipient is examined and the Foley irrigated to remove clots and demonstrate patency. A duplex ultrasound is obtained to rule out vascular thrombosis, external compression (hematoma, lymphocele), and hydronephrosis. If duplex ultrasound is not available or cannot exclude thrombosis, a renogram is done. Vascular thrombosis requires immediate exploration, but usually results in graft loss. Ureteral obstruction, usually a late complication due to stricture, requires percutaneous nephrostogram to determine the level of obstruction and a nephrostomy tube to drain the upper urinary tract. If possible, the stenosis is dilated and an internal stent placed across the obstruction into the bladder. If urine flows across the obstruction via the stent, the nephrostomy tube is elevated for 24 hours and then clamped for 24 hours. If there are no signs or symptoms of obstruction and no hydronephrosis on repeat ultrasound, the nephrostomy tube is removed. Urine leaks occur at the ureteroneocystomy. The child presents with ascites and a rising creatinine. Ultrasound shows a well vascularized kidney and ascitic fluid high in creatinine. Renal scan will show extravasation into the peritoneal cavity. Treatment requires re-exploration and ureteral reimplantation. In cases of ureteral necrosis, pyeloureterostomy with the native ureter or pyelocystostomy may be necessary. As previously discussed, acute rejection requires a biopsy. Prerenal azotemia is suspected based on clinical grounds (i.e., unbalanced in's and out's, a decrease in body weight, and low CVP) and responds promptly to volume. Acute tubular necrosis can be seen on a biopsy obtained to rule out rejection. CsA toxicity responds to lowering the CsA dose. (See Chapter on Immunosupression).
Was this article helpful?
I lost over 60 pounds and 4+ inches off my waist without pills, strenuous exercise, or any of the things that the diet experts tell you to do...and I did it in less than 4 months! If you have the desire, and can read through my e-book , then this is for you! I could have easily made it a lot more difficult, with stacks of information that people will never read, but why?