Subcapsular hematoma (SH) is a rare complication after renal transplant which may compress the renal parenchyma and cause hypoperfusion and ischemia, resulting in the clinical condition termed as the Page kidney phenomenon characterized by activation of the renin-angiotensin-aldosterone system and hypertension. Till now, 44 cases of SH in kidney graft have been reported in literature, the majority of them were due to percutaneous biopsy and only a few (5/44) had occurred immediately after transplantation. It may be caused by trauma, spontaneous rupture of cyst or tumor, anticoagulation therapy, periarteritis, lymphangiomas, and interventions such as percutaneous biopsy or shock wave lithotripsy. SH can occur immediately after transplantation due to trauma during kidney retrieval or benching. Duplex ultrasound (USG) plays the lead role in diagnosis. Treatment approaches may be conservative, percutaneous drainage or surgical reexploration and capsulotomy or nephrectomy. We report three cases of SH that developed immediately posttransplant and required surgical intervention, which resulted in complete recovery of renal allograft function.
A 52-year-old male with end-stage renal disease (ESRD) underwent a live renal transplant wherein the renal artery and vein were implanted to an internal iliac artery and an external iliac vein, respectively. On declamping, the graft turgor and urine output were good. Over the next 4 h, his hourly urine output dropped to nil. Duplex USG showed raised RI with absent diastolic flow and a large perigraft collection (8 cm × 5 cm) with crescentic outline suggestive of an SH. Immediate reexploration revealed a large SH [Figure 1]. On capsulotomy and evacuation of the SH renal blood flow increased and the RI decreased [Figure 2]. Urine production was restored immediately. He was discharged on postoperative day (POD) 12. The patient has completed 2 years of regular follow-up and presently his serum creatinine is 1.29 mg/dl.
A 37-year-old female underwent a deceased donor renal transplant for ESRD. A Carrel’s patch with three renal arteries was implanted in the external iliac artery, and the renal vein was implanted to the external iliac vein. After declamping, a small SH was found (2 cm × 2 cm), which was left undisturbed as it was not expanding [Figure 3]. At 20 h following surgery, around 800 ml of blood was noted in the perinephric drain, and the patient developed hypotension. After resuscitation, reexploration was done and during surgery, actively bleeding capsular tears were noted at the SH site [Figure 4]. The hematoma was evacuated and the capsule was repaired using Vicryl™ sutures along with the application of a hemostatic agent (Surgicel™) [Figure 5]. Her urine output was adequate throughout the hospital course. She developed ischemic hepatitis on POD one which was recovered by POD 4; this was attributed to the hypotension and use of inotropic agents during resuscitation. There was a steady fall in creatinine to 1.26 on POD 8.
A 48-year-old male patient underwent a second live donor kidney transplant following graft loss due to chronic antibody-mediated rejection at 15 years’ posttransplant. Renal artery and vein were implanted to the left internal iliac artery and external iliac vein, respectively. Postdeclamping, turgor was good, and diuresis was brisk. A small capsular tear was noted on the anterior surface but was left as such as there was minimal bleeding. Initial urine output was good, but it decreased to nil gradually after three hours postsurgery. On Duplex USG, there was a large subcapsular collection (7 cm × 5 cm) on the posterior surface of the kidney, and the Doppler waveform showed high resistance flow (RI-1) [Figure 6a and b]. On reexploration, a large posterior SH (≈10 cm × 8 cm × 5 cm) was found and evacuated [Figure 7]. Hemostasis was achieved with the application of hemostatic agent (Surgicel™). Post-SH evacuation, urine output was brisk and continuous. Biopsy was done on POD five for slow fall in creatinine, which revealed borderline cellular rejection, which was treated with steroid, following which creatinine decreased to 1.6.
SH form when blood accumulates beneath the renal capsule. Being fibrous, the renal capsule has only a limited capacity to expand; therefore, if sufficiently large, SH raises the intracapsular pressure. This occurs because SH, especially those that are fed by the renal arteriolar bed keep expanding till their internal pressure is equal to that in the renal arterial bed. At this point, the intracapsular pressure is above the glomerular capillary pressure, which causes renal blood flow to decrease and glomerular filtration to stop. Both these changes result in a drop in urine output and activation of the renin-angiotensin system, which results in hypertension. This clinical picture termed as the Page kidney phenomenon was first described in an experimental model in the 1930s. At an age when acute rejection was common in the early posttransplant period, Cromie and associates described this event as pseudo rejection; the patient had refractory hypertension, a perinephric hematoma was observed by renal ultrasonography, and blood pressure was normalized after intervention.
SH likely arises following trauma to the kidney, which may occur during allograft procurement or bench surgery, or during posttransplant biopsy. Such trauma may be trivial and unnoticed. Ischemic or preservation injury due to hypotension or prolonged cold ischemia time will lead to delayed function. On the other hand, dysfunction due to retrieval injuries may have good urine output initially and presents later on. In our cases, case 1 has no explainable cause for SH and occurred spontaneously. Case 2 has small (2 cm), nonexpanding hematoma, which got ruptured later on and led to hypotension, which warranted immediate reexploration. For case 3, capsulotomy was made on the anterior surface during transplant, but later on, SH developed on the posterior surface. Conservative management is controversial as the renal parenchyma is at risk of irreversible ischemic injury, although it can be done in cases of small nonexpanding hematoma, hemodynamically stable patients and with no signs of decreased renal perfusion, for example, preserved urine output or normal RI. Nurettin Ay has described spontaneous rupture of SH in a posttransplant patient who was decided to be managed conservatively. While signs and symptoms of SH may include flank pain/tenderness and increased blood in the drain output, the hallmarks of SH are persistent hypertension and decreasing urine output. Duplex USG is a cheap, easily available, convenient, noninvasive, and nonnephrotoxic way of diagnosing SH, and the characteristic meniscus-shaped hematoma is not easily missed. Additional Duplex USG findings include raised RI, short acceleration time, or high peak systolic velocity (PSV). In doubtful cases, such as a small hematoma in a relatively small kidney, contrast-enhanced computed tomography will clinch the diagnosis. Good outcomes require early recognition and rapid intervention to relieve intracapsular pressure. This is best achieved by evacuating the hematoma and performing capsulotomy to prevent further accumulation of blood under the capsule. In our patients also, there was significant improvement in RI, PSV, and urine output posthematoma evacuation.
SH is a rare and reversible cause of acute graft dysfunction in postrenal transplant recipients. Early diagnosis and prompt surgical treatment are the keys to preventing delayed complications such as impaired graft function or even graft loss.
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