Subcapsular renal hematomas result from a hemorrhage within the kidney that is contained by its fibrous capsule. In some cases enlarging or acute hematomas may compress the renal parenchyma and result in ischemia or impaired renal function. In the renal transplant recipient or a patient with a solitary kidney this situation requires immediate identification and aggressive intervention to preserve renal function.
The renal capsule does not allow for expansion and therefore, bleeding or accumulation of fluid will cause compression of the renal parachyma. Extrinisic compression of a kidney may also be caused by large collections surrounding the capsule. In renal transplant recipients, perinephric collections have been reported in up to 50% of patients and may be due to an abscess, a urine leak or vascular injury. Only 18% of these collections are significant and cause for concern. The clinical implications for the patient are determined by the size of the collection and the potential for expansion.
In the native kidneys as well as renal allografts, a subcapsular hematoma may result from trauma, renal cell carcinoma, angiolymphoma, periarteritis or due to anticoagulation therapy. Other causes include interventions such as renal biopsy, surgical procedures and extra corporeal shock lithotripsy.
With subcapsular hematoma, the patient’s symptoms will vary depending on the degree and duration of the bleed. Based on limited reports the clinical presentations of patients with a singular kidney and renal allografts include flank pain/tenderness, acute renal failure and decreased urine output. Additional studies in patients with subcapsular hematoma in the native kidneys showed the presence of hypertension, hematuria and a decrease in hemoglobin.
The diagnosis of acute Page kidney depends on the appearance of a subcapsular hematoma or a fibrous capsule in chronic cases . According to many authors, this is best achieved by CT scan; however MRI also can identify the hematoma and asses its age. Angiography can identify the vascular abnormalities associated with subcapsular hematoma but is invasive, expensive and nephrotoxic.
The treatment of subcapsular hematoma is aimed at maintaining the renal function and improving hypertension. In a patient with two normally functioning kidneys, conservative management may be undertaken and may include observation with oral antihypertensives. More aggressive approaches include stripping of the capsule, nephrectomy, partial nephrectomy, and surgical evacuation or percutaneous drainage.
Gray scale images of the transplanted kidney and normotropic kidneys are similar in appearance with a central hyperechoic sinus and decreased echogenicity in the cortex. In our patient, imaging revealed the subcapsular hematoma to be consistent with an acute process. Hematomas are initially echo free until the early deposit of fibrin. This creates interstices in the hematoma which result in increased echogenicity and thus, the echoes seen in our patient. As the hematoma ages a restrictive fibrous capsule is formed.
Immediate identification of venous complications in the renal allograft is critical due to the lack of the venous collaterals present in the transplanted kidneys. Renal allograft dysfunction as a result of renal vein stenosis has been previously reported. In our patient, color alaising was present in the renal vein and spectral Doppler confirmed a high velocity flow jet. This finding resulted from extrinsic compression of the renal vein by the kidney as a result of the hematoma. While there is no grading criterion for the severity of venous compression, the continuous flow pattern and increased velocity was indicative of the hemodynamic impact of the SRH on the vein.
In the transplant kidney, elevated resistive indices indicate the presence of pathologic changes similar to those seen in the native kidneys. Normal spectral Doppler waveforms obtained within a kidney should demonstrate forward flow throughout diastole, equal to approximately half of that in systole. With an increase in the intraparenchymal pressure, diastolic flow becomes absent or even reverses. Conditions that increase the resisitive indices in transplant recipients include rejection, renal vein thrombosis, infection, acute tubular necrosis, renal vein obstruction and extrarenal obstruction. In our patient the presence of the subcapsular hematoma resulted in a dramatic increase in the resistive indices and significant compression of the vein, both improving after decompression.
In summary color Doppler ultrasound provides an accurate, non-invasive and cost effective diagnosis of a subcapsular renal hematoma and its hemodynamic impact on a renal allograft.