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Original Research |
1 Department of Radiology, Division of Body Imaging, Boston University Medical
Center, Boston, MA.
2 Present address: Department of Radiology, Section of Interventional Radiology,
Northwestern Memorial Hospital, 251 E Huron St., Feinberg 4-710Y, Chicago, IL
60611.
3 Chief Radiology Service, Boston VA Healthcare System, Boston University School
of Medicine, Boston, MA.
4 Department of Radiology, Division of Body Imaging, Boston University Medical
Center, Boston, MA.
Received April 29, 2007;
accepted after revision November 6, 2007.
Address correspondence to B. L. Dunfee
(brianldunfee{at}yahoo.com).
Abstract
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MATERIALS AND METHODS. We performed a retrospective study encompassing all acute trauma patients admitted to our institution over a 42-month period found to have renal parenchyma injuries on initial MDCT and also to have undergone a follow-up CT performed at least 1 month after trauma. We identified 54 patients who sustained blunt (n = 44) or penetrating (n = 10) abdominal trauma. The renal injuries were graded by two radiologists according to the Organ Injury Scaling Committee of the American Association for the Surgery of Trauma (AAST), grades I through V. Follow-up CT was reviewed for the presence of parenchymal distortion, scarring, or perfusion defects.
RESULTS. Of the 54 patients, 12 had grade I injury, eight had grade II injury, 22 had grade III injury, 10 had grade IV injury, and two had grade V injury. Grades I and II traumatic renal injuries were undetectable on follow-up CT. Grade III injuries resulted in the development of renal scars in 14 of 22 (64%) patients. Scarring resulted in all patients with grades IV and V injuries.
CONCLUSION. Grades I and II renal injuries heal completely, whereas higher grades of renal trauma result in permanent parenchymal scarring. Hence, incidentally discovered renal scars in patients with a history of minor renal trauma should be attributed tentatively to other causes that may or may not require additional investigation.
Keywords: AAST injury scale emergency radiology renal function renal injuries renal scarring trauma
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We decided to evaluate the incidence of renal scarring after all grades of renal injury in patients who had undergone both diagnostic CT and follow-up imaging. By defining an association between grade of injury and the subsequent development of scars, one may be able to predict whether a parenchymal abnormality identified on CT is possibly due to a prior traumatic injury or to other, nontraumatic causes such as a prior infection or infarction. The purpose of this study was to determine whether there is an association between the grade of a traumatic renal injury and the subsequent development of renal parenchymal scars on CT.
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18 years) who were
evaluated on MDCT at our institution, a level 1 trauma center, after
sustaining abdominal trauma. A total of 1,473 patients underwent CT for blunt
(n = 961) and penetrating (n = 512) injuries. The original
reports of these CT examinations were reviewed, and a total of 106 patients
(7%) were identified in whom a renal parenchymal injury was documented. Of
these 106 patients, 54 (51%) had at least one follow-up CT scan obtained for a
variety of indications no earlier than 1 month after injury. These patients
constitute our study population. The remaining 52 patients (49%) had no
follow-up CT performed later than 1 month after injury and were excluded. The
mean time interval to the follow-up CT examination was 5 months (range,
1–15 months). No renal surgery was performed between initial and
follow-up imaging on any of the patients included in the study population. Thirty-six (67%) of the 54 patients were male and 18 (33%) were female, with a mean age of 35 years (range, 18–81 years). Of the 54 patients, 44 patients (81%) sustained blunt injuries and 10 patients (19%) sustained penetrating flank injuries. The mechanisms of blunt injuries included motor vehicle collisions (n = 21), pedestrians struck by motor vehicle (n = 11), assaults (n = 9), and falls from a significant height (n = 3). The mechanisms of penetrating injuries comprised gunshot wounds (n = 6) and stab wounds (n = 4).
The study was approved by the investigational review board of our medical center and was conducted in a manner compliant with HIPAA. The review board waived the need for informed consent for all patients.
CT Technique
During the time period of the study, all trauma CT scans at our institution
were obtained on either a 4-MDCT scanner (MX8000, Philips Medical Systems)
(January 2002–June 2005) (n = 37) or a 16-MDCT scanner
(LightSpeed 4.X, GE Healthcare) (September 2004–April 2005) (n
= 17) within 1 hour of emergency department admission. The scanning parameters
were as follows: 120–140 kVp; 200–250 mAs; pitch, 1.5; field of
view, 240–350 mm; and slice thickness, 3.2 mm. All patients received 100
mL of IV contrast material containing 320 mg I/mL (iohexol [Optiray,
Mallinckrodt Imaging]) administered through an indwelling IV cannula,
preferably located in an antecubital vein, at a rate of 3 mL/s using a power
injector. Oral contrast material was not administered to any of the patients
who suffered blunt trauma, in keeping with our departmental imaging protocol
for that patient population.
In addition to 100 mL of IV contrast material, patients with penetrating abdominal injuries were also given 900 mL of oral and 500 mL of rectal contrast material (2.2% barium sulfate suspension [Medescan Barium Sulfate, Lafayette Pharmaceuticals]) for a more sensitive evaluation of bowel injury [6]. Images of the abdomen and pelvis were acquired from the superior surface of the diaphragm through the ischial tuberosities in the portal venous phase after a 60-second delay from the beginning of IV contrast injection. According to our departmental protocol, the presence of a renal pedicle injury, perinephric stranding, or abnormal fluid collections within the retroperitoneum warranted a dedicated evaluation of the collecting system. As of November 2003, imaging through the abdomen and pelvis after a 5-minute delay was standard in all trauma patients who were found to have definite or possible intraabdominal injuries on the initial scan [7]. Imaging parameters were identical to those used for the initial scan except the mAs, which was reduced to 100 mAs to decrease radiation exposure to the patient. These delayed scans were acquired in 16 (30%) of the 54 patients who are the focus of this study.
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Follow-up contrast-enhanced CT of the abdomen and pelvis for 54 patients (51%) of the 106 patients was performed on a 4-MDCT scanner (n = 39), a 16-MDCT scanner (n = 9), or a single-detector CT scanner (n = 6) (PQ5000, Picker International) using scanning parameters similar to those used for the admission CT scan. Imaging was performed for various clinical indications relating to a previous trauma or for unrelated reasons. Delayed images were not acquired as part of these follow-up CT exami nations. The same radiologists evaluated both kidneys for the presence of parenchymal distortion (loss of corticomedullary differentiation), scarring (cortical thinning), or perfusion defects (decreased regional attenuation). When a renal scar was identified, the location correlated with the site of the initial injury for each case. The follow-up images were reviewed 1 month after the initial interpretation to eliminate any possibility of recall bias.
In an attempt to quantify the potential effect of renal injury on renal function, blood pressures and serum creatinine levels were identified from the patients' medical records at the time of the initial CT examination and at the time of follow-up imaging examination to assess for any change. Any other factor in the interim that may have influenced renal function, such as nephrotoxic medications or multiorgan failure, was not considered.
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Grade I renal injuries were present in 12 patients and comprised perinephric hematomas (n = 9) and small contusions (n = 3). The mechanism of injury was blunt trauma for all patients. Follow-up CT scans, obtained from 1 to 15 months after injury (mean, 6 months), showed no parenchyma abnormalities and complete resolution of the initial findings (Table 2 and Fig. 2A, 2B).
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Grade II injuries were identified in eight patients, and all were parenchymal lacerations that were less than 1 cm in depth (n = 8). The mechanism of injury in all cases was secondary to blunt trauma. Follow-up CT scans were acquired 6 weeks–7 months (mean, 3 months) after injury and showed no parenchyma abnormalities or residual hematomas (Table 2 and Fig. 3A, 3B).
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Grade IV injuries were observed in 10 patients. The injuries included segmental infarcts (n = 7) and collecting system injuries (n = 3). Small renal hematomas and contusions were also present in seven of the patients. The interval between initial imaging and follow-up imaging ranged from 1 to 9 months (mean, 6 months). The mechanisms of injury included blunt (n = 6) and penetrating (n = 4) causes. In all 10 patients (100%), the grade IV injuries resulted in the development of scars in the same region (Table 2). The scarring included regions of cortical retraction, irregularity, or decreased enhancement compared with the remaining renal parenchyma (Fig. 5A, 5B).
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Grade V injuries were identified in two patients. Both patients had renal pedicle injuries with occlusion of the main renal artery due to severe blunt trauma. Initial CT scans showed complete lack of parenchymal enhancement and delayed collecting system opacification. Follow-up CT scans, obtained 4 and 9 months later, showed persistent lack of enhancement of the entire parenchyma with marked cortical and medullary atrophy (Table 2 and Fig. 6A, 6B).
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Mean blood pressures and serum creatinine levels were available for many of the patients at both the time of initial trauma and during follow-up imaging. A significant change in mean blood pressure was defined as greater or less than 10% of the initial measurement. Of the grade I renal injuries, mean blood pressures and serum creatinine values were documented in seven of the 12 patients. There were no significant changes identified in documented blood pressure measurements. In addition, the creatinine values remained within normal limits (< 1.3 mg/dL) for all seven patients. Initial and follow-up mean blood pressures and serum creatinine levels were available for five of the eight grade II renal injury patients. The values remained within normal limits for both intervals without significant change. Of the grade III injuries, serial mean blood pressures and serum creatinine values were available for 18 of the 22 patients. The levels did not show a significant change throughout the documented time period. Both initial and follow-up mean blood pressure and serum creatinine values were available for only four of the 10 patients with grade IV renal injuries. However, there was no significant change in the values identified. One of the two grade V renal injury patients had mean blood pressures and serum creatinine levels documented initially and during follow-up imaging. Neither value showed a significant change during the interval.
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Grade I renal injuries include small parenchymal contusions and nonexpanding subcapsular hematomas. Grade I lesions constitute approximately 75–85% of all renal injuries in most studies [12–14], and management of these patients is typically conservative [15]. Grade II injuries encompass approximately 10% of renal injuries [13] and include nonexpanding perinephric hematomas and cortical lacerations extending less than 1 cm deep into cortex. A cortical laceration appears as a small linear hypoattenuating lesion originating from the periphery of the kidney. These injuries are also managed conservatively. The collecting system is not involved in grade I or II injuries.
Grade III injuries include lacerations extending more than 1 cm into the renal parenchyma without urinary extravasation. Once the laceration extends through the corticomedullary junction into the collecting system, the injury is categorized as grade IV. Delayed images in the excretory phase are required to ensure collecting system integrity [16]. Thrombosis of a segmental artery is also included in grade IV injuries, appearing as a well-defined, wedge-shaped area of decreased enhancement [17]. In addition, injury to the main renal artery or vein may be present in grade IV injuries without complete vascular occlusion. Overall, grade III and IV injuries comprise approximately 7% of renal injuries [14]. Management may be either conservative or surgical [15].
Grade V renal injuries include thrombosis or avulsion of the main renal vasculature or multiple deep lacerations, defining a "shattered" kidney. These injuries occur in less than 5% of renal trauma cases [13, 14]. Whereas thrombosis of the main renal artery appears as a nonenhancing kidney, renal vein injury is often more difficult to detect [18]. Venous outflow injury is indicated by an intraluminal filling defect, distended renal vein, diminished nephrogram, or delayed nephrographic progression. Decreased excretion of contrast material into the collecting system may also be seen with renal vein injury [19].
Most renal trauma patients are managed nonoperatively. Although the need for subsequent CT scans is not routine and is determined by both the severity injury and clinical evolution of the patient, follow-up scans are commonly obtained for a variety of other reasons. This study defines the association that exists between renal injury severity, as assessed by the CT classification of the AAST, and the potential for developing permanent renal findings on follow-up CT scans. Because the study population is limited to those individuals with follow-up CT scans, there is a greater proportion of patients with high-grade renal injuries than has been reported in other abdominal trauma series [14]. Also, a more severe renal injury is more likely to be associated with injuries to other organs [8, 20], and multiorgan trauma typically requires follow-up imaging due to increased morbidity, as compared with patients with isolated low-grade renal injuries who are typically discharged from the hospital without long-term sequelae.
Our study shows that there is a significant association between renal injury severity and the development of parenchymal scars in those regions. Numerous studies have previously shown the pathologic healing course of traumatized animal kidneys [21, 22]. The injuries progress from hematomas or active extravasation to fibrosis and eventually to scar contraction by 2–8 months [22]. The degree of pathologic scar formation has been correlated with the severity of injury. These studies support our CT findings of healing and scar formation of the posttraumatic kidney.
The results of our study can have significant clinical impact on patient management and follow-up examinations. For example, if trauma can be excluded as a cause of the renal scarring discovered on routine imaging, the findings may be the first clue to discovering an underlying abnormality. These abnormalities may be related to the cardiovascular system, such as a cardiac thrombus or hypercoagulable disorder. The early detection may initiate further workup and treatment before a more severe sequela of the disease results, such as mesenteric or cerebral infarction. In addition, we have unveiled several cases of chronic reflux nephropathy to clinicians before the patient's laboratory values changed. However, if the finding of a renal scar can be definitively associated with previous trauma, no additional workup is required.
Some potential bias should be briefly discussed. The CT images were reviewed by consensus and consequently the interobserver agreement in classifying renal injuries and in recognizing renal scars could not be estimated. In addition, six of the 54 patients had follow-up CT performed on a single-detector scanner. Theoretically, this may have decreased the effectiveness of detecting renal scarring from the injury.
In our investigation, grades I and II injuries almost invariably underwent complete resolution without any identifiable morphologic abnormality on subsequent CT scans obtained at least 1 month after the injury. Parenchymal scars developed in most patients with grade III injuries and in all patients with grades IV and V injuries. The scarring is indicated by irreversible parenchymal changes, such as cortical retraction and atrophy. Also, as we suspected, any injury to the kidney's main vascular flow resulted in permanent injury.
Of note, all 10 patients (100%) with grades III or IV injuries in our study population who sustained penetrating trauma developed a scar, whereas the frequency of scars in blunt trauma patients with grade III injuries was 64% (14/22). These results might indicate that, even though CT may show similar findings, a greater degree of parenchymal damage is present with penetrating trauma than with blunt trauma, leading to a higher frequency of scarring.
Of the 54 patients included in the study, 35 had both mean blood pressures and serum creatinine levels documented at the time of initial and follow-up imaging. Each grade of renal injury was represented in the 35 patients identified. The mean blood pressures did not significantly change for any of the documented patients and remained within 10% of the initial measurement. In addition, the serum creatinine values did not show a change of greater than 0.2 mg/dL and remained within normal limits for all patients. Despite these findings, however, blood pressure measurements and serum creatinine levels have been shown to not always correlate with renal function. Many factors affect the level of renal function after injury, and further investigation is necessary to increase the power of these findings.
In conclusion, grades I and II renal injuries were undetectable on follow-up CT performed at least 1 month after trauma in our study population. The majority of grade III and all grades IV and V renal injuries resulted in permanent parenchyma scarring in the same locations. Therefore, incidentally detected regions of renal parenchyma scarring, perfusion defects, or both can only be attributed to previous trauma if the severity of injury was grade III or higher (p < 0.0001). More importantly, however, the detection of renal scars in patients who have not sustained significant renal injury must be tentatively attributed to other causes such as prior infection or infarction. This early detection and attention may prompt additional investigation and treatment before more severe sequelae of the disease results.
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