ª Springer Science+Business Media New York 2014

Abdominal Imaging

Abdom Imaging (2014) DOI: 10.1007/s00261-014-0133-x

Asymmetric spermatic cord vessel enhancement on CT: a sign of epididymitis or testicular neoplasm Suraj A. Gupta,1 Jeanne M. Horowitz,1 Sheetal M. Bhalani,1 Hamid Chalian,2 Nancy A. Hammond,1 Senta Berggruen,1 Paul Nikolaidis,1 David D. Casalino1 1

Department of Radiology, Feinberg School of Medicine, Northwestern University, 676 St. Clair St, Suite 800, Chicago, IL 60611, USA 2 Radiology Department, University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106, USA

Abstract Purpose: To determine whether asymmetric spermatic cord vessel enhancement (ASE) on contrast-enhanced computed tomography (CECT) indicates scrotal pathology. Methods: Sixty-one male patients with scrotal symptoms who underwent both scrotal ultrasound (US) and CECT within 24 h were identified through a radiology information system. Twenty-eight emergency department patients who underwent CECT only for unrelated symptoms were included for comparison. Two blinded radiologists independently reviewed each CECT scan for qualitative ASE. These data were compared with US diagnoses, when present. A third blinded radiologist reviewed each CECT scan for quantitative ASE by measuring Hounsfield unit (HU) density ratios. McNemar, Kappa, Student’s t test, and ANOVA were used for analysis. Results: Eighty-nine total patients included 28 with CECT only and 61 with CECT and US, of which 41 had abnormal US: 15 acute epididymitis and/or orchitis, 7 testicular neoplasms, 11 varicoceles, and 8 with other pathologies. Twenty patients with normal US and 28 patients with CECT only served as control groups. Identification of ASE agreed with US diagnosis of epididymitis (and/or orchitis) or testicular neoplasm (reader 1: j = 0.79, reader 2: j = 0.75) with average 95.5% sensitivity and 88.8% specificity, and no significant difference between readers (p = 0.58). For epididymitis (and/or orchitis) or testicular neoplasm patients, the average ratio of spermatic cord HU density (ipsilateral:contralateral) was significantly different from other patients (4.01 vs. 1.26, p = 0.0025).

Correspondence to: Suraj A. Gupta; email: [email protected]

Conclusion: ASE on CECT shows stronger correlation with epididymitis (and/or orchitis) and testicular neoplasm compared with other scrotal pathologies. If discovered on CECT, this should prompt further clinical and/or imaging workup. Key words: Epididymitis—Epididymoorchitis— Testicular cancer—Spermatic cord—Spermatic vessel—Computed tomography

In men with groin pain or swelling, epididymitis and testicular neoplasm are some of the most concerning entities on a long differential diagnosis list. It can be difficult to pinpoint the etiology of such symptoms in the emergency department (ED), and occasionally patients with scrotal pathology will undergo computed tomography (CT) scans before scrotal ultrasound (US). This is in the context of dramatically increased utilization of CT in the ED [1]. A few ED patients with acute epididymitis at our institution were noted to have CT scans demonstrating asymmetric enhancement of the spermatic cord vessels (ASE). Validating such a sign might facilitate the diagnosis of epididymitis or other scrotal pathologies. A previous study associated asymmetric spermatic cord vessel enlargement and enhancement with ipsilateral scrotal pathology. The authors compared CT scans of ten patients with known asymmetric spermatic cord enlargement/enhancement and known scrotal pathology, and scans of 20 patients without asymmetric spermatic cord enlargement/enhancement nor scrotal pathology (based on normal scrotal US). The majority of the positive cases were varicoceles and the minority were either epididymitis, epididymoorchitis, or testicular neoplasm

S. A. Gupta et al.: Asymmetric spermatic cord vessel enhancement on CT

[2]. This study serves to validate this finding in a larger number of patients and looks at ASE in relation to specific types of pathology.

Materials and methods Institutional Review Board approval was obtained for this study prior to its initiation. The study was Health Insurance Portability and Accountability Act compliant and informed consent was not required.

Subjects This was a retrospective case control study where patients with known scrotal pathology had CT scans reviewed for the presence of ASE. Using the Radiology Information System (RIS), male patients who underwent both scrotal US and CT of the pelvis within a 24-h period at our institution from January 1, 2006 to June 30, 2011 were identified, yielding a total of 364 patients (Table 1). Patients were excluded if their CT scan was performed without contrast (73 patients) or if contrast-enhanced CT scans were not in the portal venous phase (3 patients). US reports of the remaining 288 patients were reviewed for the presence or absence of significant pathology, including epididymitis (and/or orchitis), neoplasm, torsion, varicocele, cellulitis, or hematoma. While testicular torsion was considered significant pathology, there were no patients in the study group with an US diagnosis of testicular torsion who also had a CT scan. The US/color Doppler criteria for diagnosing these pathologies were epididymitis: enlarged, hypoechoic, and hyperemic epididymis; orchitis: hyperemic, possibly enlarged, and/or hypoechoic testis; neoplasm: intratesticular mass; torsion: enlarged heterogeneous testis, ipsilateral hydrocele, lack of color Doppler flow; varicocele: multiple hypo- or anechoic tubular structures greater than 3 mm in diameter, possibly with increased flow during valsalva; cellulitis: scrotal wall thickening and hyperemia, with possible abscess; hematoma: focal or multiple, intra- or extrates-

ticular, hyperechoic (acute) or hypoechoic (old) collections which lack vascularity, and may be complex and heterogenous; abscess: fluid collection with irregular walls and low-level internal echoes; and edema: layers of alternating hypoechogenicity and hyperechogenicity within a thickened scrotal wall. These criteria were consistent with the literature [3, 4]. USs had been previously read at our academic tertiary care center by fellowshiptrained abdominal radiologists. Of the 62 patients with scrotal US demonstrating at least one of the above pathologies, 12 patients were excluded due to prior orchiectomy and 9 patients were excluded who had multiple (including bilateral) scrotal pathologies. Of the 226 patients with scrotal US demonstrating no significant pathology, 20 were randomly selected as controls. An additional control group consisted of 28 consecutive male patients seen in the ED who underwent portal venous phase, contrast-enhanced CT scans of the pelvis for symptoms not related to the scrotum, who did not undergo scrotal US. A power analysis was performed using a b of 0.20 and a of 0.05. Power was calculated as 0.77 for the sample size included in this study.

Procedures The CT examinations were performed using multidetector CT scanners (Somatom Sensation 64- and 16-section scanners, Siemens Medical Solutions, Malvern, PA) with 5-mm section thickness and reconstruction interval. Portal venous phase images were obtained 70 s after the initiation of intravenous contrast material injection. 125 mL of nonionic contrast material (iohexol, 350 mg iodine per milliliter, GE Healthcare, Waukesha, Wi [total dose of iodine, 43.75 g]) was administered intravenously at a rate of 3 mL/s using a mechanical power injector (Stellant; Medrad, Warrendale, PA). Sonography studies were performed on one of a few sonography systems (Acuson S2000 and Acuson Sequoia 512, Siemens Medical Solutions, Malvern, PA; and

Table 1. Inclusion and exclusion criteria N Case group Inclusion criteria CT of pelvis + scrotal US within 24 h Exclusion criteria CT scans without contrast Contrast-enhanced CT scans not in portal venous phase Prior orchiectomy Multiple or bilateral scrotal pathologies US unremarkable, not demonstrating target pathologiesa Total number of cases Control groups CT of pelvis + scrotal US within 24 h random selection from 226 with unremarkable US (above) Male ED patients with portal venous phase, contrast-enhanced CT of pelvis but no scrotal US Total included in study a

Target pathologies included epididymitis and/or orchitis, neoplasm, varicocele, cellulitis, and hematoma

364 73 3 12 9 226 41 20 28 89

S. A. Gupta et al.: Asymmetric spermatic cord vessel enhancement on CT

Philips iU22, Philips Healthcare, Andover, MA) by sonographic technologists for standard clinical purposes and not as part of a research protocol.

Collection and validation of data Three fellowship-trained abdominal radiologists (different from the study coordinator) with 10, 9, and 3 years experience, respectively, retrospectively reviewed CT scans for ASE, on a PACS workstation (National Display Systems with Centricity package Ó 2006 GE Medical Systems, Barrington, IL, USA). The radiologists evaluated scans independently and were blinded to the patients’ clinical presentation, to whether US had been performed, to the patients’ US and CT diagnoses, and to each other’s interpretations. The first two radiologists qualitatively evaluated scans for the presence of ASE (binary yes or no) and laterality (right or left). ASE was defined as the subjective perception of a difference in the relative attenuation of spermatic cord vessels within each spermatic cord. Assessment was performed at the level of the pubic tubercle on axial images, which generally provided the best cross section of spermatic cord vessels. For each CT scan, the reviewer’s interpretation was compared with the US diagnosis (when available), which was considered the gold standard. There was no clinical follow-up to confirm these diagnoses, as many of the patients were only seen in the ED in a single visit. For the 28 ED control patients without scrotal symptoms, there was no scrotal US for comparison. The third radiologist then quantitatively evaluated CT scans for ASE, measuring Hounsfield unit (HU) densities for manually traced regions of interest (ROI) containing spermatic cord vessels but minimizing adjacent fat. ROIs were retrospectively created directly on PACS, also at the level of the pubic tubercle on axial images. HU density ratios were calculated comparing spermatic cord vessel attenuation ipsilateral to contralateral in the cases of scrotal pathology (based on US diagnosis), and higher to lower in control groups. The average ratio was then calculated for each diagnostic group. ASE was defined as a HU density ratio not equal to 1.00, with average ratios used to compare the magnitude of asymmetry between different experimental groups and controls. Ratios were calculated and compared instead of absolute numbers, due to the tremendous variability of spermatic cord vessel attenuation with differences in patient anatomy, body habitus, hemodynamics, and variation in contrast bolus timing.

Statistical tests For qualitative image evaluation, the McNemar and Kappa tests were used to measure the correlation between CT interpretation and US diagnosis, as well as to assess interobserver agreement. A p value of less than 0.05 was considered significant. For quantitative image evaluation, the Student’s t test and ANOVA were used to assess the significance of HU density ratios. For statistical analysis, the pathologies of epididymitis (and/or orchitis) and testicular tumors were grouped together because these are pathologies that require treatment and are hypothesized to cause spermatic cord hyperemia.

Results Subjects A total of 89 male patients were included in this study ranging in age from 17 to 81 years old (mean 43.2 years, SD 15.6). Forty-one of eighty-nine patients had an abnormal scrotal US, including 15 with epididymitis and/or orchitis, 7 with testicular neoplasms, 11 with varicoceles, and 8 with other pathologies, including cellulitis, abscess, edema, or hematoma. Twenty of the eightynine patients had a normal scrotal US and served as one control group, and another 28 of 89 patients had neither scrotal symptoms nor scrotal US and served as another control group.

Qualitative assessment of spermatic cord vessel enhancement (Table 2) Reader 1 found ASE in 24 of 41 (59%) patients with abnormal scrotal US, including in 15 of 15 (100%) cases of epididymitis and/or orchitis, 7 of 7 (100%) cases of testicular neoplasm, 1 of 11 (9%) cases of varicocele, and 1 of 8 (13%) cases of other pathology. Reader 1 found ASE in 6 of 48 (13%) of control patients. Reader 2 found ASE in 27 of 41 (66%) patients with abnormal scrotal US, including in 14 of 15 (93%) cases of epididymitis and/or orchitis, 6 of 7 (86%) cases of testicular neoplasm, 4 of 11 (36%) cases of varicocele, and 3 of 8 (38%) cases of other pathology. Reader 2 found ASE in 0 of 48 (0%) control patients. Of the 28 control patients without scrotal symptoms or US, ASE was found in an average of 7% of cases (Figs. 1, 2, 3).

Table 2. Results of qualitative CT evaluation Diagnosis Epididymitis and/or orchitis Testicular neoplasm Varicocele Other pathology All pathology Control groups

Reader 1: Asymmetric enhancement

Reader 2: Asymmetric enhancement

15/15 (100%) 7/7 (100%) 1/11 (9%) 1/8 (13%) 24/41 (59%) 6/48 (13%)

14/15 (93%) 6/7 (86%) 4/11 (36%) 3/8 (38%) 27/41 (66%) 0/48 (0%)

S. A. Gupta et al.: Asymmetric spermatic cord vessel enhancement on CT

Fig. 1. A 28-year-old man with acute left-sided epididymitis. Portal venous phase axial contrast-enhanced CT through the pelvis demonstrates asymmetric enhancement of spermatic

cord vessels on the left (A). The color Doppler ultrasound image demonstrates enlargement and hyperemia of the left epididymis (B).

Fig. 2. A 25-year-old man with a left-sided testicular neoplasm (mixed germ cell tumor). Portal venous phase axial contrast-enhanced CT through the pelvis demonstrates

asymmetric enhancement of spermatic cord vessels on the left (A). Longitudinal gray scale scrotal ultrasound demonstrates a large testicular tumor (B).

Fig. 3. A 33-year-old man with acute left-sided scrotal cellulitis. Portal venous phase axial contrast-enhanced CT through the pelvis demonstrates scrotal edema and fat

stranding but not asymmetric enhancement of spermatic cord vessels (A). The transverse color Doppler ultrasound image demonstrates left scrotal skin thickening and hyperemia (B).

S. A. Gupta et al.: Asymmetric spermatic cord vessel enhancement on CT

Table 3. Validity measures for diagnosis of epididymitis (and/or orchitis) or testicular neoplasm Sensitivity (%)Specificity (%)PPV (%) NPV (%)Accuracy (%) Reader 1 Reader 2 Average

100.0 90.9 95.5

88.0 89.5 88.8

73.3 74.0 73.7

100.0 96.7 98.4

91.0 89.8 90.4

Table 4. Spermatic cord vessel attenuation in positive cases Patient

US diagnosis

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41

L epididymitis L epididymitis L epididymitis L epididymoorchitis L epididymoorchitis L epididymitis L epididymoorchitis R epididymitis R epididymoorchitis R epididymitis R epididymoorchitis R epididymitis R epididymoorchitis R epididymitis R epididymitis L testicular neoplasm L testicular neoplasm R testicular neoplasm R testicular neoplasm R testicular neoplasm R testicular neoplasm R testicular neoplasm L varicocele L varicocele L varicocele L varicocele L varicocele L varicocele L varicocele L varicocele L varicocele L varicocele R varicocele Scrotal cellulitis L scrotal hematoma L scrotal cellulitis L scrotal hematoma Scrotal edema, abscess Scrotal cellulitis R scrotal abscess, cellulitis Scrotal cellulitis, abscess

HU density– ipsilateral

HU density– contralateral

46 74 69 82 56 11 41 90 80 98 23 99 65 43 77 48 56 67 71 68 55 67 25 33 16 38 5 54 35 44 59 -41 -5 27 127 28 28 11 69 51 9

70 47 53 64 2 -3 19 33 34 30 15 51 3 25 21 85 33 13 49 59 9 37 22 54 21 40 4 48 58 48 22 -10 -18 20 120 14 22 -15 48 61 12

Each reader’s identification of ASE showed good agreement with US diagnoses of epididymitis (and/or orchitis) or testicular neoplasm (reader 1, j = 0.79; reader 2, j = 0.75). ASE was always found ipsilateral to the side with pathology. There was no significant difference between reader 2’s finding of ASE in cases of epididymitis (and/or orchitis) or testicular neoplasm and the US gold standard (p = 0.17), although reader 1 showed a small difference (p = .0078) when analyzed with the McNemar test. There was no significant difference in overall identification of ASE between readers (p = .058). On a caseby-case basis, both readers also had good agreement with each other (j = 0.67). Between the two readers, ASE had an average sensitivity of 95.5% and specificity of 88.8% for an US diagnosis of epididymitis or testicular neoplasm (Table 3).

Quantitative assessment of spermatic cord vessel enhancement (Table 4) The average spermatic cord vessel attenuation for each group was: 63.6 HU (ipsilateral) and 30.9 HU (contralateral) for epididymitis and/or orchitis, 61.7 HU (ipsilateral) and 40.7 HU (contralateral) for tumor, 23.9 HU (ipsilateral) and 26.3 HU (contralateral) for varicocele, 43.8 HU (ipsilateral) and 35.3 HU (contralateral) for other pathologies, and 30.1 HU for controls (Table 5). The average ratio of spermatic cord vessel HU density (ipsilateral:contralateral) for each group was: 4.68 for epididymitis and/or orchitis (15 cases), 2.56 for testicular neoplasm (7 cases), 1.31 for varicocele (11 cases), and 0.92 for other pathology (8 cases). The average ratio spermatic cord vessel HU density (higher:lower) for control groups was 1.31 (48 cases) (Table 6; Fig. 4). For all cases of epididymitis (and/or orchitis) and testicular neoplasm, the average ratio of spermatic cord vessel HU density (ipsilateral:contralateral) was 4.01 (22 cases), and for all other cases (pathology and controls) the average ratio was 1.26 (67 cases), a statistically significant difference (p = 0.0025).

Table 5. Spermatic cord vessel attenuation for experimental groups and controls Diagnosis

Range

Epididymitis and/or orchitis (ipsilateral) Epididymitis and/or orchitis (contralateral) Tumor (ipsilateral) Tumor (contralateral) Varicocele (ipsilateral) Varicocele (contralateral) Other pathology (ipsilateral) Other pathology (contralateral) Control groups

11 HU to 99 HU -3 HU to 70 HU 48 HU to 71 HU 9 HU to 85 HU -41 HU to 49 HU -10 HU to 58 HU 9 HU to 127 HU -15 HU to 120 HU -51 HU to 86 HU

Mean (HU)

Standard deviation

Number of cases

63.6 30.9 61.7 40.7 23.9 26.3 43.8 35.5 30.1

25.5 21.7 8.0 24.5 27.7 24.8 36.5 38.6 24.3

15 15 7 7 11 11 8 8 48

S. A. Gupta et al.: Asymmetric spermatic cord vessel enhancement on CT

Table 6. Spermatic cord vessel HU density ratios for experimental groups and controls Diagnosis

Epididymitis and/or orchitis Testicular neoplasm Varicocele Other pathology Control groups (higher:lower)

Average HU density ratio (ipsilateral: contralateral)

Number of cases

4.68

15

2.56 1.31 0.92 1.31

7 11 8 48

Fig. 4. A 27-year-old man with acute right-sided epididymitis. On a portal venous phase contrast-enhanced CT through the pelvis, circles 1 and 2 denote locations of manually traced regions of interest, with Hounsfield unit (HU) densities of 60 and 30, respectively. HU density ratio (ipsilateral:contralateral) is 2.0.

Discussion For the 41 patients in the study with abnormal scrotal US, ASE was found in an average of 62.5% of CT scans, compared with 6.5% of the 48 control patients. In patients with scrotal US demonstrating epididymitis (and/ or orchitis) or testicular neoplasm, however, ASE was found in an average of 96.5% and 93% of CT scans, respectively. Thus, while ASE may not be present in all etiologies of scrotal pathology, it certainly correlates well with these specific diagnoses. The readers’ qualitative assessment of ASE agreed with these two diagnoses (mean j = 0.77), and there was good interobserver agreement (j = 0.67). Qualitative assessment yielded a 95.5% sensitivity and 88.8% specificity of ASE for US diagnosis of epididymitis (and/or orchitis) or testicular neoplasm. Quantitatively, the mean ratio of spermatic cord vessel HU density in patients with these two diagnoses was statistically different from all other patients in the study (4.01 vs. 1.26, p = 0.0025). ASE on CT correlates with the presence of ipsilateral epididymitis (and/or orchitis) or testicular neoplasm.

This may relate to the relative testicular or epididymal hyperemia induced by the disease, whether by inflammation or tumor hypervascularity [4, 5]. In other pathologies evaluated (varicocele, scrotal cellulitis, hematoma, scrotal abscess, or edema), ASE on CT was not detected as frequently. Although the pampiniform plexus of veins is dilated in varicoceles, flow within varicoceles is slow [4, 6], and this may be why ASE on CT was not as frequently detected. It is also well known that hematomas do not show increased vascular flow on US [4], which is concordant with the lack of ASE on CT in cases of scrotal hematoma. Cellulitis involves the scrotal skin, which is predominately supplied and drained by the pudendal and perineal vessels. The testes and epididymes are predominately supplied by the testicular vessels, which course through the spermatic cord [7]. Thus, cellulitis may not necessarily alter hemodynamics in spermatic cord vessels. It would be expected to see ASE in patients with testicular torsion, namely decreased enhancement ipsilateral to torsion due to decreased spermatic cord vessel flow [8]. Unfortunately, there were no patients in our study group who had a sonographic diagnosis of testicular torsion as well as a contrast-enhanced pelvic CT within a 24-h period. This may be possibly due to a less ambiguous clinical presentation of torsion and symptoms limited to the scrotum. Lakhani et al. [2] found asymmetric spermatic cord vessel enhancement and enlargement to be associated with ipsilateral pathology. The majority of pathologic cases in their study were varicoceles, whereas we did not find varicocele to be associated with ASE as frequently in our study. This difference may be attributed to the smaller number of patients in their study (10 cases and 20 controls) compared with ours, and the fact that varicocele is much more common than epididymitis or testicular neoplasm in the general population [9, 10]. In their study, cases were selected using a database search for reports specifically mentioning asymmetric enhancement and enlargement of spermatic cord vessels. This method may have selected for cases where asymmetry was dramatic, and/or excluded many scans in which ASE was present but not specifically reported. In positive cases, diagnoses were confirmed by various imaging modalities and clinical records. This nonuniformity may have further limited the number of cases available for analysis and/or imposed bias. In their negative reference cases, scrotal US and CT may have been separated by as long as 6 months, an interval which likely reduced the concordance of findings in the two modalities. During quantitative evaluation of CT scans, Lakhani et al. [2] measured spermatic cord vessel diameters in addition to HU densities. While our readers noticed subtle discrepancies in vessel diameters, the decision was made to not measure diameters as the small measurements were not likely to be highly reproducible.

S. A. Gupta et al.: Asymmetric spermatic cord vessel enhancement on CT

The identification of ASE enhancement may facilitate the workup of patients with epididymitis (and/or orchitis) or testicular tumor when the diagnosis is not clinically apparent. Lakhani et al. [2] reported that this CT finding led to further workup and disease diagnosis in 3 patients. Thus, when clinically appropriate, the presence of this radiologic sign may be an indication for scrotal US. Epididymitis (and/or orchitis) or testicular neoplasm may be more likely to demonstrate avid ASE compared with varicocele, but since varicocele is much more common in the general population [9, 10], mild ASE noted incidentally on CT may frequently be due to varicocele. This is supported by the mild asymmetry in HU ratio of varicocele (1.31) vs. the more striking asymmetry in the HU ratio of epididymitis (and/or orchitis) and tumor (4.01). This study has limitations in addition to its retrospective design. Qualitative assessment of ASE was subjective, as demonstrated by the difference in ‘‘false positive’’ rates between reader 1 and reader 2. Scrotal US was considered the gold standard in this study, but diagnosis using this modality is still somewhat subjective. US reports were used for comparison and the images themselves were not reviewed at the time of the study, although all of these USs were previously interpreted by dedicated abdominal radiologists at an academic tertiary care center. There was no clinical or pathological followup to confirm diagnoses as these data were usually not available and many patients were only seen in the ED. Although the results of quantitative analysis agreed with results of qualitative analysis, it was not possible to make a direct statistical comparison between quantitative and qualitative data. Furthermore, there was no intra- or interobserver comparison for quantitative data. The purpose of our quantitative analysis was to support qualitative findings. We anticipate that in clinical practice radiologists will qualitatively detect ASE and perhaps recommend further evaluation with scrotal US if clinically indicated. Routine measurement of spermatic

cord vessel attenuation is likely impractical. Due to the tremendous variability in patient anatomy, body habitus, hemodynamics, and contrast bolus timing, it may not be possible to find a threshold ratio at which asymmetric spermatic cord attenuation becomes significant. In conclusion, asymmetric enhancement of spermatic cord vessels on contrast-enhanced pelvic CT shows stronger correlation with epididymitis (and/or orchitis) and testicular neoplasm compared with other scrotal pathologies. If discovered on contrast-enhanced pelvic CT, this sign should prompt further clinical and/or US imaging workup. Conflict of interest. None.

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