asymmetric spermatic cord vessel enhancement on ct: a sign of epididymitis or testicular neoplasm

Asymmetric spermatic cord vesselenhancement on CT: a sign of epididymitisor 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

1Department of Radiology, Feinberg School of Medicine, Northwestern University, 676 St. Clair St, Suite 800, Chicago, IL 60611,

USA2Radiology Department, University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106, USA

Abstract

Purpose: To determine whether asymmetric spermatic cordvessel enhancement (ASE) on contrast-enhanced computedtomography (CECT) indicates scrotal pathology.Methods: Sixty-one male patients with scrotal symptomswho underwent both scrotal ultrasound (US) and CECTwithin 24 h were identified through a radiology informa-tion system. Twenty-eight emergency department patientswho underwent CECT only for unrelated symptoms wereincluded for comparison. Two blinded radiologists inde-pendently reviewed each CECT scan for qualitative ASE.These data were compared with US diagnoses, whenpresent. A third blinded radiologist reviewed each CECTscan 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 CECTonly and 61 with CECT and US, of which 41 hadabnormal US: 15 acute epididymitis and/or orchitis, 7testicular neoplasms, 11 varicoceles, and 8 with otherpathologies. Twenty patients with normal US and 28patients with CECT only served as control groups.Identification of ASE agreed with US diagnosis ofepididymitis (and/or orchitis) or testicular neoplasm(reader 1: j = 0.79, reader 2: j = 0.75) with average95.5% sensitivity and 88.8% specificity, and no significantdifference between readers (p = 0.58). For epididymitis(and/or orchitis) or testicular neoplasm patients, theaverage ratio of spermatic cord HU density (ipsilat-eral:contralateral) was significantly different from otherpatients (4.01 vs. 1.26, p = 0.0025).

Conclusion: ASE on CECT shows stronger correlationwith epididymitis (and/or orchitis) and testicular neo-plasm compared with other scrotal pathologies. If dis-covered on CECT, this should prompt further clinicaland/or imaging workup.

Key words: Epididymitis—Epididymoorchitis—Testicular cancer—Spermatic cord—Spermaticvessel—Computed tomography

In men with groin pain or swelling, epididymitis andtesticular neoplasm are some of the most concerningentities on a long differential diagnosis list. It can bedifficult to pinpoint the etiology of such symptoms in theemergency department (ED), and occasionally patientswith scrotal pathology will undergo computed tomog-raphy (CT) scans before scrotal ultrasound (US). This isin the context of dramatically increased utilization of CTin the ED [1]. A few ED patients with acute epididymitisat our institution were noted to have CT scans demon-strating asymmetric enhancement of the spermatic cordvessels (ASE). Validating such a sign might facilitate thediagnosis of epididymitis or other scrotal pathologies.

A previous study associated asymmetric spermaticcord vessel enlargement and enhancement with ipsilateralscrotal pathology. The authors compared CT scans often patients with known asymmetric spermatic cordenlargement/enhancement and known scrotal pathology,and scans of 20 patients without asymmetric spermaticcord enlargement/enhancement nor scrotal pathology(based on normal scrotal US). The majority of the po-sitive cases were varicoceles and the minority were eitherepididymitis, epididymoorchitis, or testicular neoplasm

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

ª Springer Science+Business Media New York 2014

AbdominalImaging

Abdom Imaging (2014)

DOI: 10.1007/s00261-014-0133-x

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

Materials and methods

Institutional Review Board approval was obtained forthis study prior to its initiation. The study was HealthInsurance Portability and Accountability Act compliantand informed consent was not required.

Subjects

This was a retrospective case control study where pa-tients with known scrotal pathology had CT scans re-viewed for the presence of ASE. Using the RadiologyInformation System (RIS), male patients who underwentboth scrotal US and CT of the pelvis within a 24-h periodat our institution from January 1, 2006 to June 30, 2011were identified, yielding a total of 364 patients (Table 1).Patients were excluded if their CT scan was performedwithout contrast (73 patients) or if contrast-enhanced CTscans were not in the portal venous phase (3 patients).US reports of the remaining 288 patients were reviewedfor the presence or absence of significant pathology,including epididymitis (and/or orchitis), neoplasm, tor-sion, varicocele, cellulitis, or hematoma. While testiculartorsion was considered significant pathology, there wereno patients in the study group with an US diagnosis oftesticular torsion who also had a CT scan. The US/colorDoppler criteria for diagnosing these pathologies wereepididymitis: enlarged, hypoechoic, and hyperemic epi-didymis; orchitis: hyperemic, possibly enlarged, and/orhypoechoic testis; neoplasm: intratesticular mass; tor-sion: enlarged heterogeneous testis, ipsilateral hydrocele,lack of color Doppler flow; varicocele: multiple hypo- oranechoic tubular structures greater than 3 mm in diam-eter, possibly with increased flow during valsalva; cellu-litis: scrotal wall thickening and hyperemia, with possibleabscess; hematoma: focal or multiple, intra- or extrates-

ticular, hyperechoic (acute) or hypoechoic (old) collec-tions which lack vascularity, and may be complex andheterogenous; abscess: fluid collection with irregularwalls and low-level internal echoes; and edema: layers ofalternating hypoechogenicity and hyperechogenicitywithin a thickened scrotal wall. These criteria were con-sistent with the literature [3, 4]. USs had been previouslyread at our academic tertiary care center by fellowship-trained abdominal radiologists. Of the 62 patients withscrotal US demonstrating at least one of the abovepathologies, 12 patients were excluded due to priororchiectomy and 9 patients were excluded who hadmultiple (including bilateral) scrotal pathologies. Of the226 patients with scrotal US demonstrating no signifi-cant pathology, 20 were randomly selected as controls.An additional control group consisted of 28 consecutivemale patients seen in the ED who underwent portal ve-nous phase, contrast-enhanced CT scans of the pelvis forsymptoms not related to the scrotum, who did not un-dergo scrotal US. A power analysis was performed usinga b of 0.20 and a of 0.05. Power was calculated as 0.77for the sample size included in this study.

Procedures

The CT examinations were performed using multidetec-tor CT scanners (Somatom Sensation 64- and 16-sectionscanners, Siemens Medical Solutions, Malvern, PA) with5-mm section thickness and reconstruction interval.Portal venous phase images were obtained 70 s after theinitiation of intravenous contrast material injection.125 mL of nonionic contrast material (iohexol, 350 mgiodine per milliliter, GE Healthcare, Waukesha, Wi [totaldose of iodine, 43.75 g]) was administered intravenouslyat a rate of 3 mL/s using a mechanical power injector(Stellant; Medrad, Warrendale, PA).

Sonography studies were performed on one of a fewsonography systems (Acuson S2000 and Acuson Sequoia512, Siemens Medical Solutions, Malvern, PA; and

Table 1. Inclusion and exclusion criteria

N

Case groupInclusion criteriaCT of pelvis + scrotal US within 24 h 364

Exclusion criteriaCT scans without contrast 73Contrast-enhanced CT scans not in portal venous phase 3Prior orchiectomy 12Multiple or bilateral scrotal pathologies 9US unremarkable, not demonstrating target pathologiesa 226

Total number of cases 41Control groups

CT of pelvis + scrotal US within 24 h random selection from 226 with unremarkable US (above) 20Male ED patients with portal venous phase, contrast-enhanced CT of pelvis but no scrotal US 28

Total included in study 89

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

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

Philips iU22, Philips Healthcare, Andover, MA) by so-nographic technologists for standard clinical purposesand not as part of a research protocol.

Collection and validation of data

Three fellowship-trained abdominal radiologists (differentfrom the study coordinator) with 10, 9, and 3 years expe-rience, respectively, retrospectively reviewed CT scans forASE, on a PACS workstation (National Display Systemswith Centricity package � 2006 GE Medical Systems,Barrington, IL, USA). The radiologists evaluated scansindependently and were blinded to the patients’ clinicalpresentation, to whether US had been performed, to thepatients’ US and CT diagnoses, and to each other’s inter-pretations. The first two radiologists qualitatively evaluatedscans for the presence of ASE (binary yes or no) and lat-erality (right or left). ASE was defined as the subjectiveperception of a difference in the relative attenuation ofspermatic cord vessels within each spermatic cord. Assess-ment was performed at the level of the pubic tubercle onaxial images, which generally provided the best cross sectionof spermatic cord vessels. For each CT scan, the reviewer’sinterpretation was compared with the US diagnosis (whenavailable), which was considered the gold standard. Therewas no clinical follow-up to confirm these diagnoses, asmany of the patients were only seen in the ED in a singlevisit. For the 28 ED control patients without scrotalsymptoms, there was no scrotal US for comparison. Thethird radiologist then quantitatively evaluated CT scans forASE, measuring Hounsfield unit (HU) densities for manu-ally traced regions of interest (ROI) containing spermaticcord vessels but minimizing adjacent fat. ROIs were retro-spectively created directly on PACS, also at the level of thepubic tubercle on axial images. HU density ratios werecalculated comparing spermatic cord vessel attenuationipsilateral to contralateral in the cases of scrotal pathology(based on US diagnosis), and higher to lower in controlgroups. The average ratio was then calculated for eachdiagnostic group. ASE was defined as a HU density rationot equal to 1.00, with average ratios used to compare themagnitude of asymmetry between different experimentalgroups and controls. Ratios were calculated and comparedinstead of absolute numbers, due to the tremendous vari-ability of spermatic cord vessel attenuation with differencesin patient anatomy, body habitus, hemodynamics, andvariation in contrast bolus timing.

Statistical tests

For qualitative image evaluation, the McNemar andKappa tests were used to measure the correlation be-tween CT interpretation and US diagnosis, as well asto assess interobserver agreement. A p value of lessthan 0.05 was considered significant. For quantitativeimage evaluation, the Student’s t test and ANOVAwere used to assess the significance of HU densityratios. For statistical analysis, the pathologies of epi-didymitis (and/or orchitis) and testicular tumors weregrouped together because these are pathologies thatrequire treatment and are hypothesized to cause sper-matic cord hyperemia.

Results

Subjects

A total of 89 male patients were included in this studyranging in age from 17 to 81 years old (mean 43.2 years,SD 15.6). Forty-one of eighty-nine patients had anabnormal scrotal US, including 15 with epididymitisand/or orchitis, 7 with testicular neoplasms, 11 with va-ricoceles, and 8 with other pathologies, including cellu-litis, abscess, edema, or hematoma. Twenty of the eighty-nine patients had a normal scrotal US and served as onecontrol group, and another 28 of 89 patients had neitherscrotal symptoms nor scrotal US and served as anothercontrol group.

Qualitative assessment of spermatic cord vesselenhancement (Table 2)

Reader 1 found ASE in 24 of 41 (59%) patients withabnormal scrotal US, including in 15 of 15 (100%) casesof epididymitis and/or orchitis, 7 of 7 (100%) cases oftesticular neoplasm, 1 of 11 (9%) cases of varicocele, and1 of 8 (13%) cases of other pathology. Reader 1 foundASE in 6 of 48 (13%) of control patients. Reader 2 foundASE in 27 of 41 (66%) patients with abnormal scrotalUS, including in 14 of 15 (93%) cases of epididymitisand/or orchitis, 6 of 7 (86%) cases of testicular neoplasm,4 of 11 (36%) cases of varicocele, and 3 of 8 (38%) casesof other pathology. Reader 2 found ASE in 0 of 48 (0%)control patients. Of the 28 control patients withoutscrotal symptoms or US, ASE was found in an averageof 7% of cases (Figs. 1, 2, 3).

Table 2. Results of qualitative CT evaluation

Diagnosis Reader 1: Asymmetric enhancement Reader 2: Asymmetric enhancement

Epididymitis and/or orchitis 15/15 (100%) 14/15 (93%)Testicular neoplasm 7/7 (100%) 6/7 (86%)Varicocele 1/11 (9%) 4/11 (36%)Other pathology 1/8 (13%) 3/8 (38%)All pathology 24/41 (59%) 27/41 (66%)Control groups 6/48 (13%) 0/48 (0%)


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

cord vessels on the left (A). The color Doppler ultrasoundimage demonstrates enlargement and hyperemia of the leftepididymis (B).

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

stranding but not asymmetric enhancement of spermatic cordvessels (A). The transverse color Doppler ultrasound imagedemonstrates left scrotal skin thickening and hyperemia (B).

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

asymmetric enhancement of spermatic cord vessels on theleft (A). Longitudinal gray scale scrotal ultrasound demon-strates a large testicular tumor (B).


Each reader’s identification of ASE showed goodagreement with US diagnoses of epididymitis (and/ororchitis) or testicular neoplasm (reader 1, j = 0.79;reader 2, j = 0.75). ASE was always found ipsilateral tothe side with pathology. There was no significant dif-ference between reader 2’s finding of ASE in cases ofepididymitis (and/or orchitis) or testicular neoplasm andthe US gold standard (p = 0.17), although reader 1showed a small difference (p = .0078) when analyzedwith the McNemar test.

There was no significant difference in overall identi-fication of ASE between readers (p = .058). On a case-by-case basis, both readers also had good agreement witheach other (j = 0.67). Between the two readers, ASEhad an average sensitivity of 95.5% and specificity of88.8% for an US diagnosis of epididymitis or testicularneoplasm (Table 3).

Quantitative assessment of spermatic cord vesselenhancement (Table 4)

The average spermatic cord vessel attenuation for eachgroup was: 63.6 HU (ipsilateral) and 30.9 HU (con-tralateral) for epididymitis and/or orchitis, 61.7 HU(ipsilateral) and 40.7 HU (contralateral) for tumor, 23.9HU (ipsilateral) and 26.3 HU (contralateral) for vari-cocele, 43.8 HU (ipsilateral) and 35.3 HU (contralat-eral) for other pathologies, and 30.1 HU for controls(Table 5). The average ratio of spermatic cord vesselHU density (ipsilateral:contralateral) for each groupwas: 4.68 for epididymitis and/or orchitis (15 cases),2.56 for testicular neoplasm (7 cases), 1.31 for varico-cele (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) andtesticular neoplasm, the average ratio of spermatic cordvessel HU density (ipsilateral:contralateral) was 4.01 (22cases), and for all other cases (pathology and controls)the average ratio was 1.26 (67 cases), a statistically sig-nificant difference (p = 0.0025).

Table 3. Validity measures for diagnosis of epididymitis (and/ororchitis) or testicular neoplasm

Sensitivity (%)Specificity (%)PPV (%)NPV (%)Accuracy (%)

Reader 1 100.0 88.0 73.3 100.0 91.0Reader 2 90.9 89.5 74.0 96.7 89.8Average 95.5 88.8 73.7 98.4 90.4

Table 4. Spermatic cord vessel attenuation in positive cases

Patient US diagnosis HU density–ipsilateral

HU density–contralateral

1 L epididymitis 46 702 L epididymitis 74 473 L epididymitis 69 534 L epididymoorchitis 82 645 L epididymoorchitis 56 26 L epididymitis 11 -37 L epididymoorchitis 41 198 R epididymitis 90 339 R epididymoorchitis 80 3410 R epididymitis 98 3011 R epididymoorchitis 23 1512 R epididymitis 99 5113 R epididymoorchitis 65 314 R epididymitis 43 2515 R epididymitis 77 2116 L testicular neoplasm 48 8517 L testicular neoplasm 56 3318 R testicular neoplasm 67 1319 R testicular neoplasm 71 4920 R testicular neoplasm 68 5921 R testicular neoplasm 55 922 R testicular neoplasm 67 3723 L varicocele 25 2224 L varicocele 33 5425 L varicocele 16 2126 L varicocele 38 4027 L varicocele 5 428 L varicocele 54 4829 L varicocele 35 5830 L varicocele 44 4831 L varicocele 59 2232 L varicocele -41 -1033 R varicocele -5 -1834 Scrotal cellulitis 27 2035 L scrotal hematoma 127 12036 L scrotal cellulitis 28 1437 L scrotal hematoma 28 2238 Scrotal edema, abscess 11 -1539 Scrotal cellulitis 69 4840 R scrotal abscess, cellulitis 51 6141 Scrotal cellulitis, abscess 9 12

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

Diagnosis Range Mean (HU) Standard deviation Number of cases

Epididymitis and/or orchitis (ipsilateral) 11 HU to 99 HU 63.6 25.5 15Epididymitis and/or orchitis (contralateral) -3 HU to 70 HU 30.9 21.7 15Tumor (ipsilateral) 48 HU to 71 HU 61.7 8.0 7Tumor (contralateral) 9 HU to 85 HU 40.7 24.5 7Varicocele (ipsilateral) -41 HU to 49 HU 23.9 27.7 11Varicocele (contralateral) -10 HU to 58 HU 26.3 24.8 11Other pathology (ipsilateral) 9 HU to 127 HU 43.8 36.5 8Other pathology (contralateral) -15 HU to 120 HU 35.5 38.6 8Control groups -51 HU to 86 HU 30.1 24.3 48


Discussion

For the 41 patients in the study with abnormal scrotalUS, ASE was found in an average of 62.5% of CT scans,compared with 6.5% of the 48 control patients. In pa-tients with scrotal US demonstrating epididymitis (and/or orchitis) or testicular neoplasm, however, ASE wasfound in an average of 96.5% and 93% of CT scans,respectively. Thus, while ASE may not be present in alletiologies of scrotal pathology, it certainly correlates wellwith these specific diagnoses. The readers’ qualitativeassessment of ASE agreed with these two diagnoses(mean j = 0.77), and there was good interobserveragreement (j = 0.67). Qualitative assessment yielded a95.5% sensitivity and 88.8% specificity of ASE for USdiagnosis of epididymitis (and/or orchitis) or testicularneoplasm. Quantitatively, the mean ratio of spermaticcord vessel HU density in patients with these two diag-noses was statistically different from all other patients inthe study (4.01 vs. 1.26, p = 0.0025).

ASE on CT correlates with the presence of ipsilateralepididymitis (and/or orchitis) or testicular neoplasm.

This may relate to the relative testicular or epididymalhyperemia induced by the disease, whether by inflam-mation or tumor hypervascularity [4, 5]. In otherpathologies evaluated (varicocele, scrotal cellulitis,hematoma, scrotal abscess, or edema), ASE on CT wasnot detected as frequently. Although the pampiniformplexus of veins is dilated in varicoceles, flow within va-ricoceles is slow [4, 6], and this may be why ASE on CTwas not as frequently detected. It is also well known thathematomas do not show increased vascular flow on US[4], which is concordant with the lack of ASE on CT incases of scrotal hematoma. Cellulitis involves the scrotalskin, which is predominately supplied and drained by thepudendal and perineal vessels. The testes and epididymesare predominately supplied by the testicular vessels,which course through the spermatic cord [7]. Thus, cel-lulitis may not necessarily alter hemodynamics in sper-matic cord vessels. It would be expected to see ASE inpatients with testicular torsion, namely decreasedenhancement ipsilateral to torsion due to decreasedspermatic cord vessel flow [8]. Unfortunately, there wereno patients in our study group who had a sonographicdiagnosis of testicular torsion as well as a contrast-en-hanced pelvic CT within a 24-h period. This may bepossibly due to a less ambiguous clinical presentation oftorsion and symptoms limited to the scrotum.

Lakhani et al. [2] found asymmetric spermatic cordvessel enhancement and enlargement to be associatedwith ipsilateral pathology. The majority of pathologiccases in their study were varicoceles, whereas we did notfind varicocele to be associated with ASE as frequently inour study. This difference may be attributed to thesmaller number of patients in their study (10 cases and 20controls) compared with ours, and the fact that varico-cele is much more common than epididymitis or testic-ular neoplasm in the general population [9, 10]. In theirstudy, cases were selected using a database search forreports specifically mentioning asymmetric enhancementand enlargement of spermatic cord vessels. This methodmay have selected for cases where asymmetry was dra-matic, and/or excluded many scans in which ASE waspresent but not specifically reported. In positive cases,diagnoses were confirmed by various imaging modalitiesand clinical records. This nonuniformity may have fur-ther limited the number of cases available for analysisand/or imposed bias. In their negative reference cases,scrotal US and CT may have been separated by as longas 6 months, an interval which likely reduced the con-cordance of findings in the two modalities. Duringquantitative evaluation of CT scans, Lakhani et al. [2]measured spermatic cord vessel diameters in addition toHU densities. While our readers noticed subtle discrep-ancies in vessel diameters, the decision was made to notmeasure diameters as the small measurements were notlikely to be highly reproducible.

Fig. 4. A 27-year-old man with acute right-sided epididymi-tis. On a portal venous phase contrast-enhanced CT throughthe pelvis, circles 1 and 2 denote locations of manually tracedregions of interest, with Hounsfield unit (HU) densities of 60and 30, respectively. HU density ratio (ipsilateral:contralat-eral) is 2.0.

Table 6. Spermatic cord vessel HU density ratios for experimentalgroups and controls

Diagnosis Average HU densityratio (ipsilateral:contralateral)

Numberof cases

Epididymitis and/ororchitis

4.68 15

Testicular neoplasm 2.56 7Varicocele 1.31 11Other pathology 0.92 8Control groups

(higher:lower)1.31 48


The identification of ASE enhancement may facilitatethe workup of patients with epididymitis (and/or orchi-tis) or testicular tumor when the diagnosis is not clini-cally apparent. Lakhani et al. [2] reported that this CTfinding led to further workup and disease diagnosis in 3patients. Thus, when clinically appropriate, the presenceof this radiologic sign may be an indication for scrotalUS.

Epididymitis (and/or orchitis) or testicular neoplasmmay be more likely to demonstrate avid ASE comparedwith varicocele, but since varicocele is much more com-mon in the general population [9, 10], mild ASE notedincidentally on CT may frequently be due to varicocele.This is supported by the mild asymmetry in HU ratio ofvaricocele (1.31) vs. the more striking asymmetry in theHU ratio of epididymitis (and/or orchitis) and tumor(4.01).

This study has limitations in addition to its retro-spective design. Qualitative assessment of ASE wassubjective, as demonstrated by the difference in ‘‘falsepositive’’ rates between reader 1 and reader 2. Scrotal USwas considered the gold standard in this study, butdiagnosis using this modality is still somewhat subjective.US reports were used for comparison and the imagesthemselves were not reviewed at the time of the study,although all of these USs were previously interpreted bydedicated abdominal radiologists at an academic tertiarycare center. There was no clinical or pathological follow-up to confirm diagnoses as these data were usually notavailable and many patients were only seen in the ED.Although the results of quantitative analysis agreed withresults of qualitative analysis, it was not possible to makea direct statistical comparison between quantitative andqualitative data. Furthermore, there was no intra- orinterobserver comparison for quantitative data. Thepurpose of our quantitative analysis was to supportqualitative findings. We anticipate that in clinical prac-tice radiologists will qualitatively detect ASE and per-haps recommend further evaluation with scrotal US ifclinically indicated. Routine measurement of spermatic

cord vessel attenuation is likely impractical. Due to thetremendous variability in patient anatomy, body habitus,hemodynamics, and contrast bolus timing, it may not bepossible to find a threshold ratio at which asymmetricspermatic cord attenuation becomes significant.

In conclusion, asymmetric enhancement of spermaticcord vessels on contrast-enhanced pelvic CT showsstronger correlation with epididymitis (and/or orchitis)and testicular neoplasm compared with other scrotalpathologies. If discovered on contrast-enhanced pelvicCT, this sign should prompt further clinical and/or USimaging workup.

Conflict of interest. None.

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asymmetric spermatic cord vessel enhancement on ct: a sign of epididymitis or testicular neoplasm

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