imaging vesika seminalis dan vas deferen

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Imaging of the Seminal Vesicle and Vas Deferens Presented by : dr Rivani Kurniawan Lecturer : dr H.A BUNYAMIN SpRad(K) Bohyun Kim, MD, et all RSNA, 2009• radiographics.rsnajnls.org

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Diseases involving the sv and vd

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Page 1: imaging vesika seminalis dan vas deferen

Imaging of theSeminal Vesicle andVas DeferensPresented by : dr Rivani KurniawanLecturer : dr H.A BUNYAMIN SpRad(K)

Bohyun Kim, MD, et allRSNA, 2009• radiographics.rsnajnls.org

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Introduction

The seminal vesicle (SV) and vas deferens (VD) are ancillary but essential urogenital organs

Understanding their embryologic features and anatomy can be helpful in evaluating various disorders of these organs.

The development of these organs is closely related to that of urinary organs, including the kidneys and ureters

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In this article, the embryologic features and anatomy of the SV and VD are reviewed with illustrations of normal and abnormal imaging findings

Various pathologic conditions of the SV and VD, including agenesis, congenital SV cyst, seminal vesiculitis and SV abscess, amyloidosis, primary and secondary neoplasms, and postoperative and postirradiation changes

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Embryologic Features

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Developmental anomalies of the SV and VD are often associated with renal or ureteral anomalies

Any alteration occurring during ureteric bud development may affect the formation of the SV

For example, if the ureteric bud arises from a more proximal portion of the mesonephric duct, it fails to blend with the metanephric blastema and renal agenesis or dysgenesis will develop .

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Anatomy

The SV produces and secretes the seminal fluid, which contributes 50%–80% of the ejaculate volume

The normal SV measures 3.0 cm ± 0.8 in length and 1.5 cm ± 0.4 in diameter, and the ampulla of the VD measures 0.4 cm ± 0.1 in diameter

The ED measures approximately 4–8 mm in diameter

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The normal volume of the SV is 13.7 mL ± 3.7

The wall of the SV normally measures 1–2 mm in thickness at MR imaging

however, to our knowledge, there are no reports in the literature on measurement of normal wall thickness of the SV and VD

The size of the SV increases with age and then decreases with advancing age

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The SVs are located posterior to the bladder and distal ureters

The SV joins the distal portion of the VD and becomes the ED, which drains into the prostatic urethra through the verumontanum

The proximal portion of the VD is continuous with the epididymal tail and runs within the spermatic cord and through the inguinal canal

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The distal portions of the VD and SV are located in the extraperitoneum, just above the prostate.

Owing to their extraperitoneal location, these organs can be involved by disease processes of adjacent organs such as the prostate, bladder, and rectum

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Normal Imaging Findings

Ultrasonography

The SVs are seen as elongated septate cystic structures above the prostate .

The distal portion of the VD is seen as a slightly dilated tubular structure (the ampulla of the VD) medial to the SV.

If scanned obliquely, the SV and the terminal portion of the VD can be seen joining to form the ED, which may be traced to the region of the verumontanum

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Computed Tomography

At contrast-enhanced computed tomography (CT), the SVs are seen as fluid-containing structures of “bow tie” configuration.

Fine septa can be seen. The vasa deferentia are seen as tubular structures running posteriorly along the pelvic sidewall

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MR Imaging

The SVs are seen as elongated fluid-containing structures with thin septa

The intraabdominal portion of the VD is seen as a tubular structure of low signal intensity in each side on both T1- and T2-weighted images

In the ampulla of the VD, a small amount of intraluminal fluid can be seen as high signal intensity on T2-weighted images, similar to that of the SV

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Clinical Features

Abnormalities of the SV and VD are often found incidentally at cross-sectional imaging

Sometimes, patients may present with infertility or hematospermia.

Azoospermia due to occlusion of the SV, VD, or ED may result in male infertility

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SV Agenesis or Hypoplasia

Unilateral SV agenesis develops if an embryologic insult occurs before the 7th week of gestation, when the ureteric bud arises from the mesonephric duct

It is often associated with ipsilateral renal agenesis (79% of cases) or other renal abnormalities (12%)

Bilateral SV agenesis is associated with mutations in the cystic fibrosis transmembrane conductance regulator gene in 64%–73% of cases and may be related to luminal obstruction by thick secretions

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Hypoplasia of the SV refers to a congenitally small SV

At US or MR imaging, the SV looks small with fewer septa

SV hypoplasia can be associated with hypogonadism , cryptorchidism, or other congenital genitourinary anomalies but can also be an isolated finding

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Congenital SV Cyst

A congenital SV cyst is often found in the second to third decades

Often, it is found incidentally but patients may present with hematuria, hematospermia,infertility, or urinary tract infection

Although congenital SV cyst can occur as an isolated finding, it is more often associated with other genitourinary anomalies

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It is associated with ipsilateral renal agenesis or dysgenesis in two-thirds of cases

Bilateral SV cysts have been reported to occur in 44%–60% of patients with autosomal dominant polycystic kidney disease

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Other SV Cystic Lesions

Various pathologic processes can arise in or around SV areas and mimic SV cysts

These lesions may be incidentally found at imaging or may manifest as lower urinary tract symptoms such as hematuria, dysuria, hematospermia, and urinary incontinence

Differentiation can be made on the basis of characteristic location, contents, and association with renal or genital anomalies, but such differentiation may be difficult

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Hemorrhage in the SV or VD or in a utricular or mullerian duct cyst is often seen in patients with hematospermia

Mullerian duct remnants may become a utricular cyst or a mullerian duct cyst

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Seminal Vesiculitis

Bacterial vesiculitis is often secondary to bacterial prostatitis

Chronic bacterial vesiculitis is rare.

US, CT, or MR imaging may demonstrate diffuse SV wall thickening .

Diffuse enhancement of the wall and septa of the SV can be seen at CT or MR imaging

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SV Abscess

An SV abscess may be related to diabetes mellitus, instrumentation, or a surgical procedure.

It is often associated with a prostatic abscess.

A thickwalled cystic lesion can be seen in the SV at US, CT, or MR imaging

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SV Amyloidosis

Deposition of amyloid in the SVs is relatively common, particularly in the elderly

The prevalence has been reported to be up to 21% in men older than 76 years

At MR imaging, the SVs demonstrate diffuse wall thickening, along with low signal intensity on T2-weighted images

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SVs involved by amyloidosis may contain areas of hemorrhage with increased signal intensity on T1-weighted images

Because of the signal intensity characteristics, SV amyloidosis often mimics tumor invasion by prostate cancer

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Primary and SecondaryNeoplasms of the SVs

Primary neoplasms of the SVs are extremely rare

Reported benign tumors include cystadenoma, papillary adenoma, leiomyoma, teratoma, neurilemoma, and epithelial stromal tumor

At imaging, benign tumors may mimic an SV cyst

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Cystadenoma is often seen as a unilateral multiseptate cystic mass in the retrovesical space .

On T1-weighted MR images, teratoma may be seen as a heterogeneous cystic lesion with areas of high signal intensity, which are suppressed on fat-saturated images

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Primary malignant neoplasms of the SV include adenocarcinoma (most common), leiomyosarcoma, angiosarcoma, mullerian adenosarcoma–like tumor, carcinoid, seminoma, and cystosarcoma phyllodes

At imaging, these tumors may appear as a retrovesical mass with or without prostatic or ureteral obstruction or as an infiltrating lesion in the SV with enhancement similar to that of advanced prostate cancer

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Secondary neoplasms of the SV are much more common

The most common tumors arise from the prostate, bladder, and rectum

The presence or absence of SV invasion is an important prognostic factor for patients with prostate cancer

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A solid mass extending into the SV can be seen at US .

CT may demonstrate a soft-tissue mass in the SV area with obliteration of the angle between the prostate and SV

MR imaging has been shown to be most accurate in evaluating SV invasion by prostate cancer

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The diagnostic criteria include loss of normal SV architecture, SV enlargement with a low-signal-intensity mass on T2-weighted images, and obliteration of the angle between the prostate and SV

Low signal intensity in the SV is reported to be highly predictive of SV invasion, if tumor with extracapsular extension is seen at the prostatic base

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Miscellaneous SV Findings

During radical prostatectomy, both SVs are removed

Sometimes, remnant SV tissue can be present after surgery

This finding should be differentiated from a postoperative scar or fluid collection and from recurrence

After resection of the rectum, the SVs may demonstrate enlargement and posterior displacement and mimic a mass

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After radiation therapy, chemotherapy, or hormonal therapy, the SVs often demonstrate decreased size, diffuse wall thickening, or diffuse low signal intensity on T2-weighted images

These findings may mimic tumor invasion into the SVs.

Reflux of contrast material into the SV or VD can be seen on contrast-enhanced CT or MR images after transurethral resection of the prostate.

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Abnormalities of the VD

Although very rare, congenital anomalies of the VD may occur

As with anomalies of the SV, congenital anomalies of the VD are often associated with other genitourinary anomalies

Agenesis of the VD is commonly associated with unilateral or bilateral hypoplasia or agenesis of the wolffian duct derivatives, such as the epididymis and SV

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In a series of 104 patients with VD agenesis, Schlegel et al (35) reported that bilateral SV agenesis was present in 45% of patients with bilateral VD agenesis.

Ipsilateral and contralateral SV agenesis were encountered in 86% and 20% of patients with unilateral VD agenesis, respectively.

Renal agenesis was found in 11% of cases with bilateral VD agenesis and in 26% of cases with unilateral VD agenesis

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Like SV agenesis, bilateral VD agenesis is closely associated with cystic fibrosis.

Bilateral VD agenesis is present in approximately 99% of male patients with cystic fibrosis.

Mutation of the cystic fibrosis transmembrane conductance gene is seen in two-thirds of patients with bilateral VD agenesis

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Bilateral calcification of the VD is often seen in patients with diabetes

Sometimes, chronic inflammation may cause calcification of the VD

Unlike diabetic calcification, inflammatory calcification is intraluminal.

It is often unilateral and segmental and may be associated with SV calcification

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Tumors arising from the VD are extremely rare.

Sporadic cases of leiomyoma, sarcoma, fibroma, and inflammatory malignant fibrous histiocytoma have been reported

Secondary tumors are much more common.

Tumor invasion of distal portions of the vasa deferentia is commonly seen in patients with prostate cancer , and invasion from a bladder tumor is not uncommon

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Conclusions

Diseases involving the SV and VD are rare.

Secondary tumor invasion is often seen in patients with prostate, bladder, or rectal cancer. Although very rare, primary neoplasms can also occur.

Because of the close embryologic relationship with the urinary tract, congenital anomalies of the SV and VD and SV cysts are often associated with other urologic or genital anomalies

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US and MR imaging are commonly used for diagnosing various abnormalities of these organs.

Owing to its excellent tissue contrast and multiplanar capability, MR imaging is best suited for evaluation of these organs.

Knowledge of the embryology and anatomy of the SVs and vasa deferentia can be helpful in interpreting cross-sectional imaging findings

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TERIMA KASIH