Male infertility: the role of imaging in diagnosis and management

Abstract

The investigation of male infertility is assuming greater importance, with male factors implicated as a causal factor in up to half of infertile couples. Following routine history, examination and blood tests, imaging is frequently utilised in order to assess the scrotal contents for testicular volume and morphology. Additionally, this may give indirect evidence of the presence of possible reversible pathology in the form of obstructive azoospermia. Further imaging in the form of transrectal ultrasound and MRI is then often able to categorise the level of obstruction and facilitate treatment planning without resort to more invasive imaging such as vasography. Ultrasound guidance of therapy such as sperm or cyst aspiration and vasal cannulation may also be performed. This article reviews the imaging modalities used in the investigation of male infertility, and illustrates normal and abnormal findings that may be demonstrated.

Infertility is defined as a failure to achieve pregnancy during 1 year of frequent, unprotected intercourse [1]. In the general population (which includes people with fertility problems), it is estimated that 84% of females would conceive within 1 year of regular unprotected sexual intercourse. This rises cumulatively to 93% after 3 years [2,3]. As most couples conceive within a year, assessment of the presenting couple is usually initiated after 12 months, but may be instigated earlier if there is a high clinical suspicion of infertility or if the female partner is older than 35 years [4]. A careful history and physical examination of each partner can suggest a single or (more usually) multifactorial aetiology and directs further investigation [5]. A multicentre study by the World Health Organization [6] found that in 20% of infertility cases the cause was predominantly male, and in 27% abnormalities were found in both partners; therefore, a male factor is present in approximately 50% of infertility cases.

Once male infertility is diagnosed, a physical cause is identified in one-third of these patients (Table 1) [7]. In the remainder, idiopathic male infertility is diagnosed. Testicular failure or dysfunction, also referred to as primary hypogonadism, is the most common identifiable cause in males [4]. Imaging plays a vital role in identifying potentially correctable causes of infertility especially congenital anomalies and disorders that obstruct sperm transport.

Table 1. Causes of male infertility.

Causes of male infertility
Pre-testicular	Acquired endocrinopathies
	Genetic endocrinopathies
	Disorders of production or secretion of gonadotrophin-releasing hormone
	Disorders of luteinising hormone, follicle-stimulating hormone and androgen function
Testicular	Varicocoele
	Genetics
	Cryptorchidism
	Exposure to gonadotoxins
Post testicular	Obstruction
	Immunologic infertility
	Disorders of ejaculation
	Erectile dysfunction

Evaluation of male infertility

Simple initial screening for male infertility involves semen analysis, repeated at 4–6 weeks if abnormal. If male subfertility is established, urological referral is undertaken. Similarly to any other medical condition, evaluation of the infertile male starts with a detailed history and physical examination. This is followed by laboratory tests and imaging in order to identify a possible correctable cause. Laboratory tests routinely include follicle-stimulating hormone and testosterone levels, with further tests carried out when needed. Causes of male infertility include congenital or acquired urogenital abnormalities, genetic and immunological factors, endocrine disturbances, genital tract infections and erectile dysfunction. These can be conveniently divided into pre-testicular, testicular and post-testicular causes (Table 1).

Imaging techniques used for evaluation of male infertility

In addition to identifying possible causes of infertility, imaging often allows the selection of the best method for impregnating the female partner, such as image-guided sperm aspiration from the epididymis or seminiferous tubules, allowing in vitro fertilisation or intracytoplasmic sperm injection [7]. The three main imaging modalities used for investigation of the male reproductive system are ultrasound, MRI and invasive techniques such as venography and vasography. Ultrasound remains the mainstay as it is non-invasive, safe and widely available, and is able to define many of the abnormalities relevant to male infertility. MRI is useful in problem solving, and the invasive techniques are generally reserved for therapeutic intervention in previously defined abnormalities.

Ultrasound techniques

Ultrasound is almost always the initial imaging investigation in male infertility. Assessment is aimed at evaluation of testicular morphology, patency of the efferent ducts and prostatic anomalies. Erectile dysfunction may also be assessed.

Scrotal ultrasound

Scrotal ultrasound is excellent for initial evaluation of the scrotum and can directly demonstrate abnormalities within the testis and the peritesticular structures, such as varicocoeles and epididymal abnormalities, as well as visualising secondary changes caused by distal genital duct obstruction.

The examination is performed with a high-frequency (7–12 MHz) linear-array transducer with adequate length for longitudinal measurement of the testis [7]. The patient is examined in a supine position. The testes should be examined in orthogonal transverse and longitudinal planes, and colour Doppler evaluation and volume measurements should be performed routinely. Volume measurement is usually calculated as length×height×width×0.51. A total volume (both testes) of >30 ml and a single testicular volume of 12–15 ml is generally considered normal [8] (Figure 1).

Figure 1.

(a) Normal longitudinal ultrasound image of the testis, demonstrating a uniform texture and reflectivity with a length of 5.0 cm (normal 3.5–5.0 cm). Volume measurement is calculated as length×height×width×0.51. (b) Longitudinal ultrasound image of a small (length 2.5 cm) testis with an abnormal texture and reflectivity in a patient being investigated for infertility.

Transrectal ultrasound

Transrectal ultrasound (TRUS) enables high-resolution imaging of the prostate, seminal vesicles and vas deferens and is the modality of choice in diagnosing congenital and acquired abnormalities implicated in the cause of obstructive azoospermia (OA). The patient is positioned in a left lateral decubitus position. A high-frequency endorectal transducer should be used with a condom cover. Systematic evaluation of the terminal vas deferens, seminal vesicles, ejaculatory duct and prostate are carried out in axial and sagittal planes (Figure 2). TRUS is also used to guide prostatic cyst aspiration.

Figure 2.

Normal ultrasound anatomy of the seminal vesicles and vasa deferentia. Transverse image from a transrectal ultrasound image, obtained superior to the prostate, shows symmetric seminal vesicles (short arrows) and more medially located vasa deferentia (long arrows).

B-mode and dynamic colour Doppler ultrasound of the penis

Penile ultrasound is performed when evaluating physical causes of erectile dysfunction. These include structural penile abnormalities, problems with arterial inflow and malfunction of the venous occlusive mechanism [9]. It is important to obtain informed consent prior to intracavernosal injection of prostaglandin regarding the small risk of priapism. Greyscale ultrasound is initially performed to exclude structural abnormalities, including fibrotic plaque diseases, focal cavernosal fibrosis or calcification, and tunica albuginea disruption [7]. Intracavernosal injection of prostaglandin E1 (PGE1) is then undertaken. The transducer is placed on the ventral surface of the base of the penis and the cavernosal artery is sampled with Doppler angle correction to allow for accurate velocity measurements. The peak systolic velocity and end diastolic velocity (EDV) are assessed every 5 min after the administration of PGE1 for up to 30 min [7]. Although complete reversal of EDV is not always observed, in our experience with young patients EDV reversal is the rule if an adequate grade of erection is achieved (Figure 3).

Figure 3.

Ultrasound evaluation of a normal cavernosal artery response post intracavernosal injection of prostaglandin E1. Reversal of end diastolic velocity at 15 min is demonstrated, with a peak systolic velocity measured at 141.5 cm s⁻¹ (normal >35 cm s⁻¹) and an end diastolic velocity measured at −27.9 cm s⁻¹.

MRI techniques

MRI is useful for both detection and characterisation of prostatic cysts detected on a TRUS and evaluation of the vas deferens, seminal vesicles and ejaculatory ducts. A typical protocol for imaging of the prostate for this purpose would include triplanar T₂ weighted spin echo [long repetition time (TR)/long echo time (TE)] and T₁ weighted turbo spin echo (short TR/short TE) triplanar high-resolution images (3–4 mm slice thickness) with a small field of view (Figure 4). A pelvic body coil is generally used although some centres use endorectal coils. The use of the endorectal coil requires bowel preparation and may be less favoured by the patient [7].

Figure 4.

Normal T₁ (a) and T₂ (b) weighted axial MR images through the prostate (long arrow). The peripheral zone is of high signal on the T₂ weighted images (short arrows).

Invasive imaging techniques

Testicular venography and embolisation

Venography is regarded as the gold standard for diagnosis of a varicocoele by demonstrating reflux of contrast into the testicular vein [7]. However, as it is an invasive technique it is reserved for when embolisation of the testicular vein is to be undertaken following clinical and ultrasound diagnosis. Conventionally, access is from a femoral vein approach; however, a basilic or an internal jugular approach can be used. The majority of varicocoeles are unilaterally left sided. The left testicular vein flows into the left renal vein while the right testicular vein usually joins the inferior vena cava directly. With a groin approach to the right a coaxial microcatheter is often required. A hydrophilic catheter minimises vasospasm and once the testicular vein is selectively catheterised the catheter is advanced down to the level of the inguinal ligament with deployment of embolisation coils proximally from this point (Figure 5). Once embolisation coils are deployed within the distal testicular vein a check venogram is performed at the midpoint of the vein to ensure the absence of collateral vessels. If these are identified, then embolisation coils are deployed across their junction with the testicular vein to prevent collateral drainage leading to therapeutic failure.

Figure 5.

A difficult and less frequently performed right testicular vein embolisation, as the right testicular vein drains directly into the inferior vena cava. (a) An 0.018 inch coaxial microcatheter (arrow) is used on the right owing to the sharp reverse angle of the testicular vein and the inferior vena cava. Collaterals are seen at the mid-testicular vein level (short arrow). (b) Coil embolisation (arrows) of the testicular vein with successful obliteration of collateral filling.

Vasography

This is an invasive procedure requiring either blind or ultrasound-guided puncture of the vas deferens and retrograde contrast injection with filling of the ducts and spill into the bladder confirming patency. Long considered the gold standard for vas deferens and ejaculatory duct evaluation, it is now used much less frequently because of the widespread acceptance of ultrasound, TRUS and MRI. Vasography is invasive and carries a risk of infection and possible stricturing of the vas deferens at the site of puncture.

Causes of male infertility

The prerequisites for successful male fertility are normal spermatogenesis, successful epididymal maturation and storage of sperm, normal sperm transport and normal accessory gland function. The absence of both spermatozoa and spermatogenic cells in semen and post-ejaculate urine is termed azoospermia. In non-idiopathic infertility this can be subdivided into OA and non-obstructive azoospermia (NOA). OA is less frequent than NOA and represents only 15–20% of cases of azoospermia [10]. OA manifests because of blockage of sperm transport or abnormalities of the epididymis, vas deferens or ejaculatory duct. Non-obstructive OA results from defective sperm production by the testicles. The importance in differentiating these entities and correctly identifying OA is that the latter may be amenable to surgical correction.

Obstructive azoospermia

Imaging is directed at a mechanical reason for the obstruction and evaluation of the entire tract from the testis to the distal ductal system is essential. In patients with OA, testicular ultrasound is often abnormal. In a study performed by Moon et al [11], 86% of cases of OA had an abnormal ultrasound. They found abnormalities associated with obstruction included tubular ectasia of the epididymal head, tapering of the epididymal tail, absence of the epididymis and the presence of heterogeneous mass along the epididymal course [11] (Figure 6). This study also demonstrated a larger testicular volume in OA than NOA. Thus scrotal ultrasound is a useful preliminary test in diagnosing OA and differentiating it from NOA; however, TRUS is the modality of choice for assessing the actual cause of OA. Using TRUS, a systematic evaluation of the terminal vas deferens, seminal vesicles, ejaculatory ducts and prostate can be carried out in both axial and sagittal planes. Kuligowska and Fenlon [12] assessed 276 patients with OA using TRUS: 25% were found to have a normal TRUS, 34% congenital bilateral absence of the vas deferens, 15% absent seminal vesicles and ejaculatory ducts, 9% obstructing cysts and 4.4% obstructing calculi (Figure 7).

Figure 6.

Heterogeneous testis with associated ectasia of the rete testis (short arrows) and dilated body of the epididymis (long arrow) in keeping with long-standing obstruction.

Figure 7.

A transrectal ultrasound examination demonstrating calcification within the ejaculatory duct (short arrow) with dilatation of the vas deferens proximally (long arrow).

Obstruction may occur at any level in the reproductive tract from the epididymis proximally to the ejaculatory duct distally. At each of these levels, obstructive causes can be categorised into congenital and acquired (Table 2). The level of obstruction has direct relevance to possible treatment of correctable causes, with proximal obstruction being amenable to vasoepididymostomy and distal obstruction often treated by transurethral resection of the ejaculatory ducts.

Table 2. Classification of obstructive azoospermias.

Classification	Conditions
Epididymal obstruction
Congenital	Idiopathic epididymal obstruction
Acquired	Post infective (epididymitis)
	Post surgical (epididymal cysts)
Vas deferens obstruction
Congenital	Congenital absence of the vas deferens
Acquired	Post vasectomy
	Post surgical (hernia, scrotal surgery)
Ejaculatory duct obstruction
Congenital	Prostatic cysts (Müllerian cysts)
Acquired	Post surgical (bladder neck surgery)
	Post infective

Epididymal obstruction

Infection is a common cause of obstruction anywhere along the course of the male reproductive tract, especially the epididymis (Figure 8). Acute Gonococcus or subacute chlamydial infections can lead to scarring and subsequent obstruction (Figure 9). Iatrogenic epididymal obstruction may be sustained after surgical removal of an epididymal cyst. Epididymal obstruction is treated surgically. Vasoepididymostomy is a microsurgical technique where the epididymis is anastomosed to the vas deferens bypassing the level of obstruction. Pregnancy can be achieved in 20–40% of post-vasoepididymostomy cases without the use of assisted reproductive techniques [13].

Figure 8.

Scrotal ultrasound demonstrating thickening and enlargement of the epididymal body (arrow) in a case of infective epididymitis. The testis is spared from the infective process.

Figure 9.

(a) Longitudinal scan demonstrating a small testis with a heterogeneous echo-texture and a varicocoele (arrows) in a patient being investigated for infertility. (b) Focal dilatation of the epididymis (arrow) in keeping with chronic obstruction secondary to infection.

Vas deferens obstruction

Vasectomy is the most common cause of vasal obstruction. The post-vasectomy epididymis has a characteristic dilated inhomogeneous appearance on ultrasound described as ectasia of the epididymis (Figure 10). About 2–8% of patients request reversal of vasectomy. Although vasectomy reversal is technically possible, some authors have reported testicular fibrosis with impairment of germ cell function with prolonged obstruction secondary to vasectomy. Therefore, reduced fertility may persist following reversal [14]. Other acquired causes include inguinal hernia repair, scrotal sac surgery and chronic infection (Figure 11). The most common cause of congenital vas deferens obstruction is congenital bilateral absence of the vas deferens (CBAVD), which is seen in 2% of patients under investigation for infertility. Up to 82% of patients with CBAVD have at least one mutation within the cystic fibrosis gene [15]. Therefore, patients with CBAVD must be considered for cystic fibrosis screening and genetic counselling prior to sperm retrieval/intracytoplasmic sperm injection treatment [16].

Figure 10.

Longitudinal ultrasound of the epididymis demonstrating the classical appearance associated with a vasectomy (long arrow) and an additional less well appreciated view of the dilated vas deferens (short arrows).

Figure 11.

Bilateral thickening of the vas deferens on a transrectal ultrasound examination in keeping with vesiculitis (arrows).

In patients with CBAVD scrotal ultrasound demonstrates dilatation of the efferent ducts with the epididymis stopping abruptly at the junction of the body and tail beyond which no vas deferens is seen. TRUS of the caudal junction of the vas deferens and the seminal vesicles shows absence of the ampulla of the vas deferens [17]. CBAVD is nearly always associated with abnormalities of the seminal vesicle and ejaculatory duct [18,19]. Vas deferens agenesis is known to be associated with renal anomalies, including agenesis, cross-fussed ectopia and ectopic pelvic location. In view of this, renal ultrasound is advised when agenesis of the vas deferens is diagnosed. In a similar fashion to epididymal obstruction, vas deferens obstruction may also be amenable to microsurgical reconstruction [13].

Ejaculatory duct obstruction

Ejaculatory duct obstruction (EDO) is relatively uncommon, with the incidence of complete bilateral EDO reported as less than 1% in infertile males [20]. The incidence of incomplete EDO is unknown because of variations in definitions between authors [21]. Congenital causes of EDO include duct atresia or stenosis as well as compression by midline prostatic cystic lesions, e.g. cysts of the prostatic utricle (previously named Müllerian duct cysts), cystic dilatation of the prostatic utricle and ejaculatory duct cysts [22]. Cystic obstruction of the ejaculatory tracts is usually congenital and acquired lesions are rare [8].

Cysts and cystic dilatation of the prostatic urethra

Prostatic urethra cysts and cystic dilatation of the prostatic utricle are both midline anomalies. Prostatic urethra cysts and cystic dilatation of the prostatic utricle may be difficult to distinguish on TRUS, as they both appear as spherical cystic structures within the midline of the prostate [12]. However, prostatic urethra cysts may grow above the prostate and are prone to haemorrhage; therefore, distinction from cystic dilatation of the prostatic utricle can be made on the bases of the cyst size and contents. MRI is a useful technique for characterisation of these cysts. The presence of blood and or proteinaceous fluid within a prostatic urethra cyst gives it a high T₁ weighted signal distinguishing it from cystic dilatation of the prostatic utricle [23] (Figure 12).

Figure 12.

Small cyst lying within the midline within the prostatic utricle (arrow). This returns a low signal on the T₁ weighted images (not shown) and a high signal on the T₂ weighted images in keeping with cystic dilatation of the prostatic utricle.

Ejaculatory duct cysts

Ejaculatory duct cysts are far less common than prostatic urethra cysts or cystic dilatation of the prostatic utricle [24]. Ejaculatory duct cysts are midline or paramedial prostatic cysts derived from the Wolffian duct and urogenital sinus, into which the ejaculatory ducts empty, and therefore these cysts will contain sperm. Conformation of the diagnosis of an ejaculatory duct cyst can be obtained by demonstrating spermatozoa from cyst fluid on ultrasound aspiration. They can become very large and may extend beyond the prostate [25]. Although large cysts can be aspirated transrectally under ultrasound guidance, the results are often short lived; reaccumulation of the cyst contents occurs [25].

Acquired causes include calculi in the distal ejaculatory ducts at the level of the ampulla, which may be associated with dilatation of the proximal duct and evidence of obstruction [18]. Iatrogenic causes include surgery to the base of the bladder and infections acquired post catheterisation [7]. Despite the low overall incidence of ejaculatory duct obstruction, correct diagnosis is important as it can be treated by transurethral resection of the ejaculatory duct. This is followed by the appearance of sperm in the ejaculate in approximately 50–73% of cases with a 25% pregnancy rate [13].

Non-obstructive azoospermia

The causes may be divided into testicular abnormalities, varicocoeles and primary testicular tumours.

Testicular abnormalities

Cryptorchidism

The term cryptorchidism is derived from the Greek words “kryptos” meaning “hidden” and “orchis” meaning “testis”. Cryptorchidism is the most common congenital abnormality of the male urogenital tract at birth. The failure of descent of the testis into the cooler environment of the scrotal sac is thought to impair spermatogenesis and predispose to malignancy [26]. In males with bilateral cryptorchidism, the rate of paternity is approximately 50% but unilateral cryptorchidism results in little, if any, impairment of fertility [7].

Scrotal ultrasound confirms the clinical diagnosis of cryptorchidism by demonstrating the absence of the testis within the scrotal sac. As most undescended testis are located within the inguinal canal, ultrasound may also directly visualise the testis in this location (Figure 13). Either abdominal CT or MRI evaluation is useful in cases where the undescended testis is not identified with ultrasound [27].

Figure 13.

Ultrasound image of the left groin in a patient with testicular maldescent demonstrates a heterogeneous, with focal areas of low reflectivity and a small testis in keeping an infracted undescended testis within the inguinal canal.

Testicular atrophy

Testicular atrophy is associated with reduced spermatogenesis and a reduction in fertility. Atrophy may occur following previous inflammation, liver cirrhosis, oestrogen treatment, hypopituitary disorders and aging. On ultrasound, there is a global reduction in the volume of the testis (Figure 14). A decrease in both testicular reflectivity and vascularity are common findings. The epididymis usually appears normal [8].

Figure 14.

Scrotal ultrasound image demonstrating global reduction in testicular volume and reflectivity on the right (arrow) on this “spectacle” view of both the testes.

Orchitis and epididymo-orchitis

Despite the absence of conclusive epidemiological data, infections and inflammations of the genital tract are considered the most frequent causes of reduced male infertility [28]. Both clinical and pathological evidence exist to support the theory that chronic inflammatory conditions of the testes disrupt spermatogenesis and irreversibly alter both the number and quality of sperm [28]. Chronic epididymitis and epididymo-orchitis can also result in testicular atrophy. Pure orchitis is uncommon and is most often associated with the mumps virus [29]. As discussed above, epididymitis may also result in post-inflammatory obstruction of the epididymis causing OA.

A range of organisms including Neisseria gonorrhoea and Chlamydia trachomatis may be implicated in acute epididymo-orchitis. Less frequent causes such as mumps and sarcoidosis tend to cause bilateral changes [30]. Early diagnosis and appropriate management of epididymo-orchitis is important, as early therapeutic intervention may prevent loss of fertility. Greyscale ultrasound findings of epididymo-orchitis include testicular enlargement and heterogeneity of echo texture associated with an enlarged hypoechoic or hyperechoic epididymis. Colour Doppler ultrasound shows increased blood flow to both testis and epididymis [27] (Figure 15).

Figure 15.

A severely affected testis following orchitis, demonstrating mixed reflectivity with pockets of high reflectivity likely to represent areas of infarction and haemorrhage.

Varicocoele

A varicocoele is an abnormal venous dilatation of the pampiniform plexus, which may lead to symptoms of pain and discomfort, failure of ipsilateral testicular growth and development, or infertility [31]. A varicocoele is a common finding in approximately 20% of adolescents and adult males, and in up to 40% of infertile patients [32]. The direct connection between varicocoele and infertility is not clear. It is well known that after operative therapies on a varicocoele an improvement in sperm quality is found [32]. A recent Cochrane review [33] found no evidence that treatment of varicocoeles in males from couples with otherwise unexplained subfertility improved pregnancy rates. However, of the eight studies in this review two included some males with normal semen analysis and three studies specifically addressed only males with subclinical varicocoeles. In a multicentre trial specifically looking at infertile males with moderate oligozoospermia and a clinically apparent varicocoele with no other demonstrable cause for infertility, varicocoele correction improved sperm parameters and the fertility rate [34]. Thus there is still likely to be a place for varicocoele treatment in improving fertility when there is a clinically detectable varicocoele and abnormal sperm parameters.

Diagnosis of a varicocoele is made on clinical examination and usually confirmed by ultrasound with high accuracy (sensitivity 97%, specificity 94%) [35]. On greyscale imaging a varicocoele is seen as serpiginous tubules posterior to the testis, and may extend to the inferior pole of the testis with at least two or three veins of the pampiniform plexus measuring >2–3 mm in diameter (Figure 16). Colour Doppler ultrasound is a routine component of the examination as identification of flow reversal on Valsalva improves diagnostic accuracy. The degree of venous reflux during the Valsalva manoeuvre may be graded 1–3: Grade 1, reflux induced by the Valsalva manoeuvre; Grade 2, intermittent spontaneous reflux; and Grade 3, continuous spontaneous reflux [27,31,36]. Treatment may be surgical or radiological (see above) with similar success rates and rates of recurrence.

Figure 16.

(a) On greyscale imaging a varicocoele is seen as serpiginous tubules inferior to the testis (arrow). (b) Colour flow Doppler confirms flow within the varicocoele (arrow).

Primary testicular tumours

Testicular cancer dominates as the leading cancer in young males aged 15–34 years. It is also widely accepted that males with infertility have an increased risk of testicular cancer, even after excluding the common risk factors for testicular cancer and infertility, such as a history of undescended testes and chromosomal aberrations [37-39]. Similarly, patients presenting with a primary testicular tumour often have decreased semen quality and reduced fertility that appears to be specific for germ cell tumours [7]. Peterson et al [40], using patients with testicular lymphoma as a control group, demonstrated a reduction in fertility in patients with a germ cell tumour compared with preserved fertility in the control group. Scrotal ultrasound is the modality of choice for assessment of testicular tumours. The features of testicular malignancy are varied but most tumours are homogeneous and of low reflectivity when compared with the surrounding testicular parenchyma [8]. Increased vascularity may also be present (Figure 17). As testicular cancer usually affects young males, preservation of semen prior to therapy (either surgery or radiotherapy) is an important consideration, and semen cryopreservation may be indicated.

Figure 17.

Longitudinal ultrasound image of a testicular mass demonstrating increased Doppler flow within the lesion; a histologically proven seminoma.

Conclusion

The investigation of infertile male patients is essential in order to identify potentially treatable causes of infertility and to guide therapy. A key element in the pathway is separation of NOA from OA. Imaging techniques have now become well established with scrotal ultrasound indicating whether OA or NOA is likely and further modalities such as TRUS and MRI defining levels of obstruction and often the cause in cases of OA. Scrotal ultrasound findings may prompt treatment of varicocoele, testicular maldescent or tumour.

A scrotal ultrasound finding suggesting OA is usually followed by TRUS with differentiation of proximal from distal obstruction. Vasoepididymostomy may be offered to patients with proximal obstruction. In those with distal obstruction TRUS and/or MRI will define whether urogenital cysts are present: if so, these can be aspirated under ultrasound guidance, although results are often short lived. Ultrasound-guided aspiration for sperm harvesting is also possible. If no cysts are identified then transurethral resection of the ejaculatory ducts can be performed on the assumption there is distal duct abnormality causing obstruction.