Hematospermia may be associated with several pathological conditions of the urogenital tract, involving the prostate, seminal tract (seminal vesicle, vas deferens, ejaculatory ducts), verumontanum, urethra, bladder, epididymis, or testes; it can also result from various iatrogenic or systemic conditions. In the past, and even in recent years, most cases were considered idiopathic, with the cause remaining unknown. However, with the improvement of imaging techniques, the number of idiopathic cases has decreased significantly, and the seminal vesicles (Fig. 1) have been recognized as an important site of bleeding [4].

Infectious or inflammatory conditions of the urogenital tract are the most common aetiologies of hematospermia, especially in men under 40 years of age, accounting for approximately 40% of all cases [5]. Some of the most common aetiological agents of hematospermia include Chlamydia trachomatis, Herpes Simplex Virus (the most common), bacteria, Ureaplasma, Cytomegalovirus, and parasites [6]. Inflammatory processes can lead to irritation of the mucous membranes, hyperemia, and edema of the accessory sex glands and their ducts, resulting in bleeding and the manifestation of hematospermia. Chronic prostatitis, with associated seminal vesiculitis, is a common cause of hematospermia and is usually associated with elevated PSA levels

On mpMRI, the signal and size of the prostate in patients with prostatitis (Fig. 2) can be highly heterogeneous, as there are different clinical forms of prostatitis (acute bacterial or viral prostatitis, prostatic abscess, chronic bacterial prostatitis, chronic nonbacterial prostatitis, and prostatodynia) [7]. The inflammation typically presents with ill-defined margins and a linear or wedge-shaped morphology, without mass effect, and with diffuse, lobar, or focal distribution. It shows low signal on T2-weighted morphological sequences and moderate enhancement on dynamic post-contrast sequences (DCE). In the presence of an abscess (Fig. 3) as a complication of prostatitis, a fluid collection may be observed, characterized by restricted diffusivity on high B-value scans (hyperintensity in DWI, hypointensity in ADC), with characteristic post-contrast "ring" enhancement.

Seminal vesiculitis (Fig. 4) is a condition typically associated with chronic prostatitis, and its MR appearance depends on the course of the disease [8]. In the subacute phase, the vesicles are frequently enlarged and often show elevated signal on T1-weighted sequences, as hematospermia commonly accompanies vesicular infection. On T2-weighted images, the signal may vary depending on the chronicity of the disease and the presence of bleeding (Fig. 5). Parietal enhancement is observed due to hyperemia. In chronic inflammation, MRI typically shows small seminal vesicles, either bilaterally or unilaterally, with reduced signal intensity on both T1- and T2-weighted images.

There are many obstructive conditions that can cause haematospermia, including the common case of benign prostatic hyperplasia (BPH) (Fig. 6).

Prostate utricle cysts (Fig. 7), of endodermal origin, communicate with the posterior urethra or ejaculatory duct and may be associated with genitourinary abnormalities. On MRI, they are typically small, located along the midline, and do not extend beyond the base of the prostate. They show a fluid-like signal intensity on T1- and T2-weighted sequences; however, in some cases, they may have altered signal due to hemorrhage or pus [9].

Müllerian duct cysts (Fig. 8), of mesodermal origin, are not associated with congenital genitourinary conditions. On MRI, they are typically larger, often "teardrop"- or "elongated"-shaped, and extend beyond the postero-superior margin of the prostate. These cysts show fluid signal intensity on T1- and T2-weighted sequences but may have an elevated signal due to mucinous, hemorrhagic, or infected material.

Seminal vesicle cysts (Fig. 9), whether congenital or acquired, may occur in isolation, be associated with abnormalities of the upper urinary tract (e.g., Zinner syndrome), or be associated with autosomal dominant polycystic kidney disease. The acquired form typically arises from infection or inflammation. Seminal vesicle cysts are generally unilocular, with thin walls and a fluid signal on T1- and T2-weighted MRI sequences [10]. However, the T1 signal may appear elevated due to haemorrhage or concentrated protein fluid, though these cysts do not show enhancement after the administration of contrast medium (mdc).

Calculi can form in the prostate, seminal vesicles, ejaculatory ducts, bladder, or urethra. More than 50% of calculi are composed of urinary components and result from reflux and stasis phenomena [11]. On MRI, they appear as low signal intensity on both T1- and T2-weighted sequences. However, they are more conspicuous on CT imaging due to their high attenuation. Seminal vesicle stones (Fig. 10) are a rare condition and thus are often misdiagnosed in clinical practice [12].

The association between hematospermia and prostate cancer [13] is uncommon, and urological or genital neoplasms are rarely the underlying cause (approximately 3.5% of cases).

Prostate cancer (Figs. 11 and 12) arises in 70% of cases in the peripheral zone, 25% in the transition zone, and 5% in the central zone. On MRI, prostate cancer typically presents as:

• Low signal intensity on T2-weighted sequences.
• Intermediate signal intensity on T1-weighted sequences.
• Restricted diffusion characterized by hyperintensity on DWI (diffusion-weighted imaging) at high B-values and hypointensity on ADC (apparent diffusion coefficient) maps.
• Post-contrast enhancement on dynamic-perfusion sequences (DCE).

Signs of extracapsular extension include infiltration of the seminal vesicles, extensive contact with the capsular surface (>1 cm), capsular bulging or retraction, encasement or asymmetry of the neurovascular bundles, obliteration of the recto-prostatic angle, and direct invasion of adjacent organs or structures. MRI criteria for seminal vesicle invasion include: low signal intensity of the seminal vesicles on morphological sequences, obliteration of the normal angle between the seminal vesicles and the prostate base, and direct extension of the tumor along the seminal vesicle ducts.

Systemic factors that can cause haematospermia include severe arterial hypertension, blood clotting disorders (e.g., purpura, Von Willebrand disease, haemophilia), and amyloidosis [14] affecting the seminal vesicles. Vascular abnormalities, such as urethral haemangiomas, venous fistulas of the seminal vesicles, and arterio-venous malformations, can also contribute to its occurrence.

Finally, haematospermia can result from iatrogenic causes or traumatic injuries.