Hematospermia

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Background

Hematospermia is defined as blood in the semen. While often perceived as a symptom of little significance, blood in the ejaculate can cause great concern to the men who experience it. The condition is common, and many episodes go unnoticed; therefore, the prevalence of hematospermia remains unknown. In most patients with hematospermia, no further diagnostic workup is needed; however, in some patients, hematospermia may be the first indicator of other urologic diseases.

Hematospermia has been written about for centuries. Hippocrates, Galen, Pare, Morgagni, and Fournier all commented on this condition. The first American report appeared in 1894, and Fletcher,[1] Leary,[2] Marshall,[3] and Ganabathi[4] have subsequently published excellent contemporary reviews on the subject. The advent of newer imaging modalities has altered both the diagnosis and the treatment of hematospermia.

Pathophysiology

For an understanding of the causes of hematospermia, a working knowledge of the relevant anatomy of the ejaculatory complex is useful.

The seminal vesicles are androgen-dependent accessory organs that produce and store seminal fluid, which is essential to male fertility. The seminal vesicles are best studied ultrasonographically. Normal seminal vesicles are flat paired structures that lie cephalad to the prostate behind the bladder and have a bow-tie appearance on transverse imaging. They are symmetric, well-defined, saccular, elongated organs. In its normal collapsed state, the center of the gland is homogenous, with areas of increased echogenicity corresponding to the folds of secretory epithelium. In the distended state, the wall is visibly composed of 2 distinct layers. Caudally, the seminal vesicles diverge laterally.

The dimensions of the seminal vesicles vary with age, but not with the ejaculatory state. Upon transrectal ultrasonography (TRUS), the dimensions are estimated to be 30 ± 5 mm in length, 15 ± 4 mm in width, and 13.7 ± 3.7 mL in mean volume. The age of the patient and degree of prostate enlargement have been shown to cause variation in the size of the seminal vesicles.

MRI findings may also help delineate the normal anatomy of the seminal vesicles. Using MRI, the signal intensity of the seminal vesicles can be compared with the tissues surrounding them (ie, skeletal muscle, fat, urine). The signal intensity on T1-weighted spin-echo images of normal seminal vesicles in men is similar to or slightly higher than that of skeletal muscles and is always greater than that of urine. On T2-weighted images, the signal intensity varies. In prepubertal boys and men older than 70 years (androgen-deprived males), the signal intensity is generally lower than that of skeletal muscle or urine. Convolutions of the seminal vesicles are best observed on T2-weighted images or on T1-weighted images with the use of intravenous contrast agents.

The vasa deferentia act as conduits, carrying sperm between the epididymis and the ejaculatory ducts via the vasal ampullae. The vasal ampullae pass medially to the seminal vesicles and are best seen using transaxial TRUS views.

The seminal vesicles and vasal ampullae join together to form the ejaculatory duct. The ejaculatory duct travels through the prostate and enters the urethra at the level of the verumontanum. The junction between the seminal vesicle and the ejaculatory duct lies within the prostate and is difficult to see in a healthy unobstructed system. Small echodensities are frequently seen at the junction of the ejaculatory ducts and the verumontanum in the urethra. These areas provide useful landmarks and are thought to represent concretions within the periurethral glands surrounding the verumontanum.

Epidemiology

Frequency

United States

The true prevalence of hematospermia is unknown because most ejaculations occur intravaginally and hematospermia often remains unrecognized.

Recent data collected after TRUS-guided biopsy of the prostate suggest that up to 36.3% of men undergoing 6-15 cores develop postprocedure hematospermia. Increasing the number of cores did not significantly increase the frequency of hematospermia.[5]

Sex

Hematospermia affects only males.

Age

Hematospermia can occur in males of any age. In younger men (< 40 y), hematospermia is uniformly benign. Even in older men, it is rarely associated with malignancy.

History

Physical

The physical examination should include measuring the patient's blood pressure because severe hypertension is associated with hematospermia. This association is well recognized; however, the exact mechanism by which it occurs is unclear. It may have a similar basis to the association of hypertension with epistaxis (nosebleeds).

Causes

Hematospermia is usually associated with inflammatory conditions of the seminal vesicles or prostate. The condition is often self-limited and resolves within 1-2 months. If hematospermia persists beyond 2 months, further workup is recommended to determine the cause. In approximately half the cases, the etiology is declared idiopathic. However, this may reflect an incomplete evaluation.

Laboratory Studies

Imaging Studies

Procedures

Medical Care

Surgical Care

Patients in whom bleeding prostatic variceal veins are suggested as the cause of hematospermia are candidates for fulguration. After infectious causes have been excluded in cases of persistent hematospermia, cystourethroscopy is performed. If large friable prostatic veins are discovered and examination findings are otherwise normal, fulguration with a Bugbee or loop electrode can be performed. Prior to fulguration, a biopsy should be performed on any suggestive lesions.

More recently, a technique of endoscopy of the ejaculatory ducts and seminal vesicles has been described.[21, 22] This technique involves using a semirigid ureteroscope to cannulate the ejaculatory duct and allows the surgeon to examine the duct, seminal vesicle, and ampulla of the vas. However, the author reserves this technique for only the most refractory cases of hemospermia that cause significant physiologic (urinary retention or persistent hematuria) or psychological (avoidance of ejaculation) trauma.

Further Outpatient Care

Prognosis

Author

Jonathan D Schiff, MD, Assistant Clinical Professor of Urology, Department of Urology, Mount Sinai Medical Center; Adjunct Assistant Clinical Professor of Urology, Weill-Cornell School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

from Memorial Sloan-Kettering – John P Mulhall, MD, Director, Sexual and Reproductive Medicine Program, Memorial Sloan-Kettering Cancer Center

Disclosure: Nothing to disclose.

Specialty Editors

Edmund S Sabanegh Jr, MD, Chairman, Department of Urology, Glickman Urological and Kidney Institute, Cleveland Clinic Foundation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

J Stuart Wolf Jr, MD, FACS, The David A Bloom Professor of Urology, Director, Division of Endourology and Stone Disease, Department of Urology, University of Michigan Medical School

Disclosure: Nothing to disclose.

Chief Editor

Edward David Kim, MD, FACS, Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center

Disclosure: Lilly Consulting fee Advisor; Astellas Consulting fee Speaking and teaching; Watson Consulting fee Speaking and teaching; Allergan Consulting fee Speaking and teaching

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