Physiology of Urine Voiding and Ejaculation

Emission, defined as the release of sperm and accessory gland fluids into the pelvic urethra, and ejaculation, defined as the forceful expulsion of the combined fluids from the urethra, are reflex actions that also involve nervous pathways from the cerebral cortex. Emission occurs as the result of a thoracolumbar reflex arc that causes contraction of the smooth muscle of the ductus deferens and accessory glands. This same reflex arc also is responsible for the simultaneous contraction of the smooth muscle of the bladder trigone, thus preventing urine voiding during emission and subsequent ejaculation. Both emission and bladder neck closure primarily involve α-adrenergic, sympathetic fibers (Figure 17.2-1). Similarly, ejaculation is predominantly an α-adrenergic, sympathetic event and is mediated primarily by a sacral reflex involving the pudendal nerve. The reflex initiates rhythmic contractions of the bulbocavernosus, ischiocavernosus, and urethralis muscles.^2,3 Sensory stimulation of the penis, usually together with psychic input from the brain, are the physiologic triggers for the ejaculatory reflex. However, both emission and ejaculation also can occur without prior sensory stimulation (e.g., pharmacologically induced).^4,5

Pathophysiology

Any disease process that interferes with the normal synchronization of emission/ejaculation and bladder neck closure theoretically could result in urospermia. Reported causes of urospermia in stallions include neuritis of the cauda equina, equine herpesvirus 1, and sorghum toxicosis. In addition, urospermia can arise secondary to fractures, osteomyelitis, and neoplasias that impinge on the normal nervous pathways of the lumbosacral region.^1,6–8 Urospermia also has been reported in association with hyperkalemic periodic paralysis.⁹ All of these problems typically result in multiple neurologic deficits, and so clinical signs may not be limited to those involving bladder neck closure.

However, in the author’s experience, the majority of cases of urospermia in stallions are idiopathic, and the only apparent clinical sign is inappropriate urination during ejaculation. If carefully examined, some of these animals also may demonstrate mild urinary incontinence and/or subtle bladder dysfunction (e.g., an inability to completely void the bladder during voluntary urination) outside of the breeding situation. However, because the signs in breeding stallions are most dramatic at the moment of ejaculation, urospermia is often the only presenting complaint. In cases of idiopathic urospermia, the cause is typically attributed to some unidentified dysfunction of the emission and/or ejaculatory reflexes that permits a varying degree of bladder neck laxity at the moment of ejaculation, thus allowing for anterograde passage of urine through the urethra and resulting urine contamination of the ejaculate.

In men, incomplete bladder neck closure more typically is associated with retrograde ejaculation. During emission and ejaculation, semen passes in a retrograde fashion through the lax bladder neck and into the bladder, rather than moving anterograde through the penile urethra and urethral orifice.¹⁰ Although a case of retrograde ejaculation has been documented in a stallion,¹¹ this condition appears to be a much less common manifestation of incomplete bladder neck closure in the horse than is urospermia.

Regardless of the pathophysiology of urospermia, it has been documented that urine contamination of the equine ejaculate negatively affects sperm motility.¹² This effect is most likely the result of changes in pH and osmolarity caused by the presence of urine in the ejaculate. The more urine present and the more concentrated the urine in the ejaculate, the more profound will be its negative impact on sperm motility and subsequent fertility.

Clinical Signs and Diagnosis

Stallions breeding by natural cover whose semen is not evaluated on a regular basis may present for infertility.¹³ An accurate diagnosis of urospermia generally can readily be made in most stallions by collecting semen into an artificial vagina (AV) and observing gross urine contamination of the ejaculate. In more mild cases, the presence of urine in the semen may not be grossly apparent. Because sperm motility is severely adversely affected by the presence of urine,¹² reduced sperm motility may be the most apparent problem in more mildly affected animals. Microscopic examination of the ejaculate may reveal a large number of urine crystals. Even when urine contamination is not visibly evident, the presence of small amounts of urine often will alter the odor of the ejaculate. Urine also may increase the pH of the ejaculate.¹⁴

In cases in which small, grossly undetectable amounts of urine are suspected to be contaminating the ejaculate, creatinine or urea nitrogen levels can be run on a sample of whole ejaculate. A creatinine level of over 2.0 mg/dl or a urea nitrogen level of over 30 mg/dl is suggestive of urospermia.¹⁵ These are simple tests that readily can detect the presence of even small amounts of urine contamination. As an alternative, commercially available test strips for the semiquantitative detection of urea nitrogen (Azostix, Miles, Inc.,) or nitrite (Multistix, Miles, Inc.) also can be used. However, care must be taken when using these stall-side tests because false positives are common when the appropriate protocol is not strictly followed. Specifically, when using the Azostix test to detect urospermia, it is recommended that the reagent pad be rinsed with distilled water after only 10 seconds horizontal exposure to the sample. After rinsing, the result can be read. A change in color of the test pad from yellow to green indicates the presence of urine. When using the Multistix test, the test pad should be placed in a horizontal position and exposed to the sample for 3½ minutes before the test is read. A color change of the test pad from yellow to orange indicates the presence of urine.¹⁵

Urospermia can vary in severity from one ejaculate to another and often is sporadic. Thus collection of a single, urine-free ejaculate does not rule out the possibility of this condition. If urospermia is suspected, multiple semen collections, preferably when the stallion has a full bladder, are recommended to determine whether or not the disorder is present.

Observation and/or videotaping of the stallion in a box stall also may reveal some clinical signs. Affected animals may show evidence of neurologic or infectious disorders of the urinary system including dysuria, polyuria, and/or stranguria. In addition, videotaping of the stallion allows for ready evaluation of masturbation activity and penis control. Abnormalities in either of these areas may suggest the presence of either a localized or systemic neurologic problem involving the reproductive tract.

Once a diagnosis of urospermia is made, it is recommended that the stallion have a full neurologic examination, including examination of cranial nerve function, limb function, anal tone, anal reflex, tail tone, and defecation pattern and frequency. Standard neurologic evaluations may reveal subtle deficits in other areas of the body, thus suggesting a more systemic cause for the urospermia. In addition, the urinary tract should be carefully examined. Palpation and ultrasonographic examination of the bladder before and after voluntary urination may reveal an incomplete ability to fully evacuate the bladder contents. In addition, the bladder wall and contents can be evaluated for lesions or for the presence of uroliths. An attempt can be made to express the bladder by palpation per rectum. The amount of pressure that is required to expel urine from the bladder can be used as an indirect measure of bladder sphincter and neck control. To evaluate the ability of the detrusor muscle to contract, bethanechol chloride, a cholinergic agent that normally causes evacuation of the bladder within 15 minutes of subcutaneous administration, can be given at a dose of 0.07 mg/kg body weight. Following urination, the bladder can be reexamined to determine if complete evacuation has occurred. A urinalysis and culture and sensitivity of a catheterized urine sample also should be performed to rule out possible infectious causes of bladder irritation. If a problem is identified, it should be addressed directly (e.g., systemic antibiotic administration for cases of bacterial cystitis) in hopes that correction of the underlying problem will improve or eliminate the urospermia.

Treatment

Limited therapeutic options are available for the treatment of idiopathic urospermia in stallions. And of these, none has been consistently effective. The nonspecific nature of most treatments for urospermia in the stallion reflects our poor understanding of the pathophysiology of the disease. In reality, urospermia is generally managed, rather than treated. Most management changes designed to minimize or eliminate urospermia focus on minimizing the amount of urine present in the bladder at the time of semen collection or natural breeding. Treatments addressed at correcting the suspected underlying cause(s) of the problem (e.g., a neurologic condition) could in theory be more effective. However, because most cases of urospermia are idiopathic, this generally is not an option.

The simplest and most established method for the management of urospermia is to encourage the stallion to completely empty the bladder immediately before semen collection or natural breeding.¹⁶ This can usually be accomplished by moving the animal to a freshly bedded stall before he is taken to the breeding shed. Alternatively, fresh feces from another stallion can be placed in the subject stallion’s stall. Most stallions will be stimulated to urinate with either one or both of these techniques. As a final option, diuretics can be used.¹⁷ In the author’s experience, these techniques can be quite helpful in reducing the frequency and severity of urospermia; however, they do not always result in a urine-free ejaculate. Many horses retain some variable amount of residual urine in the bladder after voluntary voiding, and this urine still can be expelled and adversely affect sperm quality. Nonetheless, practices such as these remain the mainstays of management of urospermia.

In animals in which voluntary voiding is not sufficient, or in cases in which a urine-free ejaculate must be obtained in a single session, the stallion’s bladder can be completely emptied by passing a urinary catheter into the bladder to facilitate complete drainage.¹⁸ The bladder then can be lavaged with several liters of sterile physiologic saline to insure that any residual bladder contents will not be harmful to the sperm should they be expelled during ejaculation. If a sufficient number of trained personnel are available, the bladder can be manually expressed completely per rectum following the final lavage and before the urinary catheter is removed. This more extreme method of emptying the bladder has been reported to be highly successful and reliably resulted in urine-free ejaculates.⁸ In highly tractable animals, the procedure can be performed in the breeding shed, after the stallion has obtained an erection, thus avoiding the need for sedatives or tranquilizers and thus allowing for semen collection to proceed as soon as the bladder is fully evacuated. It should be kept in mind that repeated use of urinary bladder catheterization will predispose the stallion to urethritis and bacterial cystitis.¹⁸ The owners should be informed of the risk before using this technique, and it may be advantageous to place the stallion on a prophylactic course of an appropriate antibiotic if catheterization is to be performed routinely.

Stallions typically ejaculate in a series of seven or eight pulses of semen.¹⁹ Methods for separating an ejaculate by collecting individual pulses (fractions) have been described.²⁰ Theoretically, by fractionating the ejaculate, it should be possible to collect only the urine-free portions of the ejaculate, thus avoiding the problem of urine contamination.^17,18,21 However, in practice, the pattern of urine contamination of the ejaculate can vary from one ejaculate to the next.²¹ Some ejaculates may be urine-free, whereas in other instances, urine contamination may precede, coincide with, or follow ejaculation. Even within the same stallion, the frequency and pattern of urospermia can vary from one ejaculate to the next. Nonetheless, collection of the ejaculate into different fractions may allow one to at least sporadically separate the urine-free fractions from the urine-contaminated fractions. The variable pattern of urine contamination seen in most stallions can make this approach frustrating and only occasionally successful.

Depending on the amount of urine contamination present in an individual ejaculate, it may be possible to improve the longevity of sperm motility by immediately diluting the raw ejaculate with a standard semen extender. In one study the addition of semen extender to urine-contaminated semen restored sperm motility to values similar to uncontaminated control ejaculates.¹²

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