Genitourinary and Gynecological Systems

At the completion of this chapter the reader should be able to do the following:

1. Name common genitourinary and gynecological disorders that athletic personnel encounter in the care of the athlete

2. Describe conditions of the genitourinary and gynecological systems that warrant referral

3. Explain the physiology of ovulation and menstruation

4. Describe the physiological changes that occur in pregnancy

5. Identify the limitations of the pregnant athlete

6. Describe preventive strategies for genitourinary and gynecological disorders, and for sexually transmitted infections (STIs)

7. Refer patients with signs or symptoms of an STI to a physician

Introduction

Whereas injury to the genitourinary and gynecological systems is rare in athletics, disorders of these systems are common in the athletic population. This chapter focuses on these systems and discusses how an athletic trainer might recognize and refer conditions to a physician. Although athletic trainers do not perform most of the evaluations in this chapter, they do have a relationship with their athletes whereby they may be able to gather enough symptomatic data to warrant referral to the team physician. In addition, knowledge of the types of diagnostic tests will better enable the athletic trainer to explain them to the affected athlete.

Overview of Anatomy and Physiology

Anatomy of the Kidneys, Ureters, and Urinary Bladder

The kidneys act to remove excess water, salts, and products of metabolism from the blood in order to maintain proper acid–base status. The body’s waste products are then conveyed in the urine to the urinary bladder by the ureters. Normally, an individual has two kidneys, two ureters, and a single urinary bladder (Figure 10-1). The kidneys lie posterior to the peritoneum in the retroperitoneal space on the posterior abdominal wall, alongside the spine and against the psoas major muscles. The kidneys are bean-shaped organs whose upper poles are protected by the lower bony thorax. Because of the large size of the right lobe of the liver, the right kidney lies at a slightly lower level than the left. In muscular individuals and those with well-developed abdominal musculature, the kidneys are generally not palpable on examination.

FIGURE 10-1 Anatomical location of the kidneys in the retroperitoneal aspect of the abdomen. (From Seidel HM, Ball JW, Dains JE, et al: Mosby’s guide to physical examination, ed 6, St. Louis, 2006, Mosby.)

The surrounding anatomy of the two kidneys differs anteriorly (Figure 10-2). The right kidney is associated with the liver and separated from it by the hepatorenal recess. The left kidney is associated with the left adrenal gland, stomach, spleen, pancreas, a portion of the small bowel, and the descending colon. They lie well protected posteriorly by the costovertebral angle between the twelfth rib and the vertebral spine. In addition, both kidneys are attached superiorly to the diaphragm and move slightly on respiration.

FIGURE 10-2 Posterior view of the kidneys protected within the costovertebral angle between the twelfth rib and the spine. (From Jarvis C: Physical examination & health assessment, ed 5, St. Louis, 2008, Saunders.)

The kidneys are enclosed in a strong fibrous capsule that is surrounded by a layer of fat called perirenal fat. The unique characteristics of the density of the kidney itself and the perirenal fat allow for the kidneys to be visualized on abdominal radiographs. The kidney is a solid organ with a thick cortex under the fibrous capsule (Figure 10-3). Filtration begins at the medulla, continues interiorly in the calyx structures, and ends in the collection area before the ureter.

FIGURE 10-3 Cross-section reveals two views of the internal structure of the kidney. (From Copstead LC, Banaski JL: Pathophysiology, ed 4, St. Louis, 2010, Saunders.)

The ureters are muscular ducts, or tubes, that carry urine from the kidneys to the urinary bladder. Urine passes from the kidneys through the ureters by peristaltic waves of muscular contraction. The ureters are approximately 25 cm long and retroperitoneal in location. Each descends almost vertically along the psoas major muscle just anterior to the tips of the transverse processes of the lumbar vertebrae (L2–L5). In the female, the ureters and uterine arteries are closely associated. The uterine artery crosses the ureter at the side of the cervix; therefore, during a surgical procedure to remove the uterus and cervix, the ureter may be inadvertently damaged.

The urinary bladder is a muscular sac or vesicle that functions to store urine. Its shape, size, position, and relation to other structures vary with the amount of urine it contains. It is composed chiefly of smooth muscle. In the adult, the empty urinary bladder lies posterior to the symphysis pubis within the pelvis (Figure 10-4). As it fills, it ascends into the lower abdomen. A full bladder may reach as high as the level of the umbilicus. The ureters enter at the superolateral aspect of each side of the bladder. The bladder is then drained by a single urethra that empties from the central inferior aspect.

FIGURE 10-4 Anatomy of the urinary bladder. (From Copstead LC, Banaski JL: Pathophysiology: biological and behavioral perspectives, ed 2, Philadelphia, 2000, Saunders, p 710.)

The blood supply to the kidneys is provided by the right and left renal arteries, respectively. These branch off from the descending aorta at nearly right angles. Venous drainage is provided by the right and left renal veins that empty into the inferior vena cava. Blood supply to the ureters is more complex, but it is principally supplied by arterial branches from the renal, aortic, common iliac, vesicular, or uterine arteries. The main arteries supplying the urinary bladder are branches of the internal iliac arteries. In the female, however, branches of the uterine and vaginal arteries also supply a portion of the blood supply to the bladder. Venous drainage occurs via the vesicular venous plexus that drains to the internal iliac vein (see Figure 10-1).

Lymphatic drainage from the kidneys and upper ureter empties into the aortic lymph nodes, whereas lymphatic drainage from the middle and lower ureter is directed to the common iliac lymph nodes. Drainage from the superior portion of the urinary bladder is directed to the external iliac lymph nodes, and the inferior portion of the bladder drains to the internal iliac lymph nodes.

The urinary bladder is supplied by parasympathetic motor fibers to the detrusor muscle of the bladder, and sensory fibers. The sensory fibers are stimulated by stretching of the bladder, causing a sensation of fullness and activating the micturition, or urination, reflex. Micturition is preceded by contraction of the diaphragm and abdominal wall. The neck of the bladder descends, the detrusor muscle contracts by reflex, and urine is voluntarily expelled from the bladder (see Figure 10-4).

Anatomy of the Urethra

The urethra is a fibromuscular tube that conducts urine from the bladder (and semen from the ductus deferens in the male) to the exterior. The urethra originates at the central lower portion of the urinary bladder, traverses the pelvis, and terminates at the external urethral orifice.

The female urethra is approximately 4 cm long. It is closely associated, often fused, with the anterior vaginal wall. The urethral orifice is located between the clitoris (anteriorly) and the vagina (posteriorly).

The male urethra is considerably longer, averaging 20 cm in length. The male urethra consists of three parts: prostatic, membranous, and spongy. The proximal prostatic portion descends through the prostate gland. The membranous portion of the urethra descends from the lower portion of the prostate to the bulb of the penis. This portion of the urethra is surrounded by a sphincter (i.e., muscle). The lowermost portion of the membranous urethra is most susceptible to rupture or penetration by a catheter. The spongy portion of the urethra lies in the corpus spongiosum and traverses the bulb, shaft, and glans of the penis, terminating at the external urethral orifice or meatus.

Male Genital Anatomy

The male genital organs comprise the penis, ejaculatory duct, prostate gland, bulbourethral gland, and paired testes, each with an epididymis, ductus or vas deferens, and seminal vesicle (Figure 10-5). Spermatozoa, formed in the testes and stored in the epididymides, are contained in the semen, which is secreted by the testes and epididymides, seminal vesicles, prostate, and bulbourethral glands. The sperm, on leaving the epididymides, pass through the ductus deferens and ejaculatory ducts to reach the urethra and pass through the external urethral orifice.

FIGURE 10-5 Anatomy of the male genitourinary system. (Adapted from Jarvis C: Physical examination & health assessment, ed 5, St. Louis, 2008, Saunders.)

The testes are paired ovoid glands located in the scrotum and responsible for production of spermatozoa and steroid hormones. They reside away from the core of the body to maintain a slightly lower temperature of approximately 1° to 2° F below that of the body proper. The left testicle often lies slightly lower than the right testicle in the scrotum. The epididymis is associated with the posterior portion of each testicle. The testes and epididymides are covered by a dual-layered tunica vaginalis testis, which is derived prenatally from the processus vaginalis of the peritoneum (Figure 10-6). The potential cavity between these two layers or some part of the processus vaginalis may become distended with fluid, forming a hydrocele.

FIGURE 10-6 Anatomy of the testis and epididymis. Turner’s syndrome results because of the absence of one X chromosome. (From Epstein O, Perkin GD, Cookson J, et al: *Clinical examination,* ed 4, Philadelphia, 2008, Mosby.)

The testes and epididymides receive their blood supply from the testicular artery, and venous drainage occurs via the pampiniform plexus, which forms the bulk of the spermatic cord. The veins of the pampiniform plexus can become varicose, leading to the formation of a varicocele. Lymphatic drainage from the testes empties into the lower aortic lymph nodes.

The scrotum is a cutaneous pouch that houses the testicles and epididymides. A median raphe indicates the subdivision of the scrotum by a septum into right and left compartments. Smooth muscle, known as the dartos muscle, is firmly attached to the overlying skin. The dartos muscle contracts in response to cold, exercise, and sexual stimulation. Loose connective tissue underlying the dartos allows free movement and is the site for the accumulation of edema.

The prostate gland is a fibromuscular pelvic organ surrounding the male urethra and containing glands that contribute to the semen. It is located behind the symphysis pubis and directly in front of the rectum, which is where it can be palpated by a digital rectal examination. Venous drainage and lymphatic drainage of the prostate are important because these contribute to the distinct areas for the spread of prostate cancer. Venous drainage occurs via the prostatic venous plexus that drains into the internal iliac vein and communicates with the vertebral plexus, thereby allowing metastatic spread of prostate cancer to the vertebrae. Lymphatic drainage terminates in the internal and external iliac lymph nodes.

Female Genital Anatomy

The female genital organs comprise the ovaries, fallopian tubes, uterus, vagina, and external genitalia, specifically the mons pubis, labia majora and minora, vestibule of the vagina, bulb of the vestibule, vestibular glands, and clitoris (Figure 10-7, A).

FIGURE 10-7 Anatomy of the female genitourinary system. (A, from Jarvis C: *Physical examination & health assessment,* ed 5, St. Louis, 2008, Saunders; B, from Seidel HM, Ball JW, Dains JE, et al: Mosby’s guide to physical examination, ed 6, St. Louis, 2006, Mosby.)

The ovaries are paired organs that produce oocytes (i.e., eggs) and secrete steroid hormones. The ovaries are situated on the lateral wall of the pelvis where they can be palpated bimanually. The paired fallopian tubes act to transmit the oocyte from the ovaries and spermatozoa from the uterus.

The fallopian tube is the usual site of fertilization because it conveys the early embryo to the uterus. As such, the fallopian tubes are the site of a tubal pregnancy and are susceptible to scarring associated with ascending infections (e.g., pelvic inflammatory disease [PID]), which can ultimately lead to an inability of the tube to transmit either oocytes or spermatozoa, resulting in infertility.

The uterus is a muscular organ that lies within the pelvis (Figure 10-7, B). The uterus functions to accept the fertilized egg and allow for implantation and development of the fetus. The upper uterine segment receives the fallopian tubes. The lower uterine segment terminates in the cervix, which opens to the vagina. The uterus has three distinct layers: a mucosa or endometrium, a muscular coat or myometrium, and a serosa or perimetrium.

The vagina lies posterior to the urinary bladder and anterior to the rectum. It serves as a receptacle for the penis, as the lower end of the birth canal, and as the excretory duct for the products of menstruation. The anterior and posterior walls of the vagina are approximately 7.5 and 9 cm long, respectively. The opening of the vagina into the vestibule may be partially closed by a membrane called the hymen. The opening is located posterior to the urethral orifice and anterior to the anus. The vagina and cervix can be inspected through a speculum placed in the vagina. A Papanicolaou (Pap) smear is taken from the cervix to aid in the detection of cervical cancer.

Blood supply to the ovaries (i.e., ovarian arteries arising from the lower abdominal aorta), fallopian tubes (i.e., ovarian and uterine arteries), and uterus (i.e., uterine artery) is provided by their respective arteries and forms a complex anastomosis. The vagina and cervix are supplied by branches from the internal iliac arteries. Venous drainage for the ovaries is distinct for each side. The right ovarian vein drains to the inferior vena cava, whereas the left ovarian vein empties into the left renal vein. The veins of the fallopian tubes drain into the ovarian and uterine veins. The uterine veins form a uterine venous plexus on each side of the cervix and drain to the internal iliac veins. The uterine venous plexus connects with the superior rectal vein, forming a portal–systemic anastomosis. The vaginal veins form the vaginal venous plexuses and lie along the sides of the vagina, draining into the internal iliac veins. Lymphatic drainage, again, is related to the metastatic spread of cancer. The ovaries drain to the lumbar lymph nodes. The fallopian tubes have their lymphatic drainage directed to the lower lumbar lymph nodes with the ovaries and uterus. The uterus drains to the lower aortic and external iliac lymph nodes. The superior and middle portions of the vagina drain into the external and iliac lymph nodes, and the lower portion of the vagina (vestibule) drains into the superficial inguinal lymph nodes. The cervix drains to the external and internal iliac nodes and sacral lymph nodes.

Physiology of Ovulation and Menstruation

Normal menstrual cycles depend on an intact hypothalamic–pituitary axis, functioning ovaries, and a normal outflow tract. The menstrual cycle, which averages 28 days, requires a well-coordinated series of events (Figure 10-8). The normal menstrual cycle is divided into two parts: a proliferative, or follicular, phase and a secretory, or luteal, phase. During the follicular phase, estrogen and luteinizing hormone (LH) levels increase as follicle-stimulating hormone (FSH) levels decrease. The endometrium thickens during this phase. Before ovulation, estrogen sharply declines, followed by a surge in LH and a steady rise in progesterone. It is shortly after this that ovulation occurs, followed by a slight increase in core body temperature. The remnant of the follicle (i.e., corpus luteum) supplies the progesterone for the second half of the cycle. During this time, the endometrium prepares itself for implantation. If fertilization and implantation do not occur, the corpus luteum involutes and progesterone levels decline, prompting menses.

FIGURE 10-8 Diagram of the female menstrual cycle. GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; FSH, follicle-stimulating hormone. (From Lowdermilk DL, Perry SE: Maternity & women’s health care, ed 9, St. Louis, 2007, Mosby.)

Physiological Changes of Pregnancy

Noteworthy physiological changes occur in pregnancy. Cardiac output (CO), defined as stroke volume (SV) × heart rate (HR), increases during pregnancy as a result of increases in both SV and HR. Plasma volume also increases with pregnancy.¹ The high flow of blood exiting the heart can often create a benign heart murmur. Blood pressure, defined as CO × systemic vascular resistance (SVR), actually decreases because of a decrease in SVR.

Respiratory changes also occur in pregnancy and result in increased tidal volume, which translates into increased minute ventilation at rest despite a normal respiratory rate. Of note, the forced expiratory volume in 1 second (FEV₁) does not change, which is important regarding asthmatic athletes because peak flow meter values would not need to be altered. Overall airway resistance is also decreased in pregnancy.

Physiological responses to exercise are somewhat different in pregnancy than in the nonpregnant female.² Respiratory rates increase with mild exercise in pregnancy compared with nonpregnant women, whereas maximal oxygen consumption (Vo₂ max) is less in pregnant women compared with nonpregnant women. The respiratory quotient (Vco₂/Vo₂) is also increased in exercising pregnant women, suggesting that there may be a greater dependence on carbohydrates as the preferred fuel source. This may also explain the fact that hypoglycemia can develop more rapidly during prolonged strenuous exercise in pregnant athletes. In addition, the core temperature of a pregnant woman is higher than that of a nonpregnant athlete, which requires caution in the exercising expectant mother, especially in hotter climates.

Anatomical considerations because of the enlarging uterus result in common changes in pregnancy. Urinary frequency increases during pregnancy as a result of pressure of the uterus on the urinary bladder. Low back pain is another common complaint and is again the result of the enlarging uterus. In this scenario, however, changes in biomechanics lead to increased lumbar lordosis that is more commonly the cause of the low back discomfort. Lower extremity edema may also develop and is more common later in pregnancy.

Pathological Conditions of the Genitourinary System

Kidney Stones

Kidney stones, also known as renal calculi, arise in the kidney when urine becomes supersaturated with a salt that is capable of forming solid crystals. More than 5% of adults have had kidney stones.³ Renal calculi are commonly composed of calcium (75%), struvite (15%), uric acid (6%), and cystine (2%) (Box 10-1). Recurrence rates after an initial kidney stone are 14% (1 yr), 35% (5 yr), and 52% (10 yr). Males are affected approximately three times more commonly than females, and Caucasian males are affected more commonly than African-American males, although African-American males have a higher incidence of associated infection with renal calculi whereas females of all races have been noted to have a higher incidence of infected hydronephrosis. The age of onset of symptomatic renal calculi is generally in the third or fourth decades.

BOX 10-1 TYPES OF KIDNEY STONES

Each of the following five commonly identified types of kidney stone has its own causes:

1. Calcium stones are composed of calcium oxide, calcium phosphate, calcium oxalate, and uric acid. Common causes of calcium stones include hyperparathyroidism, increased gut absorption of calcium, a renal phosphate leak, hyperuricosuria, hyperoxaluria, hypocitraturia, and hypomagnesemia.

2. Struvite stones are composed of magnesium ammonium phosphate. These stones are associated with chronic urinary tract infections secondary to gram-negative rods.

3. Uric acid stones are associated with high purine intake (diet rich in organ meats, legumes, fish, meat extracts, or gravies), gout, and malignancy.

4. Cystine stones are caused by an intrinsic metabolic defect resulting in failure of renal tubular reabsorption of cystine, ornithine, lysine, and arginine.

5. Indinavir stones typically appear in individuals with human immunodeficiency virus (HIV) infection who are treated with the protease inhibitor indinavir (Crixivan). These stones are composed entirely of the protease inhibitor.

Most stones pass spontaneously, but some individuals affected require hospitalization for unremitting pain, dehydration, associated urinary tract infection, or inability to pass the stone.

Signs and Symptoms

Most kidney stones originate within the kidney and proceed distally, creating various degrees of urinary obstruction as they become lodged in the narrow canal areas. Acute passage of a kidney stone from the kidney through the ureter gives rise to pain so excruciating that it has been likened to that of childbirth. The location and quality of pain are related to the position of the stone within the urinary tract. The severity of pain is related to the degree of obstruction, the presence of ureteral spasm, and the presence of any associated infection. Pain is typically described as unilateral flank pain that radiates to the groin. The individual is often writhing in pain, moving about and unable to lie still. Nausea and vomiting are common. Examination demonstrates flank tenderness, costovertebral angle tenderness, and occasionally testicular pain, notably in the absence of any testicular tenderness. The abdominal examination is often normal although bowel sounds may be hypoactive because of a mild ileus (see Chapter 9). The presence of a fever raises the possibility of an infectious complication and warrants immediate referral.

Once a kidney stone passes to the urinary bladder it is often asymptomatic and can be passed during urination. During passage of the stone the athlete will usually note burning and some blood-tinged urine depending on the size of the stone.

Referral and Diagnostic Tests

An athlete with symptoms suggestive of a kidney stone should be referred immediately to the team physician if this is the first episode. Any athlete with new or recurrent presentation and an associated fever needs to be referred immediately for physician evaluation and a urology consultation. Also, an athlete with recurrent symptoms who is unable to tolerate oral fluids and has unrelenting pain with a history of renal failure or a single kidney should be referred for immediate physician evaluation and possible observation or hospitalization.

The mainstay of diagnostic testing for kidney stones is a urinalysis. Blood is often present in the urine and may be detectable in more than 90% of symptomatic individuals, using both a urine dipstick and microscopy. Urine pH can also be helpful because a urine pH greater than 7 suggests the presence of urea-splitting organisms and struvite stones. Alternatively, a urine pH less than 5 suggests the presence of uric acid stones. The presence of pyuria (>5 white blood cells per high-power field) in a centrifuged urine specimen should prompt a careful search for an associated infection. (Normal urine values are listed in Table 3-2.) In these cases a complete blood count (CBC) and differential, serum creatinine, and urine culture are in order.

Imaging studies may also be performed and are often done to confirm the initial diagnosis. The current imaging study most often used is the noncontrast helical computerized tomography (CT) scan.⁴ This is a rapid test with sensitivity in the range of 95% to 100%. The principal disadvantage of CT is that indinavir stones are not well visualized by this method. Radiographs may also be obtained and may demonstrate a radiopaque stone. Radiographs are occasionally used to monitor the passage of a stone under certain circumstances. An intravenous pyelogram (IVP) may be used in the diagnosis of kidney stones but has essentially been replaced by CT. Last, ultrasound can also be used to identify stones. Although the sensitivity and specificity of ultrasound are poorer than with other imaging techniques, there is no exposure to radiation, and therefore this is an ideal imaging tool for pregnant women.

Differential Diagnosis

The differential diagnosis for kidney stones is long and often depends on what side of the body is involved, as well as on the sex and age of the individual. The list includes urinary tract infection, pyelonephritis, urinary obstruction, testicular torsion, pelvic inflammatory disease, bowel obstruction, appendicitis, cholecystitis, biliary colic, and constipation. Among those older than 60 years of age, an abdominal aortic aneurysm may also be included as a differential diagnosis.⁵

Treatment

The crux of treatment for the uncomplicated passage of a kidney stone is pain management and maintenance of adequate hydration. Pain management is often obtained with narcotic analgesics or nonsteroidal antiinflammatory agents, such as ketorolac (Toradol).⁶ An antiemetic medication also may be added when nausea is present and deters the use of oral analgesics or hydration. The forcing of oral or intravenous fluids has not been shown to alter outcome or to improve the passage of a stone; therefore the focus should remain on maintenance of hydration. A strainer is useful to filter the urine during the passage of the stone in order to collect the stone for analysis. Antibiotics are necessary in the presence of an associated infection.

The incidence of sports hematuria is estimated to be as high as 80% in swimming, lacrosse, and track and field; 55% in football and rowing; and 20% in marathon runners (Figure 10-9). These incidence levels have led to the development of several possible causes of sports hematuria (e.g., increased permeability of the glomerulus, direct or indirect trauma to the kidneys, renal ischemia, dehydration, release of a hemolyzing factor), all of which appear to be related to exercise duration and exercise intensity.⁸

FIGURE 10-9 Athletes who train strenuously can present with from benign sports hematuria.

Signs and Symptoms

By definition sports hematuria is asymptomatic. The finding of hematuria may occur during a routine urinalysis, such as those that may be performed during a physical examination or preparticipation examination. On occasion individuals will present with gross hematuria (i.e., visible presence of blood in the urine) after a prolonged and strenuous workout. In these situations, the general rule is that the hematuria will resolve within 72 hours without any further intervention than rest.

Referral and Diagnostic Tests

The finding of asymptomatic hematuria in an athlete during some form of routine testing needs to be reviewed by the team physician. As a general rule, these athletes are retested at 24 to 72 hours to document resolution. Any athlete with symptomatic hematuria or systemic symptoms is referred to a physician for immediate evaluation.

Although sports hematuria is a benign condition, not all hematuria is benign and therefore the evaluation must include some basic tests. A urinalysis or dipstick test will demonstrate the presence of blood in the urine. Because drugs, dyes, and myoglobin can mimic hematuria by causing a false-positive result on the urine dipstick, microscopic examination of a spun urine specimen will confirm the presence of red blood cells. If symptoms of dysuria (i.e., painful urination) are present, a urine culture may be performed. If hypertension, renal disease, repeated urinary tract infections, or pyelonephritis is found in the athlete’s history, an initial serum creatinine may be performed. As a general rule, if hematuria persists beyond 72 hours, further evaluation is warranted. Additional tests include a renal ultrasound, CT, and possible cystoscopy.

Differential Diagnosis

The differential diagnosis includes causes of true hematuria (i.e., red blood cells in urine) and causes of a false-positive urine blood dipstick. True hematuria may result from a urinary tract infection, urethritis, interstitial nephritis, renal papillary necrosis, nephrolithiasis (i.e., renal stone), polycystic kidney disease, kidney laceration, a neoplasm arising from any structure in the urinary tract, coagulopathy, and prostatitis in males.⁹ Causes of a false-positive urine dipstick examination for blood include drugs (i.e., phenazopyridine, rifampin, nitrofurantoin, phenytoin), food dyes, menses, and myoglobin in the urine.

Treatment, Prognosis, and Return to Participation

The treatment of sports hematuria is simply rest for 24 to 72 hours. Resolution is the rule and should be documented with a repeat urinalysis after rest. The prognosis is excellent because sports hematuria is a benign and self-limiting condition.¹⁰

Urinary Tract Infection

Urinary tract infection (UTI) occurs in either the upper or lower urinary tract. These infections most commonly involve the urinary bladder, but they can also involve the urethra, ureters, and kidneys (i.e., pyelonephritis). UTIs are a leading cause of morbidity and health care expenditures in persons of all ages.

Anyone can develop a UTI; however, sexually active young women are at highest risk. Several factors have been attributed to this higher risk: a short urethra; sexual activity; delays in micturition, particularly after intercourse; and the use of diaphragms and spermicides.¹¹ Fortunately, the risk of a complicated UTI in this population is very low, yet up to 20% of young women with a UTI will develop recurrent UTIs.¹²

UTIs in men are less common than in women but can occur. Overall, most UTIs in men are accounted for by older men: this is attributed to risk factors such as prostatic disease, which can cause some degree of urinary obstruction, and urinary tract instrumentation. Among younger men, UTIs may occur in men who participate in anal sex, who are not circumcised, or whose sexual partner is colonized with a uropathogen.¹³ Catheter-associated UTIs are also known to occur.

Signs and Symptoms

In most individuals a UTI is signaled by a constellation of symptoms, including dysuria, increased frequency of urination, and voiding small amounts of urine relative to their normal pattern. On occasion, lower pelvic discomfort or cramping may also be present. The presence of gross hematuria, abnormal vaginal bleeding, or fever warrants prompt physician attention.

Referral and Diagnostic Tests

Because of the relative discomfort associated with a UTI and the possibility of developing an ascending infection, symptomatic athletes need to be referred to a physician for evaluation and treatment. The presence of gross hematuria, fever, abdominal pain, nausea, or vomiting warrants immediate referral.

The diagnosis of an uncomplicated UTI is often made on the basis of the history, physical examination, and examination of a urine specimen. The urine specimen is examined specifically for the presence of leukocyte esterase, nitrite (i.e., a surrogate marker for bacteria), and the finding of leukocytes on microscopic examination. A urine Gram stain can also aid in the identification of bacteria. The finding of a single bacterial organism, under high-power oil immersion, on an unspun urine specimen correlates with a count of more than 100,000 colony-forming units on urine culture. Because of the limited added value in determining treatment for most uncomplicated UTIs, a urine culture may not be performed in the initial evaluation. The evaluation of a recurrent, complicated, or catheter-associated UTI often necessitates obtaining a urine culture.

Urine culture results must be viewed in light of certain threshold values that have been shown to correlate with significant bacteriuria. In young women, a urine culture producing more than 100,000 colony-forming units of bacteria per milliliter of urine is considered a positive culture because of its high specificity for the diagnosis of a true infection. In men, a urine culture yielding more than 1000 colony-forming units of bacteria is considered a positive culture, and in catheterized individuals this value falls to more than 100 colony-forming units of bacteria.

The use of additional urological testing for anatomical abnormalities is generally unrewarding. However, a urological evaluation should still be performed in an adolescent male with his first UTI and in men with pyelonephritis or recurrent UTI.¹⁴

Differential Diagnosis

Differential diagnoses for UTIs include urethritis, noninfectious cystitis, pyelonephritis, vulvovaginitis, sexually transmitted infections (STIs), dehydration, mittelschmerz, endometriosis, and balanitis.

Treatment

UTIs are treated with antibiotics. An uncomplicated UTI can be treated with antibiotics such as trimethoprim-sulfamethoxazole, ciprofloxacin, or ofloxacin for a 3-day course (see Chapter 5). Recurrent UTIs in women or UTIs in men should be treated with a 7- to 10-day course of antibiotics with antibiotic choice based on the results of the urine culture. If a woman experiences more than three UTIs in a given year, prophylactic antibiotics may be used to prevent recurrence. Studies have challenged the use after coitus of prophylactic antibiotics, given continually at a lower dose than treatment dose, for recurrent UTIs.¹⁵ Complicated UTIs require a longer course of treatment and should be treated for 10 to 14 days.

Prognosis and Return to Participation

The prognosis for an uncomplicated UTI is excellent and generally will not preclude participation in athletics. For the few individuals developing a complicated UTI, return-to-play decisions need to be based on the athlete’s unique complication. Athletes with fever or poor fluid intake as a result of nausea or vomiting should be observed and return to play after symptoms resolve with treatment.

Prevention

Common sense will help prevent recurrent UTIs. Modification of risk factors associated with UTI includes urination after intercourse, avoidance of delays in urination, and limited use of either diaphragms or spermicides. Wearing breathable (cotton) underwear also reduces the chances of contracting a UTI.

Urethritis

Urethritis is an inflammation of the urethra caused by an infection and is typically reserved to describe a syndrome of sexually transmitted infections (STIs), namely gonococcal urethritis (GU) and nongonococcal urethritis (NGU). Urethritis, in a more general definition, may also be a posttraumatic irritation and inflammation of the urethra.

Infectious causes of urethritis are typically sexually transmitted and include Neisseria gonorrhoeae (GU) and nongonococcal organisms such as Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, and Trichomonas vaginalis (NGU).¹⁶ Less common infectious causes of urethritis include lymphogranuloma venereum, herpes genitalis, and syphilis and may be associated with infectious conditions such as epididymitis, orchitis, prostatitis, or UTIs. The incidence of GU is in decline. Conversely, the incidence of NGU is rising and is notably higher during the summer months. Urethritis affects males and females equally, although up to 50% of females may be asymptomatic and homosexual males are more commonly infected than heterosexuals or homosexual females. Infectious urethritis may occur in any sexually active person, but the incidence is highest among people 20 to 24 years of age.

Signs and Symptoms

Despite the infectious causes of urethritis, up to 25% of those with NGU will be asymptomatic. Symptom onset typically occurs between 4 and 14 days after contact with an infected partner. Urethral discharge may be present and may be yellow, green, brown, or blood tinged. Dysuria is usually localized to the urethral orifice and worst with a first-morning void. Urethral itching may be present. Males may report heaviness or aching in the testicles although associated tenderness should suggest orchitis or epididymitis. Females may report a worsening of symptoms with their menses. The presence of fever, chills, sweats, or nausea suggests a more systemic infection and warrants immediate referral to a physician.

Referral and Diagnostic Tests

Athletes suspected of having urethritis are referred to a physician for diagnosis and treatment. In the interim, the athlete should be counseled to refrain from sexual intercourse until seeing the physician so as to avoid infecting any other people.

The diagnosis of urethritis is most often based on history and examination. A urinalysis is not particularly helpful in establishing the diagnosis but may be helpful in the exclusion of cystitis or pyelonephritis. More than 30% of individuals with NGU do not have leukocytes in their urine. A urethral culture may be performed to examine for the presence of gonococcus or chlamydia. In cases of confirmed GU or NGU, testing for syphilis, hepatitis B, and human immunodeficiency virus (HIV) is encouraged. Women of child-bearing age who have experienced unprotected intercourse need a pregnancy test before treatment.

Differential Diagnosis

The differential diagnosis for urethritis is best considered by gender. Differential diagnoses to be considered in both men and women include STIs such as chancroid, chlamydia, gonorrhea, herpes, mycoplasma, syphilis, or trichomoniasis, dermatological diseases involving the urethral orifice (e.g., contact dermatitis secondary to spermicides), molluscum contagiosum, urethral stricture, urethral trauma, urethral warts, urethral diverticulum, and urethral cancer. Differential diagnoses affecting females include oophoritis, pelvic inflammatory disease, salpingitis, vaginitis, and vulvovaginitis. Differential diagnoses exclusive to males are epididymitis and prostatitis.

Treatment

Antibiotics are the mainstay of treatment for urethritis. Symptoms will resolve in all individuals with urethritis over time regardless of treatment. The use of antibiotics in the treatment of infectious urethritis is to prevent morbidity and to reduce transmission to others. The antibiotic choice or choices are based on the likelihood of whether it is GU or NGU. Current recommendations are to treat individuals for both GU and NGU. Azithromycin in a single 2 g dose treats both GU and NGU, is the treatment of choice for urethritis, and is well tolerated. Ceftriaxone (intramuscularly), cefixime (oral), ciprofloxacin (oral), or ofloxacin (oral) can be used in single doses to treat GU only. Doxycycline can be taken for 7 days to treat NGU only. In the case of recurrent NGU, a prolonged course of erythromycin for 14 to 28 days is recommended. Antibiotic treatment is recommended for sexual partners of those with culture-positive urethritis, including Trichomonas.

Prognosis and Return to Participation

The overall prognosis for urethritis is excellent. The use of antibiotics helps to decrease any associated morbidity and prevent further transmission. Any individual with urethritis is counseled to abstain from sexual intercourse until all partners have been treated and is further encouraged to use barrier devices (condoms) when engaging in sexual intercourse with multiple partners. Uncomplicated urethritis should not interfere with an athlete’s ability to train or compete.

Prevention

Prevention of urethritis equates to education. Sexually active athletes are encouraged to use barrier methods during intercourse. Education regarding STI risk factors can be beneficial. Risk factors include intercourse at a young age, unprotected intercourse, multiple sexual partners, intercourse with partners known to have infections, and drug abuse. The early diagnosis and treatment of individuals with urethritis help to limit the transmission, as does the identification and treatment of all partners.

Testicular Torsion

The testicle is covered by the tunica vaginalis, which attaches to the posterolateral surface of the testicle and allows for limited mobility. In the event that the testicle is able to twist or freely rotate (i.e., torsion), venous occlusion can occur, which subsequently leads to arterial ischemia causing infarction of the testicle (Figure 10-10).

The incidence of testicular torsion in males younger than 25 years is approximately 1 per 4000. The highest incidence is among males 12 to 18 years of age, with a peak incidence at age 14 years.¹⁷ Torsion predominantly affects the left testicle. A subgroup of individuals has a higher frequency of testicular torsion because of an extremely narrow attachment of the epididymis to the tunica vaginalis (i.e., bell clapper deformity).¹⁷ This attachment allows the testicle to rotate freely on the spermatic cord within the scrotal sac.¹⁸ This congenital abnormality is found in as many as 12% of males. Testicular torsion can also occur after exercise, sexual activity, or trauma, or it may develop at rest.

Signs and Symptoms

The history of testicular torsion includes the sudden onset of severe unilateral scrotal pain. The most common symptoms include scrotal swelling, abdominal pain, nausea, and vomiting.¹⁹ Less frequently a fever or urinary frequency may be documented. Examination of the scrotum reveals a tender and painful testicle that is often elevated in relationship to the contralateral testicle. The involved testicle often is in a horizontal position rather than its usual vertical orientation. The testicle may be enlarged with scrotal swelling and erythema.¹⁷ In general, elevation of the involved testicle provides no relief of pain as compared with epididymitis, in which pain relief is notable with elevation of the involved testicle.

Referral and Diagnostic Tests

Testicular torsion is a urological emergency.

The consideration of a diagnosis requires immediate and emergent evaluation by the team physician or immediate referral to an emergency department. Diagnosis and treatment within 6 hours of the onset of pain result in an 80% to 100% salvage rate for the affected testicle. Beyond this time frame, the salvage rate steadily decreases and approaches 0% at 12 hours.²⁰

RED FLAGS FOR TESTICULAR TORSION

Testicular torsion is a urological emergency requiring emergent medical attention. It presents as follows:

• Scrotal swelling

• Abdominal pain

• Nausea and vomiting

• Tender testicle

• Elevated testicle compared with uninvolved one

• Possible horizontal rather than vertical orientation

Initial laboratory tests often include a urinalysis and complete blood count. The urinalysis is most often normal but may demonstrate leukocytes in up to 30% of cases.

Imaging studies can provide useful information, but because testicular torsion is a clinical diagnosis, treatment should not be delayed for imaging if the diagnosis is clear. For those cases in which the diagnosis is less clear, color Doppler ultrasonography can be performed.21,22 A color Doppler is used to assess arterial blood flow to the testicle. A radionuclide scan can also be performed to assess arterial blood flow, with decreased uptake indicating a lack of blood flow to the testicle.

Differential Diagnosis

Because testicular torsion is a urological emergency there is little room for error in diagnosis. The differential diagnosis, however, should include epididymitis, orchitis, hydrocele, varicocele, a hernia, and acute appendicitis.

Treatment

Early diagnosis and referral are the keys to successful treatment. Once testicular torsion is diagnosed, a manual reduction can be attempted by the physician. Because most testicular torsion involves a “turning in” toward the midline, the process of detorsion involves rotating the affected testicle 180 degrees from medial to lateral. This rotation may need to be repeated two or three times for a complete detorsion. Success is determined by a marked decrease in pain. Detorsion can be accomplished manually in 30% to 70% of affected individuals.¹⁷ If manual detorsion is not successful, surgery is indicated for definitive treatment and involves detorsion and orchiopexy.

Prognosis and Return to Participation

The prognosis for testicular torsion depends on rapid referral and diagnosis. If detorsion is obtained within 6 hours of onset of symptoms, nearly 100% of torsive testicles can be salvaged. A delay in treatment up to 12 hours results in decreasing rates of salvage.¹⁹ Return to participation is based on the result of the torsion and physician clearance.

Prevention

Other than early identification of the bell clapper deformity, no preventive measures can prevent a testicular torsion. Wearing an athletic supporter may lower the risk of torsion.

Hydrocele

Hydroceles are fluid collections within the tunica vaginalis of the scrotum or along the spermatic cord. Most hydroceles are developmental in origin because of persistence of a patent processus vaginalis. However, for unknown reasons hydroceles can also develop as a result of an imbalance between scrotal fluid production and absorption. It is estimated that approximately 6% of adult males have a clinically apparent hydrocele.

Signs and Symptoms

Hydroceles are usually asymptomatic. Increased fluid collections, however, can cause a scrotal aching. A hydrocele typically manifests itself as a nontender fullness in the hemiscrotum and is palpable just anterior to the testicle. Inability to clearly delineate or palpate the testicular structures or the presence of tenderness raises the possibility of an alternative diagnosis (Figure 10-11).

FIGURE 10-11 Hydrocele is a painless swelling in the scrotum. (From Jarvis C: Physical examination & health assessment, ed 5, St. Louis, 2008, Saunders.)

Referral and Diagnostic Tests

Athletic trainers should immediately refer any male with painful scrotal swelling to a physician. Although a hydrocele is not an emergency, nontender scrotal swelling that is consistent with a hydrocele needs to be examined by a physician to document its presence. An experienced physician can confirm the diagnosis of a hydrocele. An ultrasound may be performed to confirm the diagnosis in some cases. Box 10-2 lists the differential diagnoses for hydroceles.

BOX 10-2 DIFFERENTIAL DIAGNOSES: HYDROCELES AND VARICOCELES

Both hydroceles and varicoceles are differential diagnoses for each other. In addition, the differential diagnoses include the following:

For hydrocele, another differential diagnosis is an inguinal hernia.

For varicocele, another differential diagnosis is spermatic vein compression.

Treatment, Prognosis, and Return to Participation

Asymptomatic adults with an isolated hydrocele can be observed indefinitely or until they become symptomatic. Surgical intervention is warranted for the following indications: inability to distinguish hydrocele from an inguinal hernia, failure to resolve spontaneously after an appropriate interval of observation, inability to clearly examine the testes, or association of hydroceles with suggestive pathology, such as testicular torsion or tumor. Return to sport may take 2 to 6 weeks after a simple hydrocele repair.

The presence of a hydrocele does not preclude participation in athletics. If the hydrocele is symptomatic or has been surgically repaired, the treating physician will need to make a decision regarding return to play.

Varicocele

A varicocele is a dilation of the pampiniform venous plexus and the internal spermatic vein within the scrotum (Figure 10-12). The etiology of a varicocele is unclear. Varicoceles occur in approximately 20% of the adult male population; however, about 40% of infertile men may have a varicocele.²³

Signs and Symptoms

Approximately 80% to 90% of varicoceles occur on the left side of the scrotum because of anatomical vascular differences.²³ Men are generally asymptomatic but will occasionally report an aching pain or heaviness in the scrotum. Physical examination demonstrates a soft thickening just above the testicle and has been described as feeling like a “bag of worms.” Varicoceles are staged according to size (Box 10-3).

BOX 10-3 STAGING OF VARICOCELES

Varicoceles are staged according to size:

• Large: Those easily identified by inspection alone

• Moderate: Those identified by palpation without Valsalva’s maneuver

• Small: Those identified by palpation, using Valsalva’s maneuver to increase intraabdominal pressure, which will impede venous drainage and increase varicocele size

Referral and Diagnostic Tests

The development of a new varicocele or sudden onset of testicular swelling or pain requires immediate physician evaluation. Any male athlete with a known varicocele who develops increasing testicular pain also warrants physician evaluation. Referral to a urologist for a surgical opinion is indicated when there is significant testicular pain, impairment of testicular function as evidenced by decreased semen quality, or testicular atrophy (volume <20 ml or length <4 cm).

The diagnosis of a varicocele is typically clear by physical examination; Valsalva’s maneuver may aid diagnosis (Figure 10-13). If the physical examination is equivocal a Doppler ultrasonogram may be performed to demonstrate the varicocele. Individuals who have a new or sudden-onset varicocele or a nonreducible varicocele in the recumbent position may warrant abdominal CT to evaluate for renal or vascular pathology as a cause of spermatic vein compression. Box 10-2 lists the differential diagnoses for varicoceles.

FIGURE 10-13 In Valsalva’s maneuver the athlete is asked to exhale against a closed epiglottis (bearing down).

Treatment, Prognosis, and Return to Participation

There is no medical treatment per se for an asymptomatic varicocele. Surgical treatment involves the ligation of the involved veins in order to prevent continued abnormal blood flow.

The presence of a varicocele poses no known risks to the athlete involved in individual or team sports. After surgical correction of a varicocele, return to play is generally within 2 to 6 weeks but will depend on the specific circumstances for the athlete and the recommendations of the surgeon. Use of a protective cup is recommended for involvement in contact or collision sports if early return is allowed.²³

Testicular Cancer

Testicular cancer is an abnormal growth of cells in the testicles. It accounts for 1% to 2% of all cancers in men and typically affects a single testicle. Because of the high cure rate if diagnosed early, nearly 100% of men with this cancer are cured.

Testicular cancer typically affects men between the ages of 18 to 44 years. The American Cancer Society’s statistics on cancer state that in 2009, about 8400 men were diagnosed with testicular cancer, but only 380 will die of the disease.²⁴ Hispanic men were the group who experienced the largest increase in incidence ²⁵ whereas northern European populations were still the most affected. Asian and African populations have a low incidence of testicular cancer.²⁶ There is increasing evidence that there may be a slight genetic component to this cancer.²⁷ Conditions that are associated with an increased risk of testicular cancer include cryptorchidism (i.e., failure of one or both testicles to descend into the scrotum during development), maternal exposure to diethylstilbestrol (DES) while pregnant, testicular atrophy, and some possible environmental and drug exposures.²⁸