The Prostate and Transrectal Ultrasound

Zonal Anatomy

Original textbook anatomic descriptions of the prostate referred to lobar anatomy, describing anterior, posterior, lateral, and median lobes; this designation has not been useful in identification and evaluation of carcinoma of the prostate. Detailed anatomic dissections of the prostate reveal zonal anatomy in which the prostate is divided into the four glandular zones surrounding the prostatic urethra ( Fig. 10.1 ):

• Peripheral zone

• Transition zone

• Central zone

• Anterior fibromuscular zone

These zones have differing embryologic origins and disease susceptibilities. In the normal young gland, sonography can rarely identify these zones separately unless a pathologic condition is present ( Figs. 10.2 and 10.3 ). At sonography it is helpful to consider the prostate as having a peripheral or outer gland (peripheral zone plus central zone) and inner gland (transition zone plus anterior fibromuscular stroma plus internal urethral sphincter).

The prostate does not have a true anatomic capsule, but it is surrounded by an outer fibromuscular band that is visible as a clear line demarking the prostate from the surrounding fat but that becomes blurred at the posterolateral margins at sites of entry of the neurovascular bundles.

The peripheral zone, the largest of the glandular zones, arises from the urogenital sinus and in a young man before the onset of benign prostatic hyperplasia (BPH) contains approximately 70% of the prostatic glandular tissue and is the site for about 70% of prostate cancers. It is separated from the transition zone and central zone by the surgical capsule, a hypoechoic line that is rendered hyperechoic by the frequent accumulation of corpora amylacea or calcifications along it. Traditionally, urologists at the time of suprapubic or transurethral prostate resection believed that they dissected to this line, which demarked hypertrophied periurethral glands from posterior lobe—hence “surgical” capsule. The peripheral zone occupies the posterior, lateral, and apical regions of the prostate, extending anteriorly around the margins, like an egg cup holding the “egg” of the central gland ( Fig. 10.4A ).

The young transition zone contains about 5% of the prostatic glandular tissue. It is visible as two small glandular areas positioned like saddlebags adjacent to the proximal urethral sphincter, which is a muscular tube up to 2 cm in diameter. It is the site of origin of most BPH and about 20% of prostate cancers.

The central zone along with the seminal vesicles (SVs) arises from the wolffian ducts. It constitutes approximately 25% of the glandular tissue and is wedged at the prostate base between the peripheral and transition zones. The ducts of the vas deferens (VD) and SVs enter the base of the prostate at the central zone, where they are renamed the ejaculatory ducts and pass through it en route to the verumontanum. The central zone is relatively resistant to disease processes and is the site of only about 5% of prostate cancer.

At the base of the prostate at the bladder neck is the thick, muscular, continence-providing, internal urethral sphincter. Its substantial homogeneous muscle content can make it appear hypoechoic. It contains periurethral glands that often contain calcifications.

Vascular and Neural Structures

The prostate is supplied by the prostaticovesical arteries, which arise from the internal iliac arteries on each side and give rise to the prostatic artery and inferior vesical artery. The prostatic artery gives rise to the urethral and capsular arteries. The inferior vesical artery supplies the bladder base, SVs, and ureter. The urethral artery supplies about one-third of the prostate, and the capsular branches supply the remainder.

On Doppler ultrasound the prostate is mildly to moderately vascular. The neurovascular bundles are visible at the posterolateral angles ( Fig. 10.5 ). The capsular and urethral arteries are easily seen, and branches to the inner gland and peripheral zone are visible in a somewhat radial pattern with the periurethral vessels as the axle. A dense cluster of vessels is often seen capping the base of the prostate, and care must be taken not to mistake these for tumor vascularity.

Nerve supply to the prostate has been clarified. Parasympathetic supply is through the S2-S4 sacral roots, and sympathetic supply is through the hypogastric nerve. These combine in the pelvic plexus just above and lateral to the prostate and give rise to about 6 to 16 small branches that supply the SVs, prostate, levator ani, and corpora cavernosa. The cavernosal branches are responsible for erections. The nerves and blood vessels travel together as the neurovascular bundle in the Denonvilliers (rectoprostatic) fascia at the posterolateral aspect of the prostate, where the vessels are visible with color flow Doppler ultrasound. These nerves are vulnerable to injury during surgery, radiotherapy, and other interventions and are avoided at nerve-sparing prostatectomy to preserve potency.

Normal Variants

Benign ductal ectasia is seen in older men who develop atrophy and dilation of peripheral prostatic ducts and has no clinical significance. The ducts appear as single or grouped, 1- to 2-mm-diameter tubular structures in the peripheral zone radiating from the capsule toward the urethra. Clusters of these can form hypoechoic areas that could be mistaken as prostate cancer ( Fig. 10.7 ).

Prostatic calcifications and corpora amylacea are normal findings visible as bright echogenic foci or clumps consisting of proteinaceous debris in dilated prostatic ducts, most often in periurethral glands and along the surgical capsule. When densely clustered they can attenuate sound and block anterior visibility, and on Doppler they create a prominent “twinkle” artifact (see Fig. 10.7D ). Subclinical infections, inflammation, and atrophy may contribute to their formation. Corpora amylacea have no clinical significance and are not usually palpable even if dense or clumped. Peripheral zone calcifications should not be accepted as a cause for palpable firmness or nodules. Patients with palpable abnormality need further evaluation, frequently with biopsy.

Benign Prostatic Hyperplasia

Prostate enlargement with benign prostatic hypertrophy (BPH) is a common cause of lower urinary tract symptoms (LUTS) in older men and affects about 50% of men older than 60 years and over 90% older than 70. The cause of BPH is unclear but is probably related to hormonal changes with aging and results in hypertrophy and hyperplasia of the fibrous, muscular, and glandular elements, primarily affecting the transition and periurethral zones.

Lower urinary tract symptoms, also called prostatism and bladder outlet obstruction, can relate to increases in prostate size and muscular tone, both causing urethral constriction. Symptoms include frequency, nocturia, weak stream, hesitancy, intermittence, incomplete emptying, and urgency and are quantified using the American Urological Association (AUA) symptom index. Many men have a misguided concern about prostate size. The issue is urinary obstruction, not prostate size. Prostate size correlates poorly with urinary obstruction. Urinary dysfunction is multifactorial and can also arise from abnormalities of the central nervous system, spine, bladder, prostate, and urethra. Patients with urinary dysfunction need evaluation of all these systems, not just the prostate. Ultrasound investigation of the patient with symptoms of prostatism is best done transvesically to assess prostate size, identify median lobe enlargement, and evaluate bladder volume and postvoid residual, bladder wall character, trabeculation, diverticula, tumors, and calculi, and the kidneys and ureters should be evaluated for hydronephrosis and masses. TRUS plays only a small role but helps if there is a clinical concern for prostate cancer (BPH is one cause for PSA elevation) or there is need for precise gland volume determination to plan surgical or medical treatment.

The appearance of BPH is heterogeneous and depends on underlying histopathologic changes. This heterogeneity hinders cancer detection for both TRUS and mpMRI. Typically there is enlargement of the inner gland (transition zone) with hypoechoic, isoechoic, or hyperechoic nodules. The specific echo pattern depends on the admixture of glandular, stromal, and muscular elements and nodules, which may be fibroblastic, fibromuscular, muscular, adenomatous, or fibroadenomatous. Hyperplasia of the periurethral glandular elements results in “median lobe” enlargement manifesting as a bulge into the urinary bladder (see Fig. 10.4E ). Calcifications and degenerative or retention cysts are common. Benign BPH nodules tend to have distinct margins, whereas transition zone cancer usually manifests as a diffuse, poorly marginated, usually hypoechoic nodule that may cause an asymmetrical bulge of the adjacent anterior contour similar to findings on mpMRI.

Because of the distortion of the gland in patients with BPH, some hyperplastic nodules may bulge into the peripheral zone when they actually originate in the transition zone. Hypoechoic, well-circumscribed transition zone nodules are virtually always benign. Although BPH nodules are generally confined to the transition zone, on occasion they can form entirely within the peripheral zone, appearing as an isoechoic nodule with a well-circumscribed halo and often containing a small degenerative cyst and frequently create a prominent bulge at the capsule. They are similar in appearance to BPH nodules seen in the transition zone on TRUS and mpMRI (see Fig. 10.4G ). Because these benign, peripheral zone nodules are palpable as a firm or hard, cancer-like nodule, they should undergo biopsy to confirm their benign nature and obviate continuing concern.

After exclusion of other systemic causes of the symptoms, such as neurologic disease, diabetes, and local urinary conditions, treatment focuses on the prostate. Transurethral resection of the prostate (TURP) is considered the standard of care for many patients, but other treatments can include watchful waiting, medical therapy, minimally invasive therapies, open surgery, and laser therapy.

TURP initially leaves a large basal surgical defect that rapidly contracts as the gland collapses into the defect, often surprising unwary urologists who may think they have removed considerably more tissue than the visible defect suggests (see Fig. 10.4F ).

Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Understanding of the condition called “prostatitis” has changed over the years. It is not merely “infection in the prostate.” Rather, prostatitis refers to a chronic pain syndrome in which, surprisingly, infection, inflammation, and even involvement of the prostate are not always present. It is commonly termed chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Prostatitis and pelvic pain complaints encompass many clinical syndromes and can severely affect the quality of life of many men who have chronic pain, sexual dysfunction, and LUTS. Patients and physicians are often frustrated because diagnosis and treatments can be time-consuming and ineffective. The impact of prostatitis on quality of life has been likened to the morbidity of myocardial infarction, angina, or Crohn disease. Interestingly, men with CP/CPPS also have an increased incidence of cardiovascular disease, neurologic disease, sinusitis, anxiety or depression, and sexual dysfunction. Prostatitis can elevate PSA and on mpMRI can mimic cancer, leading to potential unneeded cancer investigations. An estimated 9% to 13% of all men in the 40- to 50-year-old age group are affected. About 25% of visits to urologists are related to prostatitis symptoms. In men younger than 50 years, CP/CPPS is the leading cause of visits to a urologist, and in men older than 50, it is the third most common cause, after BPH and cancer. The lack of public awareness of this condition likely relates to men's general reluctance to discuss “personal” concerns.

A consensus group at the National Institutes of Health produced a Chronic Prostatitis Symptom Index (NIH-CPSI) and diagnostic flowcharts to help in diagnosis and characterization of symptom severity.

• I

  Acute bacterial prostatitis

• II

  Chronic bacterial prostatitis

• III

  CP/CPPS

  • A

    Inflammatory

  • B

    Noninflammatory

• IV

  Asymptomatic inflammatory prostatitis

Acute bacterial prostatitis is the least common form of prostatitis, seen in about 2 of 10,000 office visits, and 5% to 10% of cases become chronic. Patients have symptoms of acute urinary or systemic infection usually caused by infection with gram-negative organisms such as Escherichia coli. TRUS is generally of little use in acute prostatitis and can be very painful. About half of these men have findings including edema, prostate enlargement, increased blood flow, venous engorgement, hypoechoic peripheral halo, and altered patchy echo changes that can be decreased, increased, or both. TRUS and mpMRI findings can mimic neoplasia ( Fig. 10.8 ). The diagnosis is mainly clinical. Symptoms should subside promptly with antibiotic therapy, but treatment is continued for 4 to 6 weeks. If symptoms do not subside quickly, abscess formation should be considered. Abscesses occur in 0.5% to 2.5% of patients with acute bacterial prostatitis and are more common in those with underlying diabetes mellitus or immunosuppression (including human immunodeficiency virus [HIV] infection) and after catheterization or instrumentation (see Fig. 10.8E ). In such patients, TRUS should be promptly performed for diagnosis. Small abscesses may not need drainage, but larger abscesses over about 1.5 cm in diameter can be easily drained transrectally or transperineally using TRUS guidance, or they can be unroofed at cystoscopy. Experience has shown that simple transrectal aspiration can be effective without need for a drainage catheter. Abscesses have resolved even after a single drainage, but repeat aspiration is easily performed if needed.

Chronic bacterial prostatitis is also uncommon. Patients are typically afebrile but have recurrent episodes of bacterial urinary infection–like symptoms. Most have no ultrasound findings, but during acute episodes this condition may appear similar to acute prostatitis on TRUS and mpMRI. In general, urine cultures are negative but some have gram-negative organisms, most often E. coli. Empirically, about half of patients with chronic bacterial prostatitis respond to 6- to 12-week courses of antimicrobial therapy.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is the most common form of prostatic inflammation. These men have lower genitourinary pain with variable voiding and sexual dysfunction but no evidence of bacterial infection or other cause of pain. CP/CPPS accounts for about 90% of cases and affects about 2 per 100 men. It is the most difficult to understand and treat. CP/CPPS is classified into two types: inflammatory type (diagnosed by seeing leukocytes in prostate secretions, urine, or semen) and noninflammatory type (no evidence of inflammation; also called prostatodynia ). The cause is unknown, and the CP/CPPS name takes into account that the prostate may not be the sole source of discomfort. The symptoms, however, are identical to those of true prostate infection. Neurologic factors, psychological factors, stress, and genetic predisposition have been implicated, as well as association with other conditions such as fibromyalgia, irritable bowel syndrome, and chronic fatigue syndrome. No cause is identified in the majority of men with CP/CPPS. Patients may respond to antibiotics, alpha blockers, nonsteroidal antiinflammatory drugs (NSAIDs), and analgesics, which are often used in multimodal fashion. In most cases the prostate appears normal on ultrasound. Some sonograms show nonspecific findings such as peripheral hypoechoic areas, calcifications, venous congestion, increased arterial flow, bladder neck thickening, hypoechoic prostatic rim, and periurethral hypogenicity, and on TRUS and mpMRI the findings can mimic neoplasia.

Asymptomatic inflammatory prostatitis is diagnosed in men who have no history of genitourinary pain complaints but who are shown to have inflammatory changes at histology. Often biopsy is done because of PSA elevations that are common with prostate inflammation, even with asymptomatic inflammation.

Diagnostic protocols have attempted to differentiate among the various types of prostatitis using history, physical examination, and urine or other cultures. An issue for TRUS and biopsy is that many of these men have chronically elevated but often fluctuating PSA levels, even in excess of 10 ng/mL, and the often-multiple inflammatory areas can mimic cancer on ultrasound and mpMRI, leading to biopsy to exclude cancer (see Fig. 10.8 ).

Other infectious or inflammatory conditions affecting the prostate do not fit easily into these groups. These include conditions such as malacoplakia, eosinophilic prostatitis, cytomegalovirus (CMV) prostatitis, and granulomatous prostatitis. Granulomatous prostatitis is usually idiopathic but can follow prior instrumentation and may be caused by bacteria (e.g., tuberculosis, brucellosis, syphilis), fungi (e.g., coccidioidomycosis, blastomycosis, histoplasmosis, cryptococcosis), and parasites (e.g., schistosomiasis). Most cases in North America are caused by bacille Calmette-Guérin (BCG). BCG is commonly instilled into the bladder to treat transitional cell carcinoma. It leaks into the prostate, where it can cause granulomatous inflammation. Granulomatous prostatitis mimics cancer on DRE, TRUS, and mpMRI and elevates PSA level. A history of BCG instillation can be reassuring, but biopsy generally is needed to exclude cancer.

Prostate Cysts

Prostate cysts are common and have been grouped into six categories: (1) parenchymal cysts, (2) isolated medial cysts (utricle and müllerian), (3) ejaculatory duct cysts, (4) abscesses, (5) cystic tumors, and (6) cysts related to parasitic disease (schistosomiasis, hydatid disease). By far, the most common cysts are parenchymal degenerative cysts in hyperplastic nodules in the transition zone. These have no clinical significance but on occasion can become large enough to contribute to urinary or ejaculatory obstruction. Typically, these are seen as unilocular or thinly septated multilocular cysts in a typical BPH nodule in the transition zone (see Fig. 10.9A ). Some patients develop atrophic dilation of prostate ducts, which appear as 1- to 2-mm-diameter clusters of radially oriented tubules or cysts in the peripheral zone. These have no significance (see Fig. 10.9A,B ).

Retention cysts are focal cysts typically smaller than 1 cm at the surface of the prostate and result from duct obstruction. They can be very tense and become palpable as a hard prostate nodule mimicking cancer on DRE but on ultrasound appear as a typical cyst. They have no significance, but if they are palpable, aspiration helps confirm their benign nature and avoids future clinical concern when a hard “nodule” is again palpated at that site (see Fig. 10.9D ).

Congenital cysts of the prostate occur in or close to the midline and are related to the wolffian (mesonephric or pronephric [archinephric]) ducts or müllerian (paramesonephric) ducts ( Fig. 10.9B–C ). Most men with congenital cystic lesions in the prostate and SV are asymptomatic, but occasional symptoms arise if the cysts become large or infected.

Congenital abnormalities are common in and around the prostate and SVs. The müllerian tubercle gives rise to the prostatic utricle, a small, midline blind pouch situated near the summit of the verumontanum. Prostatic utricle cysts are caused by dilation of the prostatic utricle. Utricle cysts rarely contain spermatozoa but can be associated with genitourinary anomalies including unilateral renal agenesis, hypospadias, and undescended testis. Utricle cysts are always in the midline and are usually small but occasionally can enlarge to several centimeters in diameter (see Fig. 10.9B–C ). Müllerian duct cysts may arise from remnants of the paramesonephric duct. Müllerian duct cysts are usually small and usually midline but may extend lateral to the midline and enlarge to extend above the prostate. They have no other associations and never contain spermatozoa. As with utricle cysts, they have a teardrop shape pointing toward the verumontanum, a thick visible wall, and occasional mural or contained calcifications. In practice, utricle and müllerian cysts appear similar and their differentiation is not important. When large, both may obstruct ejaculatory ducts or develop calcifications (see Fig. 10.9E ) and become painful or infected and rarely may develop tumors.

Ejaculatory duct cysts are usually small and probably represent cystic dilation of the ejaculatory duct, possibly as a result of obstruction. Alternatively, they may be diverticula of the duct. They tend to be fusiform in shape and are typically pointed at both ends. Ejaculatory duct cysts contain spermatozoa when aspirated. They can be associated with infertility and may be seen in patients with a low sperm count. Some may cause perineal pain.

Other disorders that mimic prostate cysts include SV cysts, ectopic ureterocele, Cowper duct cysts (in urogenital diaphragm below apex of prostate), and bladder diverticula.

Prostate abscesses are cystlike cavities with thick, irregular walls and debris containing fluid and resemble abscesses seen elsewhere (see Fig. 10.8E ). Coliform organisms such as E. coli are the most common cause. Predisposing conditions include diabetes, instrumentation, and immunodeficiency. Transrectal aspiration or TURP drainage can be an effective treatment in addition to antimicrobial therapy. Cysts caused by parasites are rare in Western countries and can result from schistosomiasis (bilharziasis) or hydatid (echinococcal) disease.

Cystic neoplasms are rare, but cystadenoma and cystadenocarcinoma have been described.

Seminal Vesicles and Vas Deferens

The seminal vesicles and vas deferens develop from the mesonephric duct and are associated with renal and ureteric development. Developmental anomalies of the SV/VD are often associated with renal and ureteric abnormalities. Normal SVs measure about 1 × 5 cm, and VD, about 6 mm. The SVs function to produce and secrete seminal fluid and not to store sperm. The vasa deferentia drain via the ejaculatory ducts through the prostate into the verumontanum. Primary pathology of the SV and VD is being increasingly detected with use of TRUS and MRI.

Hypoplasia or agenesis of the SV occurs surprisingly commonly. It may be unilateral or bilateral and can be associated with agenesis or ectopia of the VD and ipsilateral kidney. Patients with cystic fibrosis commonly have bilateral agenesis of the SV and VD but normal kidneys.

Seminal vesicle cysts are rare and usually solitary ( Fig. 10.10C ). Most are asymptomatic. The cysts can enlarge and become symptomatic and can be aspirated with TRUS guidance. They may be associated with ipsilateral renal anomalies, including renal agenesis, because the SVs are derivatives of the wolffian (mesonephric) ducts, which also give rise to the ureter and VD. Congenital SV cyst and absence of the ipsilateral kidney is known as Zinner syndrome. Other associations include adult polycystic disease, hemivertebra, and ipsilateral absence of testis. The SV is a common site of ectopic insertion of the ureter.

Calcification of the SV and VD can occur with diabetes or infection. Diabetic calcification tends to involve the walls and resembles “tram tracks” on x-ray films, whereas infectious or inflammatory calcification is luminal and segmental and may be associated with SV calcifications. In endemic areas, tuberculosis and schistosomiasis should be considered.

On occasion, a 1-cm-diameter eggshell calcification is seen in the SV. These calcifications are asymptomatic and likely related to inflammation.

Malignancy in the SV is most commonly secondary to carcinoma of the prostate, bladder, or rectum and appears as a mass involving the SV. If SV involvement is suspected at time of prostate TRUS biopsy, then additional cores can be taken from the SV and may alter treatment plans. Primary neoplasms of the SV are very rare and include benign cystadenomas, leiomyoma, fibromas, and others and malignant lesions such as adenocarcinoma. Tumor mimics such as amyloid deposits are increasingly becoming recognized.