BENIGN PROSTATIC HYPERPLASIA
Benign prostatic hyperplasia (BPH) is a common condition of the prostate gland seen in older men. BPH is clinically important because it is the most common cause of urinary outlet obstruction in men older than 50 years. Untreated, stasis occurs, which increases the risk of urinary tract infection and bladder stones. Over time, bladder decompensation can result in chronic urinary retention with overflow or renal failure secondary to high-pressure urinary retention.
PATHOGENESIS
Prostate gland growth is influenced by steroid hormones. However, the exact mechanism of prostatic hyperplasia remains unclear. Interestingly, BPH does not occur in castrated men or pseudohermaphrodites, both of whom lack dihydrotestosterone, the active metabolite of testosterone. Estrogens have also been implicated in prostatic hyperplasia, because in aging men, the levels of estrogens increase and those of androgens decrease.
The specific area of cellular hyperplasia is the transitional zone or periurethral area of the prostate. The periurethral glandular elements undergo hyperplasia, causing an increase in glandular mass that results in compression of the prostatic urethra and the onset of obstructive symptoms (Figs. 22-1 and 22-2).
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Figure 22-1 • Benign prostatic hyperplasia causing urethral compression. The enlarged periurethral glands are enclosed by the orange peel–like surgical capsule, which is composed of compressed true prostatic tissue. |
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Figure 22-2 • Normal prostate and nodular hyperplasia. In pros-tatic hyperplasia, the nodules distort and compress the urethra and exert pressure on the surrounding normal prostatic tissue. Image from Rubin E, Farber JL MD. Pathology. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 1999. |
EPIDEMIOLOGY
The prevalence of BPH increases with age. Autopsy studies show that at least 50% of men older than 50 years have significant enlargement of the prostate as a result of BPH. Rarely does a patient present before age 50 years, because the doubling time of the hyperplastic gland is slow. By age 90 years, roughly 90% of males have a significant degree of hyperplasia. All men with intact functional testes are at risk for development of BPH.
CLINICAL MANIFESTATIONS
History
Any older man presenting with obstructive urinary symptoms must be suspected of having BPH. Symp-toms include urinary hesitancy, intermittency, decreased force of urinary stream, and a sensation of incomplete bladder emptying after voiding. Secondary symptoms are a consequence of urinary stasis. High postvoid residual volumes promote bacterial growth, leading to urinary tract infection. Stasis can also promote the formation of bladder calculi. Most seriously, high-pressure chronic retention can cause bilateral hydroureteronep-hrosis and subsequent renal failure.
Physical Examination
A careful rectal examination reveals an enlarged symmetric rubbery gland. The size of the gland has no relationship to symptomatology. A small gland may produce a high degree of outflow obstruction, whereas a large gland may produce no symptoms at all. The suprapubic region should be palpated to rule out a grossly distended bladder.
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Diagnostic Evaluation
Urine should be obtained for sediment analysis and microbiologic cultures. Serum blood urea nitrogen and creatinine levels should be checked for evidence of renal insufficiency. If chronic urinary retention is suspected, a postvoid residual can be checked by straight catheterization or bladder ultrasonography. Urinary flow rate is assessed by measuring the volume of urine voided during a 5-second period. A flow rate of <50 mL in 5 seconds is evidence of bladder outlet obstruction. Ultrasonography, intravenous pyelography, or computed tomographic (CT) scan can be used for imaging the urinary tract. Information regarding size of the prostate, presence of bladder stones, the postvoid residual volume, and hydronephrosis can be obtained. Transrectal ultrasonography is used to evaluate either an irregular prostate when found on examination or an elevated prostate-specific antigen level.
Treatment
The goals of drug therapy for BPH are to relax smooth muscle in the prostate and bladder neck or to induce regression of cellular hyperplasia, thereby enhancing urinary outflow from the bladder to the urethra. Alpha blockade of adrenergic receptors produces smooth muscle relaxation of both prostate and bladder neck. An infrequent side effect of alpha-antagonists (e.g., terazosin) is postural hypotension (2% to 8%). Prostatic hyperplasia can also be treated with 5-alpha reductase inhibitors (e.g., finasteride), which block the conversion of testosterone to dihydrotestosterone without lowering serum levels of circulation testosterone. However, the effectiveness of 5-alpha reductase inhibitors is less than half that seen with alpha-blockers.
Surgical relief of obstruction is necessary when medical therapy fails. The indications for surgery are a postvoid residual volume >100 mL, acute urinary retention, chronic urinary retention with overflow dribbling, gross hematuria on more than one occasion, and recurrent urinary tract infections. Additional indications are patient request for restoration of normal voiding pattern because of excessive nocturia or dribbling.
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The procedure of choice is transurethral resection of the prostate (TURP). With the patient in the lithot-omy position, the resectoscope is introduced via the urethra into the bladder. The occlusive prostate tissue is identified, and under direct vision, the tissue is shaved away using an electrified wire loop (Fig. 22-3).
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Figure 22-3 • Prostate surgery procedures. (A) Transurethral resection of the prostate (TURP). Portions of the prostate are removed at the bladder opening. (B) Transurethral incision of the prostate. One or two incisions are made in the prostate to reduce pressure on the urethra. From Cohen BJ. Medical Terminology. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2003. |
Extravasated blood and tissue fragments are evacuated as the bladder is continuously irrigated with a nonelectrolytic isotonic solution. An indwelling catheter is left in place for 1 to 7 days. To minimize the blood loss and side effects of the standard TURP technique, alternative minimally invasive outpatient procedures have been developed and are applicable to select patients. Transurethral needle ablation and focused ultrasound—both of which are less invasive modalities than TURP—ablate prostate tissue by locally heating the tissue. Although these procedures have excellent short-term results in selected patients, long-term efficacy is not well established.
PROSTATE CANCER
Prostate cancer is the most common malignancy of the male genitourinary tract. Indolent tumor growth and a long latency period account for the majority of cases (approximately 80%) being clinically silent. Most prostate cancers are only discovered on postmortem examination. Management and prognosis depend on stage of tumor.
PATHOGENESIS
The vast majority of prostate cancer (approximately 95%) is adenocarcinoma. Tumors arise from the glandular epithelium in the peripheral zone of the prostate. Tumor growth is hormonally influenced; testosterone exerts a stimulatory effect, whereas estrogens and antiandrogens are inhibitory. Tumors are histologically graded using the Gleason grading system, with scores from 2 (well differentiated) to 10 (poorly differentiated). Tumor grade is correlated with prognosis.
EPIDEMIOLOGY
Prostate cancer is a malignancy of older men, usually occurring after age 60 years. The disease is more common in Black men than in White men.
CLINICAL MANIFESTATIONS
History
Early prostate cancer is usually asymptomatic and is typically only detected on screening examination.
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Many patients present with evidence of obstructive symptoms indicating invasion or compression (poor stream, incomplete bladder emptying, nocturia). Such patients are commonly misdiagnosed as having BPH. Metastatic disease is often manifested by bony pain or ureteric obstruction.
Physical Examination
Digital rectal examination and prostate-specific antigen level measurement are the principal methods of screening. Tumor staging is based on the degree of spread: T1 to T2 indicates localized spread within the prostate, T3 to T4 indicates local spread to seminal vesicles or pelvic wall, and M1 indicates metastatic disease. Pattern of spread is via lymphatics to iliac and periaortic nodes and via the circulation to bone, lung, and liver.
Diagnosis
As for most cancers, prostate cancer requires tissue diagnosis. Typically, a hard nodule is detected on digital rectal examination and a follow-up transrectal ultrasound is obtained for needle biopsy of the prostate. The procedure is well tolerated and performed on an outpatient basis.
Chest x-ray is performed to evaluate for lung metastases. Liver function tests may detect liver metastases. If bone metastases are suspected on the basis of presenting symptoms, a bone scan is indicated.
Treatment
Treatment for prostate cancer is based on the stage and grade of the tumor. Two common staging systems are the Gleason score and the TNM stage (Tables 22-1 and 22-2). The treatment options for localized disease (T1 to T2) include radical prostatectomy, external-beam radiotherapy, or interstitial irradiation with implants.
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For local spread (T3 to T4), the treatment is external-beam radiotherapy, with the addition of hormonal therapy for more advanced cases. Treatment for metastatic disease is hormonal ablation, as most prostate cancers are androgen sensitive. Methods of androgen ablation include surgical and pharmacologic options. Bilateral surgical orchiectomy is the gold standard for ablating testosterone production. Chemical castration using luteinizing hormone-releasing hormone agonists in conjunction with antiandrogens, such as flutamide and cyproterone, produces castrate levels of testosterone. Randomized trials demonstrate that patients with hormone-refractory prostate cancer benefit from docetaxel-based chemotherapy.
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TABLE 22-1 Gleason Score |
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TABLE 22-2 AJCC Classification for Prostate Cancer |
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TESTES
Disorders of the testes requiring surgical management include congenital abnormalities, tumors, and, in the emergent setting, testicular torsion.
CONGENITAL ABNORMALITIES
Cryptorchidism
Cryptorchidism is the failure of normal testicular descent during embryologic development. The cause of failed descent is unknown but may be due to a selective hormone deficiency, gubernaculum abnormality, or intrinsic testicular defect. Such cryptorchid testes fail in spermatogenic function, but they may retain the ability to secrete androgens. The major risk of cryptorchid testes is the increased risk of testes cancer (35 to 48 times more common than in descended testes). Inguinal hernia is also found in at least 25% of patients with cryptorchidism.
Physical Examination
The testicle remains within the abdomen and cannot be palpated on physical examination.
Treatment
Because spermatogenic failure is progressive, surgical exploration and scrotal placement of the testis should be performed before 2 years of age. If placement of the testicle into the scrotum is not possible, orchiectomy is indicated, because the incidence of cancer of abdominal testes is very high.
Incomplete Descent of the Testis
Incomplete descent of the testis implies a testicle arrested at some point in the path of normal descent but palpable on physical examination. Such testes are usually located within the inguinal canal between the deep and superficial rings (Fig. 22-4).
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Figure 22-4 • Four degrees of incomplete descent of the testis. 1. In the abdominal cavity close to the deep inguinal ring. 2. In the inguinal canal. 3. At the superficial inguinal ring. 4. In the upper part of scrotum. From Snell RS. Clinical Anatomy. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2003. |
Incompletely descended testes are often associated with congenital indirect hernias as a result of the incomplete obliteration of the processus vaginalis.
Treatment
Because testicular function is less compromised than in a cryptorchid testicle, the usual treatment is repositioning and orchiopexy within the scrotum. If present, an indirect hernia is repaired concurrently.
Testicular Tumors
Tumors of the testicle are the most common genitourinary malignancy among young men between the ages of 20 and 35 years. Virtually all neoplasms of the testicle are malignant. Tumors are divided into either germ cell or non–germ cell tumors, depending on their cellular origin. Germ cell tumors predominate, accounting for 90% to 95% of all tumors.
Pathology
Non–germ cell tumors, which arise from Leydig and Sertoli cells, produce excess quantities of androgenizing
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hormones. Germ cell tumors arise from totipotential cells of the seminiferous tubules. Germ cell tumors are divided into two categories: seminomas and nonseminomatous germ cell tumors (NSGCTs). Seminomas are relatively slow growing and exhibit late invasion. They are usually discovered and surgically removed before metastasis can occur. NSGCTs exhibit greater malignant behavior and metastasize earlier. NSGCTs consist of embryonal (20%), teratoma (5%), choriocarcinoma (<1%), or mixed cell type (40%). Choriocarcinomas are fortunately rare subtypes but are highly invasive, aggressive tumors that metastasize via lymphatic and venous systems early in the disease.
Epidemiology
Seminomas are the most common malignant germ cell tumor. Embryonal carcinoma is usually seen in younger males during childhood. Non–germ cell tumors are relatively rare.
History
Tumors usually manifest as firm, painless testicular masses (Fig. 22-5). Occasionally, the mass may cause a dull ache. Hemorrhage into necrotic tumor or after minor trauma may cause the acute onset of pain. Approximately 10% of patients with testicular tumors have a history of cryptorchidism. Because of excess androgen production, non–germ cell tumors can cause precocious puberty and virilism in young males and impotence and gynecomastia in adults.
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Figure 22-5 • Early testicular tumor. From Weber J, Kelley J. Health Assessment in Nursing. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2003. |
Diagnostic Evaluation
Immediate evaluation should include serum for tumor markers (alpha-fetoprotein [AFP], beta-human chorionic gonadotropin [β-hCG]), serum lactate dehydrogenase, and ultrasound. Tumor markers are not always helpful because seminomas, the most
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common testicular neoplasm, are usually negative for both AFP and β-hCG. In neoplasms with tumor markers, the level of tumor burden directly relates to AFP/β-hCG levels that can be monitored during the postoperative period to evaluate the efficacy of treatment and to detect recurrence.
Treatment
Initial treatment is always radical orchiectomy. Subsequent therapy depends on tumor type, grade, and staging. Retroperitoneal lymph node dissection is standard therapy for stage I and II NSGCT.
Seminomas are usually highly radiosensitive. Adjuvant treatment with radiation and chemotherapy yields high 5-year survival rates for both localized and metastatic disease.
Torsion of the Spermatic Cord
Torsion of the spermatic cord is a urologic emergency because complete strangulation of the testicular blood supply renders the testicle surgically unsalvageable after approximately 6 hours.
Pathogenesis
Torsion results from an abnormally high attachment of the tunica vaginalis around the distal end of the spermatic cord. This abnormality allows the testis to hang within the tunica compartment, like a bell clapper within a bell—hence the name bell clapper deformity. As such, the testicle is free to twist on its own blood supply, causing pain and ischemic strangulation (Fig. 22-6).
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Figure 22-6 • Torsion. Left image shows normal testicular anatomy; a bell-clapper deformity in the tunica vaginalis (middle image) can permit torsion of spermatic vessels (right image). LifeART image copyright © 2009. Lippincott Williams & Wilkins. All rights reserved. |
History
Torsion is usually seen in young male patients, who present complaining of the rapid onset of severe testicle pain followed by testicle swelling.
Physical examination reveals a high-riding, swollen, tender testicle, oriented horizontally in the scrotum. Pain is worse with elevation of the testes, and the cremasteric reflex is often absent.
Diagnostic Evaluation
A color-flow Doppler ultrasound should be obtained to evaluate for blood flow within the testicle. Absence of flow confirms the diagnosis.
Differential Diagnosis
The differential diagnosis of an acutely swollen, tender testicle includes essentially two diagnoses: torsion of the spermatic cord and advanced epididymitis. Because one can mimic the other, it is vitally important to arrive at a timely diagnosis. Other less common diagnoses include torsion of an appendix testis or appendix epididymis (Fig. 22-7).
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Figure 22-7 • Torsion of appendix testis or appendix epididymis (not shown) can also cause testicular pain and tenderness. |
Treatment
Prompt surgical exploration and orchiopexy are required to save the testicle from undergoing ischemic necrosis. Because the bell clapper deformity is usually bilateral, orchiopexy of the contralateral testicle is performed concurrently. If the diagnosis is unclear, surgical exploration is required, because an uncorrected torsion will cause necrosis of the testicle.
KEY POINTS
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options include surgery, radiotherapy, and hormonal ablation.