Main cause of lower urinary tract symptoms in older men.
BPH occurs with aging and the prevalence increases from 25% among men 40-49 years of age to more than 80% among them in 70-79 years of age.
More than 50% of men in their 60s, and as many as 90% of octogenarians have lower urinary tract symptoms.
Can cause acute urinary retention, recurrent urinary tract infection, incontinence and obstructive uropathy.
Prostate size correlates poorly with lower urinary tract symptoms, and many other conditions can cause such symptoms.
Prostate size alone is not a reliable or accurate predictor of the presence or degree of urinary outlet obstruction.
BPH when accompanied by enlargement of the prostate can lead to static bladder-outlet obstruction the basis of lower urinary tract symptoms.
BPH has both a dynamic and a mechanical component.
The same time as the occurrence of mechanical obstruction, a dynamic component involving the stromal prostatic tissue and bladder is present, which is often more significant in causing urinary symptoms than simple mechanical obstruction from an enlarged prostate.
Bladder obstruction can arise from dynamic processes mediated by the alpha-adrenergic axis.
Bladder detrusor hyperactivity mediated by M2-M3 type muscarinic receptors contributes to lower urinary tract symptoms in approximately 15% of men.
Lower urinary tract symptoms in men older than 50 years are probably due to BPH, while in men younger than 40 years such symptoms due to other reasons.
Diagnosis based on symptoms, which are not specific for BPH.
Symptoms include frequency, retention, impaired stream, straining, urgency and nocturia.
Symptoms are classified as obstructive voiding or bladder storage symptoms.
Obstructive voiding symptoms include urinary hesitancy, delayed in initiating micturition, intermittency, involuntary int2242uption of voiding, weak urinary stream, straining to void, sensation of incomplete emptying, and terminal dribbling.
Classic symptoms of BPH include a slow, intermittent, or weak urinary stream; the sensation of incomplete bladder emptying; double voiding; postvoid dribbling; urinary frequency; and nocturia.
Patients may also present with acute or chronic urinary retention, urinary tract infections, gross hematuria, renal insufficiency, bladder pain, a palpable abdominal mass, or overflow incontinence.
Storage symptoms include urinary frequency, urgency,nocturia, incontinence, and bladder pain or dysuria.
Normal prostate exam does not rule out the diagnosis of BPH because the prostate size does not correlate with degree of obstruction or symptoms.
Diagnosis based on clinical symptoms, prostatic enlargement on digital rectal examination, and abnormal uroflow studies with increased postvoid residual urine.
Causes up to a 40% risk for urinary retention in a man’s lifetime.
Affects more than 14 million older men in the U.S.
Affects 40-50% of men age 51- 60 years and more than 80% of men older than 80 years of age.
BPH is thought to be caused by aging and by long-term testosterone and dihydrotestosterone (DHT) production, although their precise roles are not completely clear.
Histopathologic evidence of BPH is present in approximately 8% of men in their fourth decade and in 90% of men by their ninth decade.
BPH occurs primarily as two histological types: stromal hyperplasia, fibromuscular, and glandular hyperplasia.
Loss of testosterone early in life prevents the development of BPH.
The similarities in BPH among identical twins suggest a hereditary influence.
BPH tends to progress, as cross-sectional studies suggest that the growth rate of the prostate decreases with age.
In patients aged 31-50 years, the prostate doubling time averages 4.5 years. In men aged 51-70 years, the prostatic doubling time is approximately 10 years, while in men older than 70 years, the doubling time increases to more than 100 years.
A 5-year longitudinal study of 631 community men aged 40-79 years from Olmsted County, Minnesota demonstrated an average annual prostate growth rate of 1.6%, and in this study it remained essentially constant regardless of age, although men with larger prostates tended to have higher growth rates.
The average prostate weighs approximately 20 g by the third decade and remains relatively constant in size and weight unless BPH develops.
Symptoms of BPH tend to progress slowly over time in most individuals, with an average annual increase of 0.14-0.44 points per year in the AUA symptom index for men aged 60 years and older.
Once BPH has begun, the prostate grows an average of 0.6 mL in volume annually, with a mean decrease in average urinary peak flow rate of 0.2 mL per second each year.
Men older than 70 years and those with a baseline peak flow rate less than 10 mL/s tend to have a more rapid and dramatic decline in their peak flow rates over time.
Secondary to the growth of epithelial and stromal cells in the prostate.
The normal prostate consists of approximately 50% stroma, and the rest is divided among gland elements, acinar lumens, and epithelial elements.
The growth rate of the epithelium, and particularly the stroma, in BPH is much faster than the growth rate of in normal prostates.
Stromal hyperplasia results from proliferation of the fibromuscular stromal fibers that separate the acini of prostate glands.
Epithelial and stromal cell proliferation in the prostatic transition zone with hypertrophy of median and lateral lobes.
The transition zone is thought to be the origin of BPH.
The transition zone consists of two separate lobes on either side of the urethra and usually involves a small grouping of ductal tissue near the central portion of the prostatic urethra near the internal sphincter.
As the transition zone expands, it can comprise up to 95% of the prostate volume, compressing the other zones.
Stromal hyperplasia results from proliferation of the fibromuscular stromal fibers that separate the acini of prostate glands.
It is proposed that stromal hyperplasia may respond better to medical management with alpha-blockers that relax the tone of the muscle fibers.
Hyperplastic prostate tissue that arises primarily from the periurethral zone tends to be mainly stromal and fibromuscular.
Median lobe enlargement is primarily stromal fibromuscular tissue.
Intraoperatively, the 2 enlarged lobes of the transition zone can be seen obstructing the prostatic urethra on either side.
An enlarged median lobe may cause relatively more severe symptoms than lateral lobe hyperplasia of similar magnitude because it can act as a valve at which increased bladder pressure may actually cause further obstruction.
Thus, the term lateral lobes is often used intraoperatively for this tissue to distinguish it from any hyperplastic periurethral gland tissue.
The periurethral glands are less commonly involved with BPH.
If the periurethral glands become enlarged, they can form what is termed a median lobe, which appears as a teardrop-shaped midline structure at the posterior bladder neck.
This can ball-valve into the urethra, creating severe obstructive voiding symptoms when the detrusor pressure increases and presses this tissue against the bladder neck or across the outlet to the urethra, creating a functional obstruction.
When a bladder is trying to empty through a blocked outlet from an obstructing prostate gland, the intravesical pressure required to open the bladder neck is increased.
The bladder is initially able to produce a higher transitory voiding pressure when required, but loses muscle tone over time.
The need for a higher intravesical pressure to overcome the increased resistance to voiding, causes isolated muscle bundle hypertrophy, and bladder trabeculation often follows.
As the spaces between these hypertrophied bundles tend to become thinner, there is less functional muscle, that can progress to the point at which the bladder becomes almost nonfunctional.
As the spaces between these hypertrophied bundles tend to become thinner, there is less functional muscle, that can progress to the point at which the bladder becomes almost nonfunctional.
Bladder trabeculation is usually graded on a scale of I-IV.
Bladder trabeculation seen on cystoscopy images, it is a relative indicator of the degree and duration of any bladder outlet obstruction, such as BPH.
Proliferation of tissues is induced by testosterone and its biologically active conversion form dihydrotestosterone.
BPH is a result of the ongoing process of testosterone being converted to dihydrotestosterone which stimulates prostate growth.
Development of histologic BPH depends on biovailability of testosterone and its metabolite dihydrotestosterone.
Conversion of testosterone to dihydrotestosterone occurs via the enzyme 5α-reductase.
Congenital absence o 5α-reductase results in a vestigial prostate, and castration leads to prostate atrophy and decreased lower urinary tract symptoms.
DHT has an affinity for prostate cell androgen receptors that is 5 times greater than that of testosterone.
The levels of 5-alpha reductase are increased in the stromal tissue of men with BPH compared to controls, indicating that DHT is much more important in the development of prostatic hypertrophy than testosterone is.
Associated with increased risk is high levels of dehydroepiandrosterone, estradiol, insulin like growth factors, and inflammatory markers like CRP.
Initiated in the transition zone of the prostate.
The transitional zone of the prostate surrounds the prostatic urethra between the bladder neck and the verumontanum.
The relatively small transitional zone, which is located just lateral and distal to the internal sphincter, is the primary site of origin of the majority of BPH glandular tissue prostatic growth.
Leads to urinary outflow resistance and secondary detrusor dysfunction, bladder trabeculation and bladder contractions.
Although the risk of developing symptoms doubles each decade of life between 60 and 90 years of age the clinical symptoms of an individual patient does not necessarily progress with age.
Among men with urinary tract symptoms treated with placebo clinical progression with worsening lower urinary tract symptoms, acute urinary retention, urinary incontinence, renal insufficiency, or recurrent UTI occurred in 14% of men followed for a period of five years.
Rates of progression increase with age, increased severity of lower urinary tract symptoms, larger prostate size, increased PSA levels, and decreased rates of urinary flow.
Diagnosis has increased as a result of increased life expectancy and earlier diagnosis.
Rare below the age of 40 years.
Does not occur among those who are castrated, therefore requires the presence of functional testes with androgen production.
No direct correlation between glandular enlargement and symptomatology.
Patients with enlarged prostate 4-5 times more likely to have moderate to severe symptoms than those with normal sized prostate.
Evaluation includes a complete medical, neurologic, and urologic history to rule out other causes of lower urinary tract symptoms and bladder dysfunction.
History includes excess fluid intake, caffeine intake, use of diuretics, use of medications with antihistamine effects that may weaken bladder detrusor function.
Digital rectal examinations should be performed and a PSA measurement obtained.
A urinalysis is completed to screen for UTI and to look for hematuria.
Urinary tract infection should be treated before initiation of other therapy for the BPH.
On digital rectal exam the posterior lobes are palpable.
If patients report a sense of incomplete bladder emptying, or there is a palpable bladder on exam, a post void residual urine should be obtained to rule out silent urinary retention.
Normal androgen function required for its development.
Androgenic and estrogenic stimulation can induce prostate hypertrophy.
Factors related include race, sexual activity, smoking history, socioeconomic activity, alcohol intake, vasectomy and diet have been implicated in its development.
Higher incidence in blacks, obese, diabetics, high alcohol consumption, and physical inactivity.
5-alpha-reductase inhibitor finasteride reduces the risk of acute urinary retention, and need for surgery by 50%.
Long-term alpha-blocker and 5-alpha-reductase inhibitor reduces overall progression of benign prostatic hyperplasia more than treatment with either agent alone.
In men younger than the age of 30 years the prostate is about the size of a walnut but gradually increases in size leading to BPH by age 60 years in most men.
Progresses when untreated.
Prevalence is approximately 25% in men aged 40-49 years, 50% in men aged 50-59 years, 80% in men aged 70-79 years and 90% by age 85.
Clinical prevalence correlates with autopsy findings.
Volume of prostate increases steadily by 1.6% per year.
Peak urinary flow decreases 2.1% per year after the age of 40 years.
5-year cumulative incidence of acute urinary retention ranges from 1.6% among men 40-49 years of age to 10% in men 70-79 years.
Complications include hypotonic bladder, hematuria, bladder calculi, urinary tract infections and obstructive nephropathy.
Two forms of 5α-reductase exist, types 1 and 2 with the former in the skin, liver, and the later in the urogenital tissues.
5α-reductase inhibitors act on the anatomical component of bladder outlet obstruction.
Available 5α-reductase inhibitors decrease the conversion of testosterone to dihydrotestosterone in the prostate, limiting its growth and include finasteride (Proscar) and dutasteride (Avodart).
In men treated with finasteride or dutasteride plasma DHT levels decline by 60-95% and testosterone levels increase by 15-22% .
In men treated with finasteride or dutasteride intra- prostatic concentrations of DHT and testosterone change by similar proportions as plasma levels.
Reduced intra-prostatic DHT causes shrinkage of hyperplastic prostate tissue.
High concentrations of α1-adrenergic receptors in prostatic capsule and bladder neck associated with an increase smooth muscle tone and increase urethral resistance and pressure.
Medical blockade with α1 antagonists blocks prostatic smooth muscle contraction and decreases urethral resistance and pressure and relaxing the dynamic component.
In a randomized, placebo-controlled trial comparing the alpha blocker doxazosin, a 5 Alpha reductase inhibito, finasteride and the combination of the two: The five alpha reductase inhibitors with the without alpha blocker therapy, but not alpha blocker therapy alone, significantly reduced rates of urinary retention and the need for invasive therapy for BPH with the combination therapy versus the placebo, 81% versus 67% (McConnell JD et al).
Other causes of lower urinary tract symptoms must be ruled out and include, urinary tract infection, urinary tract stones, diabetes, urethral stricture, overactive bladder, neurogenic bladder, bladder cancer, prostate cancer and congestive heart failure.
Obstructive symptoms can be increased by tricyclic antidepressants, anticholinergic medications, diuretics, narcotics, antihistamines and decongestants.
Daily use of antidepressants and antihistamines associated with increased prostate symptoms in men 40-79 years compared to aged matched controls.
Men with subclinical BPH may develop symptoms with the initiation of a new medication. Average annual change in prostate volume is 1.6% for all ages.
Majority of patients have symptoms which are not severe or bothersome enough to warrant long term medical or surgical treatment.
The American Urological Association Symptom Index (AUASI) is a self-administered quantitative measure of the severity of lower urinary tract symptoms on a scale of 0-35.
Zero indicates no symptoms and 35 indicates the most severe symptoms and the extent to which the patient is bothered.
The AUASI score also can guide management and quantifies measure of response to therapy with a three point change considered clinically important.
In men with mild or no symptoms, or who are not bothered by their symptoms watchful waiting is the recommended management.
Benign prostatic hyperplasia-the International Prostate Symptom Score (IPPS) asks 7 questions about urinary symptoms, with a 5 point scale for each question.
Benign prostatic hyperplasia-International Prostate Symptom Score (IPSS)-
Incomplete emptying-0-5
Frequency- 0-5
Intermittency-0-5
Urgency-0-5
Weak stream-0-5
Straining-0-5
Nocturia-0-5
Mild symptoms 0-7
Moderate 8-19
Severe 20-35
Patients with IPPS of less than 8 can be treated with expectant management.
Evaluation includes PSA level, urinalysis to rule out infection, or hematuria, a serum creatinine to evaluate renal function and a urine cytologic study if irritative voiding symptoms are present.
In patients with more severe symptoms (IPSS>8) additional studies including urinary flow rate, postvoid residual and pressure flow urodynamic studies are appropriate.
Cystoscopy is usually reserved for patients that are being considered for invasive management.
For patients receiving watchful waiting, or in noninvasive treatment invasive diagnostic tests are not needed.
Decreasing evening fluid intake, avoiding caffeine, avoiding decongestants, avoiding anticholinergics and other medicines that make voiding difficult.
In a comparison of watchful waiting vs transurethral resection of the prostate in patients with moderate symptoms of BPH resulted, after 3 years of follow up, that 8% of men treated with TURP and 17% of men with watchful waiting failed treatment.
Majority of patients have symptoms which are not severe enough to receive medical or surgical treatment.
Medical management has replaced interventional therapy as the most common treatment.
Medical management available are alpha1-adrenergic antagonists and 5 alpha reductase inhibitors, which act on both dynamic and static components of bladder obstruction.
Consideration for invasive urologic approach when moderate to severe symptoms occur, gross hematuria persists, urinary retention occurs, renal insufficiency due to BPH occurs, presence of recurrent urinary tract infections and formation of bladder calculi.
TURP surgery is reserved for patients with symptomatic BPH who have acute, recurrent, or chronic urinary retention, in whom medical management failed or who have prostates of an unusual size or shape, or who have renal insufficiency due to prostatic obstruction, who have severe symptoms of prostatism, recurrent gross hematuria, bladder calculi, permanently damaged or weakened bladders, or large bladder diverticula that do not empty well secondary to an enlarged prostate.
Prostate surgery for BPH attempts to remove the obstructing tissue while minimizing damage to surrounding structures, with as little discomfort to the patient as possible.
The accessibility of the obstructing prostate via transurethral endoscopy affords the opportunity to remove the obstruction without open surgery.
It also protects the surrounding organs from injury by removing the tissue from the intraluminal surface of the prostate.
Electrosurgical TURP is the standard for endoscopic removal of obstructive BPH tissue.
Open prostatectomy is more appropriate for larger prostates, as endoscopic resection is a more lengthy procedure allowing fluid shifts and other complications.
Patients with IPSS score less than 8 are treated expectantly by minimizing evening fluid intake, avoiding antihistamines, anticholinergics, decongestants and other medications that impair urination and by avoiding caffeine.
Alpha1-adrenergic antagonists are the initial treatment of choice form most patients (tamsulosin-Flomax).