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Benign Prostatic Hyperplasia
Benign Prostatic Hyperplasia
Also known as benign prostatic hypertrophy (BPH) occurs when there is
an increase in the size of the prostate gland without the presence of a
malignancy; the condition is so common it is considered normal as the
man ages. An enlarged prostate can cause compression of the urethra as it
traverses the prostate. BPH is the most common prostate problem in men.
Most frequently it occurs in men over the age of 50 years.
The enlarged prostate can cause urinary symptoms.
BPH can impact negatively on a man’s quality of life. BPH is uncommon
before the age of 45, affecting men of Afro‐American origin more
severely than it does white men. Between the ages of 31 and 50 the
prostate gland doubles in size every 4.5a•›years but this rate reduces
subsequently.
Pathophysiology
The cause of BPH is unclear. Enlargement of the prostate is dependent on
the androgen dihydrotestosterone (DHT). DHT binds to androgen
receptors located in the cell nuclei, potentially resulting in BPH. This
results in an oestrogen and androgen imbalance. There are large numbers
of alpha‐1‐adrenergic receptors located in the smooth muscle of the
stroma and capsule of the prostate, and the bladder neck.
BPH is characterized as a hyperplastic process, resulting in prostatic
enlargement causing clinical manifestations of BPH. The prostate
enlarges with age and is hormone dependent, men who are unable to
produce testosterone do not develop BPH.
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The traditional theory behind BPH is that, as the prostate enlarges, the
surrounding capsule prevents it from radially expanding, potentially
resulting in urethral compression. However, obstruction‐induced bladder
dysfunction contributes significantly to lower urinary tract symptoms
(LUTS). The bladder wall becomes thickened, trabeculated and irritable
when forced to hypertrophy, increasing its own contractile force.
This is believed to contribute to urinary frequency and LUTS. The
bladder may gradually weaken and its ability to empty completely
disappears, causing increased residual urine volume with acute or chronic
urinary retention. Obstruction in the bladder leads to smooth‐muscle‐cell
hypertrophy. Collagen fibres limit shortening of adjacent smooth muscle
cells, leading to impaired emptying and development of residual urine.
Signs and symptoms
There is an increased frequency of micturition associated with a delay in
initiating micturition and a reduction in the force of the urinary stream.
As the condition progresses there may be inadequate emptying of the
urinary bladder, resulting in dribbling of urine and urinary over flow. The
time required by the man to void increases. With advanced BPH the man
may be unable to pass urine due to urethral compression. Urinary
obstruction can lead to urinary tract infection and if unrelieved, progress
to renal failure
Investigations
A detailed history should be taken and a physical examination. Urinalysis
should be done to check for the presence of blood, leukocytes, bacteria,
protein or glucose. Urine culture should also be performed, to exclude
infectious causes of irritative voiding, if urinalysis indicates an
abnormality. Prostate specific antigen (PSA) may be assessed, although
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screening for prostate cancer remains controversial and should be
performed after an informed discussion with the man. Evaluation of
electrolytes, blood urea nitrogen and creatinine can be used as screening
tools for chronic renal insufficiency in men who have high post‐void
residual urine volumes.
Abdominal, renal, transrectal ultrasound sonography and intravenous
urography help determine bladder and prostate size and degree of
hydronephrosis (if any) in those with urinary retention or signs of renal
insufficiency. Transrectal ultrasonography (TRUS) of the prostate can
determine the dimensions and volume of the prostate. In men with raised
PSA levels, TRUS‐guided biopsy may be indicated. Imaging of the upper
urinary tracts in those with associated haematuria, history of urolithiasis,
elevated creatinine level, high PVR volume or history of upper urinary
tract infection is indicated.
Drugs
Alpha adrenergic blockers reduce the tone in the muscle of the neck of
the bladder and should be offered to men with moderateto‐ severe voiding
symptoms. There are alpha‐1 receptors that are subdivided into types 1a,
1b and 1c. These should be avoided in men with postural hypotension or
micturition syncope.
The 5‐alpha reductase inhibitor (5‐ARI) drugs block the synthesis of
dihydrotestosterone from testosterone and can reduce symptoms, for
example finasteride and dutasteride. They should be offered to men with
LUTS and a prostate estimated to be larger than 30a•›g or PSA greater
than 1.4a•›ng/mL and a high risk of progression. These medications may
have an adverse effect on sexual performance.
Surgery
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Surgery is reserved for those with a large prostate or failure to respond to
an adequate trial of medical therapy. Surgery is needed if there is acute
urinary retention, failed voiding trials, recurrent gross haematuria, UTI,
renal insufficiency due to obstruction or failure of medical treatment.
Open prostatectomy – transurethral vaporization of the prostate
(TUVP) – is used for prostates larger than 75a•›g, bladder stones or
bladder diverticula and patients who cannot be positioned for
transurethral surgery.
Transurethral resection of the prostate (TURP) is now the standard
technique. When successful, it is an excellent operation that does not
involve entering the abdomen but it can have complications.
Holmium laser enucleation of the prostate (HoLEP) is effective, has a
lower morbidity rate and where available is first choice of treatment.
Minimally invasive therapies involve heat destruction of prostatic tissue.
Where the estimated prostate size smaller than 30a•›g, transurethral
incision of the prostate (TUIP) or transurethral needle ablation (TUNA) is
an alternative to TURP for those wishing to avoid or who are unfit for
more invasive surgery.
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Testicular torsion
Torsion of the testes is an abnormal twisting of the spermatic cord due to
rotation of a testes or the mesorchium (this is a fold in the area between
the testes and epididymis. This occurs when a testicle rotates, causing
twisting of the spermatic cord. There is a reduced blood flow as a result
and this causes sudden and often severe pain and oedema that is not
relieved by rest and elevation. The condition is most common between
the ages 12 and 16 years; however, it may occur at any age, even in utero.
Testicular torsion is a urological emergency and requires emergency
surgical intervention. If the condition is treated within a few hours, the
likelihood of saving the testicle will increase. If the condition is left
untreated then permanent damage may ensue; this can impact on the
man’s ability to father children. When the flow of blood has been
impaired for too long, infarction of the testicle can occur and it becomes
so seriously injured that orchidectomy will be required. The prognosis is
good with early detection and prompt treatment. The contents of the
spermatic cord include the following:
•a•￠ Ductus deferens and related vasculature and nerves
•a•￠ Testicular artery
•a•￠ Pampiniform plexus, this eventually forms the testicular vein
•a•￠ Genital branch of the genitofemoral nerve
Pathophysiology
The onset may be spontaneous or it may occur after physical exertion or
physical trauma. The condition is almost always unilateral. Torsion may
happen at any time, when sitting or standing, or it may awaken a person
from sleep.
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In neonates, often the testicle has not descended into the scrotal sac,
where it becomes attached within the tunica vaginalis. As a result, this
mobility of the testicle predisposes it to torsion (extravaginal testicular
torsion). The normal contraction of the cremaster muscle causes the left
testes to rotate in a counterclockwise manner with the right testes rotating
clockwise. Incompetent fusion of the testicle to the scrotal wall typically
is diagnosed within the first 7–10 days of life.
In those who have an inappropriately high attachment of the tunica
vaginalis and an abnormal fixation to the muscle and fascial coverings of
the spermatic cord, the testicle can rotate freely on the spermatic cord
inside the tunica vaginalis (intravaginal testicular torsion). This
congenital irregularity, known as the bell clapper deformity, can cause the
long axis of the testicle to be oriented transversely as opposed to
cephalocaudal (from head to toe). The bell clapper deformity allows the
testicle to twist spontaneously on the spermatic cord.
As the testicle rotates between 90° and 180° this compromises blood flow
to and from the testicle. Complete torsion occurs when the testicle twists
360° or more; incomplete torsion occurs with lesser degrees of rotation. It
is possible for the degree of torsion to extend to 720°. As the testicle
twists venous occlusion occurs and engorgement, along with arterial
ischaemia and infarction of the testicle. The degree of testicular torsion
plays a role in the viability of the testicle over time.
As well as the degree of torsion, the duration of torsion significantly
influences the rates of immediate salvage and also late testicular atrophy.
Testicular salvage is more probable if the duration of torsion is less than
6–8 hours. If more than 24 hours elapses then testicular necrosis will
develop in most patients.
Signs and symptoms
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Excruciating unilateral pain, with a sudden onset followed by inguinal
and/or scrotal swelling occurs. As necrosis becomes more complete the
pain may lessen. It is unusual for the pain to present in a gradual manner.
As torsion can also occur with sports or A physical activity it can be
associated with trauma or may happen spontaneously. There may also be
gastrointestinal upset accompanied with nausea and vomiting. Where the
duration of pain is less than six hours, pyrexia, vomiting, history of
trauma or activities, absence of cremasteric reflex and abnormal testicle
direction have all been shown to be significantly associated with the
diagnosis of testicular torsion. It is unusual for the person to relate
problems with micturition or dysuria.
Some patients describe previous episodes of recurrent acute scrotal pain
that had resolved spontaneously. This is suggestive of intermittent torsion
and detorsion of the testicle; in this instance prompt referral to a urologist
is essential as those with symptoms who have elective surgical
exploration are less likely to develop subsequent torsion and loss of the
testicle.
Typically, there is reddening of the scrotal skin with oedamtous, tender
testes retracted upwards. Lifting the testes up over the symphysis causes
an increase in pain. The epididymis may be felt in an abnormal anterior
rather than its typical posterior position in the early stages; however, this
depends upon the degree of torsion. As the condition progresses the gross
swelling prevents this finding. Unilaterally the testes are typically in the
‘bell‐clapper position’ with a horizontal long axis.
Investigations
The healthcare practitioner undertakes a clinical evaluation which
consists of medical history and physical examination; this is often
sufficient to diagnose torsion. If testicular torsion is clinically suggested,
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immediate surgical exploration is required; this is regardless of laboratory
studies, a negative finding upon exploration of the scrotum is more
suitable than the loss of a testicle, surgical intervention should not be
delayed for the sake of further investigation. No single laboratory test has
high sensitivity or specificity in diagnosing testicular torsion.
Imaging studies (ultrasonography, nuclear scans) may be useful when a
low suspicion of testicular torsion exists, otherwise they are of little
value. The most important investigation is ultrasound integrated with
colour Doppler; this investigation detects the presence/ absence of
intratesticular blood flow for the early identification of testicular torsion.
Management
If manual reduction is unsuccessful, surgical intervention is required
within six hours after the onset of injury in order to A preserve testicular
function. Surgical detorsion is the definitive treatment for testicular
torsion. Testicular torsion is treated with orchiopexy, the testes is
anchored to the scrotal wall. There may be a need for orchidectomy.
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