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=== Urology course Daniel Porav-Hodade, Mihail Radu Boja ===========

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=== Urology course Daniel Porav-Hodade, Mihail Radu Boja ===========
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=== Urology course Daniel Porav-Hodade, Mihail Radu Boja ===========
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UNIVERSITATEA DE MEDICIN I FARMACIE TRGU-MURE


CLINICA DE UROLOGIE




AUTORI

As. Univ. Dr. Porav Hodade Daniel
Prof. Univ. Dr. Boja Radu





UROLOGY COURSE






















Editura University Press - Trgu Mure 2012


=== Urology course Daniel Porav-Hodade, Mihail Radu Boja ===========
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Descrierea CIP a Bibliotecii Naionale a Romniei:
Urology Course/ Porav-Hodade Daniel, Boja Radu - Trgu Mure :
University Press Tg Mures, 2012
270, 21x30cm, 250 exemplare
ISBN 978-973-169-187-9
Porav-Hodade Daniel
















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1. Congenital anomalies of urogenital tract........................................6
2. Urogenital apparatus trauma.........................................................21
3. Non-specific infections of the genitourinary system.....................37
4. Specific urogenital infections - urogenital tuberculosis................83
5. Lithiasis of the urinary tract..........................................................96
6. Benign prostatic hyperplasia.......................................................116
7. Prostate cancer.............................................................................134
8. Kidney tumors.............................................................................148
9. Upper urinary tract urothelial cell carcinoma.............................161
10. Urinary bladder tumors...............................................................169
11. Testicular tumors........................................................................182
12. Acute renal failur in urology.......................................................191
13. Erectile dysfunction....................................................................199
14. Male infertility............................................................................205
15. Renal transplantation..................................................................210
16. Urological emergencies..............................................................217
17. Abbreviation...............................................................................233
18. References..................................................................................234


CONTENTS
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Represent 35-40 % of the total amount of congenital anomalies, being the
most common visceral malformations; in 4.5% of cases these represent a mortality
cause in the first year of life.
Sometimes they do not develop during the entire life, being randomly discovered,
during a more detailed medical exam or at the autopsy. In other cases, due functional
disorders they are severe, putting in danger the life of the patient. There are many
causes for congenital anomalies of urogenital apparatus. Apart from heritage, which
transmits some chromosomal mutation, many other factors are involved in producing
these anomalies which perturb embryo development inside the maternal organism:
infectious diseases, vitamin lacks, or hormonal lacks, ionized radiations as well as a
series of tranquilizer remedies, or contraceptives. There great impact towards other
apparatus and systems is explained by the specificity of embryonic development of
the urogenital apparatus, which is the result of complex processes, as a consequence
of two systems crossover: excretory and secretory systems.
I. ANOMALIES OF SUPERIOR URINARY SYSTEM
A. Kidney anomalies are classified according to number, volume and structure,
shape, center and vascularization.
1. Number anomalies.
a. Bilateral renal agenesis is very rare and incompatible with life.
b. Unilateral renal agenesis (one congenital kidney), consists in the absence
of one kidney along with the ureter and the orthotopic hemitrigone. The adrenal
gland can also be missing.
The absence of one kidney does not have a clinical expression as long as the
congenere kidney is normal. When the single normally developed congenital kidney
is the center of various conditions or injuries, the situation is worse, due to the
functional consecutive lack, claiming therapeutical treatment of great responsibility.
The diagnosis the first suspicion for such an anomaly is raised by the
ultrasound of both lumbar regions. On one hand, in one of the two lumbar fossae a
kidney with increased volume can be observed. On the other, on the opposite side no
1. Congenital anomalies of urogenital tract
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renal structure can be identified. Up to this point, unilateral renal agenesis cannot be
affirmed with certainty (the kidney can be in high, low or crossed ectopic). The
urography (IVU) reveals the presence of a secretion, only on one side, while the
reno-scintigraphy reveals the same thing, the unilateral setting of radioactive isotope.
The cystoscopy is the certainty clinical examination, which reveals the trigonal
asymmetry together with the absence of ureteral aperture on the side in question. The
absence of the ureteral aperture with trigonal asymmetry can be the consequence of
an abnormal opening of the ureter (ectopic ureteral aperture) in the vagina, urethra,
and labia majora. In case of doubt, computerized tomography (CT), nuclear magnetic
resonance (MRI) and the angiography will confirm or invalidate the unilateral renal
agenesis.
The renal agenesis is often accompanied by some anomalies in the
development of other organs that are related to the genital, digestive and
cardiovascular apparatus. The diagnostic of this renal anomaly is more important in
the case of urological emergencies, such as surgical interventions on the unique
kidney, which will always be conservative.
The presence of the unique congenital
kidney in abnormal position should be also
mentioned (pelvic ectopic), situation that
involves a greater responsibility in stating the
diagnostic and in establishing the therapeutical
attitude, when needed.
c. The supernumerary kidney is an
extremely rare anomaly, exceptionally
bilateral. The supernumerary kidney, situated
in one of the lomb, or medial, is usually
smaller and has a capsule, ureter which opens
in the bladder, in one of the other ureters or in
one of the adjoining organs (urethra, vagina)
and vessels (fig. 1.1).
d. The double kidney. Pretty common, this anomaly is characterized by the
presence in the space reserved to one kidney of two undelimited, or relatively

Fig. 1.1. A supernumerary kidney 1 -
The normal kidney position, 2 -
Supernumerary kidney in ectopic
position, 3 - Supernumerary ureter, 4 -
Supernumerary kidney ureter, 5 -
Supernumerary kidney ureter opens
ectopic into the urethra
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delimited parenchymal masses, with two distinct collecting systems and separate
ureters, having a distinct vascularization. At the level of excretory pathways, the
halving is limited in some cases only to the renal pelvis, which is shown bifide. In
most frequent cases, the ureters, that were initially distinct, combine (ureter fissus) in
lumbar, iliac and pelvic region (incomplete dupplicate) (fig 1.2). In the case of
complete duplicate, the ureters open separately in the bladder through two apertures
located on the same side (fig 1.3).

2. Structure and volume anomalies
Renal dysplasia is an incomplete development of renal paranchymal at the
beginning of organogenesis, the kidney being function deprived.
1. Renal aplasia when bilateral, the anomaly is life incompatible; the
unilateral one is compatible as long as the congener kidney can compensate the
function of aplastic kidney. This can be a cause of arterial hypertension (HTN) of
renal nature. In the case of unilateral renal aplasia, the contralateral kidney is
increased by the volume. The diagnostic is based on an ultrasound examination,
which discovers sometimes very hardly the kidney reduced by volume on one side,
and on the other side, the kidney increased by volume. IVU identifies the functional
absence of one kidney and provides information on the function and the morphology
of the other organ. The reno-scintigraphy, the CT and the angiography are
complementary means of diagnostic. In other cases, when it is well tolerated, it is
only discovered during the autopsy.


Fig. 1.2. Left double kidney with incomplete
ureteral duplication (ureter fissus)
Fig. 1.3. Left double kidney with complete
ureteral duplication.

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Fig. 1.4. Left renal hypoplasia
2. Renal hypoplasia represents a renal
dysplasia characterized by the incomplete
development but with normal development of the
ureter (fig 1.4). Kidneys function is diminished or
is missing. The diagnostic is established by using
the known imagistic methods: ultrasounds and
IVU, at which the radio-isotopic and the radiological methods are added. The
treatment for hypoplasic kidney is established depending on the clinical distress and
on the lesion impact on the organism, being a frequent cause of renovascular
hypertension.
The hypoplasic kidney which is not well tolerated (pyuria, nephritis or pain), or with
complications imposes nephrectomy.
3. Renal hyperplasia the kidney has an enlarged volume, with a normal
paranchymal structure and with an increased functional capacity. In most cases,
either hyperplasia or congenital renal hypertrophy is associated with agenesis, or
with congener kidney hypoplasia. The diagnostic follows the same phases as in the
case of renal hypoplasia. As the normal kidney, it can be the center of various
pathologic processes. The treatment depends of the nature of the disease. The
nephrectomy is practiced only when the opposite can ensure a normal purge of the
organism.
4. The solitary renal cyst. The anomaly is characterized by the presence of a
solitary cyst formation of variable volume, at the kidney level (polar, medial, on the
anterior or posterior hemivalve). When it is located at the level of inferior pole, it is
clinically manifested like a tumor in a flank. It is frequent in adults, but can alse be
encountered in young people. The renal cyst diagnostic is nowadays achieved mainly
by ultrasound, investigation that accurately differentiates a solid expansive process
by a fluid one.
By compression, the cyst atrophies the renal parenchymal in the vicinity and
deforms the pyelocaliceal cavities. When we are talking about a considerable
volume, it can compress the organs located in the vicinity, causing consecutive
disorders. The cysts wall, located at the level of the dome, is avascular and there is
no cleavage plan between its wall and the renal parenchymal. The solitary cyst can
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evolve without showing any clinical manifestations, and in this case, its discovery is
random. When complications (infection, malignancy, inter-cystic bleeding), or
compression effects on the parenchymal, compression or tractions on the renal
vessels appear, it has therapeutic indication.
The treatment. Nowadays, a classical surgical approach is no longer adopted
(dome resection and filling the cavity of the cyst with fat). Instead, other less
invasive methods are used: eco-guided puncture, aspiration and cyst sclerosis with
Aethoxysklerol, glucose 33%, alcohol solution 90, cyst fenestration (electrical
incision of the avascular wall), or subtotal laparoscopic cyst resection.
5. The polycystic renal disease it is a congenital malformation, autosomal
recessive genetically transmitted, being always a bilateral disease. The anomaly
consists in a deficiency in the development of convoluted and collector tubes which
are partially obstructed, but are linked to functional glomerules. These are subject
(under the accumulation of urine effect) to a distension, which transforms them in
cysts with normal dimension. The kidney aspect is similar to a cluster of grapes.
The compression that is exerted by these cavities, which contain liquid under
pressure, on the intact tubes located in the vicinity and on the vascular network, leads
to ischemia and, eventually, to renal functional deficit.
These types of lesions can simultaneously affect the lungs, the liver, the
spleen, the pancreas and the thyroid.
Pathological anatomy. The kidneys are increased by volume, with irregular
surface due to different size cysts, being similar to a cluster of grapes. On the section,
the kidney is constituted of multiple cysts. The renal tissue (parenchyma) is rarely
emphasized in the shape of some reduced areas, compressed by cyst elements. Calyx
are elongated, thinned, anarchically oriented. The renal pelvis is small, most of the
times inter-sinusal, hardly to find during dissection.
Clinical symptomatology. The anomaly can exist for a long period of time
without presenting any clinical manifestations, being accidentally discovered. In
other cases, the traction of the kidney increased by volume on the renal pedicle, the
compression on the excretory pathway of multiple cysts, and inter-cystic bleedings
increase the inter-cystic pressure and lead to the appearance of different intensity
bilateral pains. Sometimes the pains are violent, having the intensity of a nephritic
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colic. Hematuria microscopic sometimes, but discrete, can be total in other cases,
macroscopic, massive, presenting clots.
Septic complications (fever, pyuria) and the pain contribute to the
amplification of clinical picture.
Functional renal deficiency sometimes unapparent for a long period of time,
becomes in other cases evident (loss of appetite, nausea, vomiting, fatigue, lack of
weight, pallor). Arterial hypertension is encountered in more than 50% of the
patients and represents sometimes the distress that initiates exploration and diagnosis
of malformation.
Uraemia is an expression of renal insufficiency.
During the objective clinical examination, one or both kidneys can be
palpated, increased by volume, with lumbar contact, with nonregular surface, and
sometimes with increased sensitivity.
Paraclinical examinations can establish the alteration of renal function:
increased values of urea and serum creatinine, anemia, decrease of urinary density to
isosthenuria, signs of installed renal insufficiency.
KUB X-Ray increased renal shadows, erasure of the external edge of
unilateral or bilateral psoas. The ultrasound identifies both kidneys increased by
volume, sometimes impossible to catch the entire kidney in the ultrasound sector,
with multiple transonic formations (liquid) of variable sizes, on the surface and in the
interior of renal parenchymal. Parenchymal index cannot be estimated, the entire
architectonic of the kidney being altered, and the edges of the central ecogen
complex are impossible to be specified.
IVU, if the values of creatinine allow it, reveals specific images: renal
shadows increased by volume, polycyclic perimeter, calix with modifications
encountered in expansive processes (traction, elongation, disorientation, recurving),
but are not observed in amputations, being a sign of turnoral invasion.
The reno-scintigraphy delineates increased renal surfaces and report the
multiples mute areas that correspond to cysts.
The other explorations, retrograde ureteropyelography, CT and the
angiography complete the diagnostic or provide essential elements for differential
diagnosis.
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Positive diagnosis. The disorder can be suspected when one kidney is
enlarged by volume, with nonregular surface and there are signs of renal
insufficiency. It is extremely probable when both kidneys are enlarged by volume
and present the characteristics palpate examination. In this context, paraclinical
investigations sustain the polychystic kidney diagnosis.
Differential diagnosis is made with hydronephrosis, sometimes bilateral, but
the ultrasound and the IVU provide morphological aspects; with renal tumors, for the
patients presenting apparent unilateral anomaly, in which case the ultrasound
precisely differentiates a renal tumor of a polycystic kidney.
Clinical forms
The obstetrical form with polycystic liver and kidney, that develop intra-
uterus, having an impressive volume, represents a cause of fetal dystocia.
The medical form, the clinical picture is dominated by HTN, cephalalgia,
fatigue, pallor, proteinuria, which can be confused with chronic nephritis.
Sometimes, a total hematuria episode, that can be important, draws attention
on another diagnosis and discovers the anomaly.
The surgical form imitates intra-peritoneal tumors (spleen, liver, colon).
The urological form whose clinical picture draws attention on a urological
disorder: hematuria, lumbar pains.
The evolution is progressive or in leaps and is irreversibly leading to renal
insufficiency, associated with HTN. Early discovery is achieved by urological exam
of all family descendents in which one parent has this disease, or of the patients
brothers.
The treatment. The therapy is firstly conservative in front of one disorder
that implies both kidneys, having a marked evolutionary potential and causing a
progressive decrease of renal function.
The medical treatment: hypo-nitrate regime, increased hydric intake,
avoiding intense physical efforts; its purpose is the treatment of chronic renal
insufficiency (CKF). HTN and the treatment of urinary infection, if it has been
detected, should also be taken into consideration. At young patients with polycystic
kidney, without HTN, with CKF, bilateral nephrectomy, dialysis and renal transplant,
therapeutic measures that improved the prognosis of this congenital anomaly, are
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Fig. 1.5. Horseshoe kidney
recommended in order to avoid the complications inherent to the evolution of the
disease.
The surgical treatment can become necessary only when the disease
presents complications: tumors, calculus, tuberculosis and renal trauma. In the case
of big, painful cysts, a percutaneous puncture with evacuation can be performed in
order to reduce the inter-cystic pressure and to calm down the pain.
The nephrectomy is possible if the patients life is in danger, regardless of the
functionality of congener kidney. In case of functional deficiency of congener
kidney, dialysis is recommended.
Renal transplant is the elected treatment for the patients with CKF, which
reached the dialysis stage.
3. Shape anomalies
The kidneys can remain welded
due to early development disorders,
constituting a common mass. One or
both kidneys are situated in a lower
position, being close to the median line.
Vascularization and rotation
malformations are associated.
1. Horseshoe kidney it is
formed of two distinct renal masses,
situated on one side and the other of the
spine, welded at the inferior pole, exceptionally rare at superior pole. The area is
usually a fibrousisthmus, rarely parenchymal, which overlaps the spine (fig 1.5). Due
to the fact that the anomaly was produced before the ascension and the complete
kidney rotations, it has some characteristics:
The kidneys are usually situated lower than usual, the isthmus being situated
in the region of L2-L3 lumbar vertebrae;
The longitudinal axe of the kidneys is transverse, top-down and inside out,
describing a V with cranial opening;
renal pelvis is anterior facing (insufficient rotation);
The ureters descending to the bladder cross the isthmus.
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The vascularization is abnormal (from mesenteric arteries, iliac arteries and
from the aorta) and approaches the medial edge of the horseshoe and the
superior edge of the isthmus.
Clinical. The symptomatology is related to the appearance of complications,
usually the infectious ones, the tumors and the calculus being the most frequent.
Thus, the anomaly is very well tolerated. The symptomatology takes the
charactereristics of stated above disorders.
The diagnosis is based mainly on X-Ray investigations (reno bladder X -
ray, IVU) and radioisotopic ones.
The KUB X - ray can emphasize the two welded renal shadows, lower
situated, especially at patients with thin abdominal wall. IVU, in normal functioning
renal conditions, allows anomaly recognition (modification of longitudinal axes of
the kidney, the renal pelvises are anterior, the ureters cross the isthmus, the calyx
have an anarchic orientation, they look on a medial direction and less external).
The reno-scintigraphy, or ureter-pielography (retrograde
ureteropyelography) are useful in functional renal deficiency.
The ultrasound is less useful, contrasting the position modification of
kidneys, related to the normal position, both kidney masses being moved medially; it
outlines eventual dilatations (transonic formations) and/or calculus (ecogene
formations with shadow cone).
The treatment: when the anomaly is associated to calculus, the treatment
consists in extracorporeal lithotripsy (ESWL), or percutaneous extraction
(percutaneous nephrolithotomy - PNL). Rarely, pielolitotomy and the dissection of
fibrous isthmus are performed, if this is actually an obstructive factor for ureters. The
approach is on medial line, transperitoneal. Surgical interventions of any kind are
difficult due to associated anomalies: of rotation, vascularization and due to fusion
anomaly.
2. Sigmoid kidney is a rare malformation that consists in welding in front of
the spine of the inferior pole of one kidney with the superior pole of the other, which
is lowered, each kidney keeping its side (right, left). Overall, the symphysis takes the
aspect of a normal or inversed S.
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Fig 1.6. Various forms of direct renal
ectopia. High (mediastinum) and lower:
inferior lumb, iliac, pelvic

4. Location anomalies. The kidneys
dont fulfill their usual migration to the
lumbar region and remain stuck on the way,
at different levels. The situations in which
the kidney occupies the lumbar region on a
higher position than usual are well known.
Thus, the ectopies are high or low. When
the kidney stays on the same side of the
spine, the ectopy is direct, and if it passes
on the other side, the ectopy is crossed (fig.
1.6). The anomaly involves vascularization
also.
Clinical. Most of the times, the
symptoms are missing. During labor, an ectopic kidney can represent a cause for
maternal dystocia. The anomaly is most of the times accidentally discovered, during
some surgical interventions, or when some complications appear: calculus,
infections, tumors, when corresponding symptoms appear. The diagnosis is based on
the KUB X ray (radioopaque kidney stones), on IVU that provides
morphofunctional details about both kidneys, is less relied on the ultrasound, but
mostly on reno-scintigraphy and on retrograde ureteropyelography. The angiography
provides clarifications regarding vascularization anomalies. .
Medical treatment particularly aims infectious complications.
Surgical treatment is recommended in complications that are due to calculus
appearance, which is mostly fixed through ESWL being about an anomaly, and
rarely through endoscopic surgery (PCNL, antegrade or retrograde ureteroscopy) or
open, by ablation of the kidney stone. The nephrectomy is recommended in
inflammatory destructive specific and/or nonspecific processes, or in tumoral
processes. Sometimes great difficulties are encountered due to anarchic
vascularization, kidney position and to adhesion with organs in the vicinity.
5. Rotation anomalies.
During kidney migration from the pelvic region to the lumbar region, a
kidney rotation is also produced; the kidneys in normal position have the renal
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pelvises medially oriented and the calix is external. In the absence of rotation, the
renal pelvis is anterior , while the calyx are medial or posterior facing; in case of
rotation excess, the renal pelvis is posterior facing, and the calyx have an anterior
orientation and, in case of insufficient rotation the renal pelvis is facing outward and
the calyx have a medial orientation.
6. Vascular anomalies.
Several types can be observed: polar cranial or caudal veins and double or
qudruple principle renal vessels. The anomaly involves only the aorta and the
corresponding vein, or in some cases it involves only the vein. Principle renal vessels
anomalies are frequently the reasons for obstruction at the level of pielo-ureteral
junction (UPJ). Inferior polar vessels are often the cause for a hydronephrosis. By
polar vessel sectioning, ischaemia and aseptic necrosis are produced in the
parenchymal section that is irrigated in the corresponding vessel. For this reason,
when it is possible, vascular cross is preferred to the alternative of a ligation followed
by sectioning the vessel with the stroke of the corresponding renal pedicle.
The diagnosis is established based on clinical symptoms (hydronephrosys
symtoms): diffuse lumbar pains, sometimes colicative pains, pyuria, fever in case of
associated infection, or hematuria, when kidney stones appear. The most used
investigations are: the ultrasound that identifies the dilation of colecting system and
sometimes kidney stones and can outline the vessel if the Doppler module is used;
IVU that in addition provides information about the functional details of kidneys and
emphasizes the vascular imprint at the UPJ level; retrograde ureteropyelography
provides more accurate evidence, and the angiography precisely outlines the
anomalous vessel or the anomalies related to renal pedicle elements.
B. Ureter anomalies.
They are usually associated to kidney anomalies. They can be classified as
follows:
1. Number anomalies. Unilateral agenesis accompanies the renal agenesis
and it is complete, the trigone on the corresponding side being also missing. Bilateral
agenesis is life incompatible.
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Fig. 1.7. Retrocava ureter.

Ureteral duplication is an anomaly that is related to a kidney with double
collecting system, or rarely, to a supernumerary kidney. Triple or quadruple ureter are
very rare anomalies.
2. Diameter anomalies. Congenital ureteric stenosis are situated at the level
of UPJ, or in the vicinity of ureter-bladder junction at the level of juxtabladder ureter.
The megaureter is the dilation, sometimes colossal, of the ureter on its entire length,
with important tortuosity, or only segmentary, due to obstruction (stenosis), or
through bladder-ureter reflux . Ureterocele is the cystic dilation of the terminal ureter.
3. Position anomalies
retrocaval ureter is a very rare
anomaly in which the ureter,
usually the right one, crosses the
vena cava at the level of L3
vertebrae, then passes on the
posterior side and then on
medial and anterior one, coming
back in the iliopelvic region in
the normal situation (fig. 1.7). Along the way, the ureter is compressed by the vena,
caught in adhesion and fixed to the vertebral plan, making an obstacle to the passing
of urine, with consecutive hydronephrosis. The diagnosis is possible when
performing a urography and especially a ureteropyelography. The concomitent
cavography provides specifications. The treatment is surgical. The conservative
attitude consists in the cross of ureter and of the vena by sectioning the ureter and pre
or lateral vena cava anastomosis.
4. Anomalies related to the ureter opening can be in the bladder, but in
abnormal position. The condition is discovered especially in women. In women, the
ectopic orifice can open in: the vestibule, urethra, vagina, ureter, and in men, in
prostatic urethra, seminal vesicle, ejaculatory channel. Bilateral ectopic is extremely
rare.


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II. INFERIOR URINARY TRACT AND MALE GENITAL
APPARATUS ANOMALIES
A. Urinary bladder anomalies
1. Cysts and urachus fistulae. The urachus cysts are due to persistency of
middle segment of allantoic channel. They contain: urine, serum liquid, mucus, puss
or blood. The urachus fistulae are due to the absence of obliteration of allantoic
channel at the level of umbilical extremity.
2. Diverticulum de urachus is due to the persistency of the lumen of bladder
extremity. 3.Congenital sclerosis of the bladder neck (Marion disease, Bodian
fibroscleroris, congenital contracture of the Duckett bladder neck). It is clinically
manifested by obstructive syndrome: pollakiuria, dysuria with bladder response, and
then high cervical disectasia, in other words renal impairment. Treatment consists of
transurethral resection of bladder neck or cervical plastic Y-V (Young).
4. Bladder exstrophy- is a rare congenital anomaly, encountered mainly in
male. It is a complex anomaly that involves not only the bladder, but also the
abdominal wall, the skeleton, urethra, the ureters and the genitals. Essentially, it is
about the absence of the wall anterior to the bladder that leads to the fact that the
surrounding teguments are in permanent contact with the urine; complete dehiscence
of abdominal drepti pubic symphasys, the absence of sphincter apparatus. Under the
symphasys is located the gland and the deformed penis, shortened in a cranio-caudal
sense. The anterior wall of the urethra is missing (penopubic or bladder epispadias).
The prostate is missing. The testicles can be ectopic. Bladder mucus, in contact with
ambient environment, is congested, irritated; at this level, septic processes begin.
The prognostic is critical. Renal deficiency, or pyelo-renal infections with
possible septic stages, constitutes the principle causes of death.
Treatment implies rebuilding of bladder tank, urethra and abdominal wall. In
order to fight the incontinence rebuilding of an ileal or rectal bladder, implanting the
bladder trigone in the sigmoid or ureter-sigmoid implantation are requested. By its
simplicity, the cutaneous ureterostomy through an excluded ileal loop (Bricker), was
also requested.


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B. Urethra Anomalies.
These anomalies lead to severe obstructions, life incompatible, but other pass
unobserved or give uncharacteristic disorders that are attributed to other causes.
There are rare anomalies of urethra: congenital absence of urethra, congenital
obliteration of urethra, congenital stricture urethra, congenital anterior urethral
diverticula, and posterior urethral valves. This anomalys characteristic is that the
urethral valves are a major obstacle against elimination of urine, being a real
diaphragm.
1. The Hypospadias is an anomaly of the urethra opening from the ventral
side of the penis. Usually this is small and curved down. The anomaly is the
consequence of a development interruption that leads to an incomplete welding of
genital fold or to an incomplete growth of genital buds. According to the location of
the ectopic urethral meatus, several anatomic forms of hyspodias can be
distinguished: balanic, penian, penoscrotal, perineoscrotal hypospadias (vulviform).
The sponge body stops developing and with him, the urethra stops too and it is
replaced by a tissue blade that keeps the penis curved. Urethral plasty techniques use
skin flaps from the penis or scrotum.
2. The Epispadias is an anomaly characterised by urethra opening on the
dorsum of the penis, at a greater or smaller distance from the gland. There are four
anatomic varieties of epispadias balanic, penian, subpubian and bladder (actually a
bladder exstrophy).
Treatment. In the case of continent epispadias, surgical methods aim urethra
restoration, the removal of fibrous tissues that apply the penis on the pubis. In case of
incontinence (subpubian and bladder forms), the main therapeutic objective is to
ensure continence.
3. Foreskin anomalies foreskin absence, foreskin hypertrophy, adherent
foreskin.
Congenital phimosis. It is characterized by the existence of tight foreskin
orifice, the penis is not-retractable due to the foreskin orifice which is too tight, or
due to the fact that the skin is to adherent to the gland. The balanopreputial sulcus is
the location of infection, ulceration and condyloma. The sexual act and ejaculation
are difficult or impossible. The treatment consists of circumcision (postectomy).
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Fig. 1.8. Migration anomalies of the testis. 1 -
lumbar cryptorchidism, 2 iliac
cryptorchidism, 3 - external inguinal
cryptorchidism, 4 - internal inguinal
cryptorchidism, 5 - prepubic cryptorchidism, 6
- abdominal ectopy, 7 prepubic ectopy, 8
penile ectopy, 9 femoral ectopy, 10 - inguinal
external ectopy
C. Testicular ectopy.
The anomalies in testicle
migration can take place at different
levels on the usual path of the gland
(cryptorchidism), or in areas situated
outside this ectopic route. Thus, the
cryptorchidism can be lumbar, iliac,
inguinal and prepubian, while the
ectopy is abdominal, femoral, scrotal
and perineal (fig. 1.8). The causes of
this anomaly can be represented by
testicular dysgenesis and the absence of
hormonal receivers that make the
testicle insensitive to gonadotropins; pituitary hormonal impairment in case of
bilateral ectopies.
Various authors consider that the risk of appearance of some malign processes
is high for the testicle found in the abnormal position. Medical treatment consists of
administration of chorionic gonadotropin. The hormone shall not be administrated in
ectopies when testicle position is outside the nominal path of descent. Up to 5 years
old, 1000 -5000 U.I. of chorionic gonadotropin in cryptorchidism is recommended.
Surgical treatment is recommended in testicular ectopies and in cryptorchidism that
do not respond to administrated hormonal treatment and consists of discovery,
preparation, descend and fixation of testicle in the scrotum.

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Although located deep and protected by skeleton and strong muscle mass, the
urogenital system is subjected to vulnerable agents. As the lesion communicates or
not with the outside through a solution of continuity of the skin (skin wounds), there
are two varieties of trauma: closed trauma (contusions) and open trauma (wounds).
Urogenital wounds are more rare than contusions and more common in wartime.
Below are described the main aspects of diagnosis and treatment of closed
trauma of urogenital system.
I. KIDNEY CONTUSIONS
Etiopathogenesis. It is more common in men than women and it is more
common in adults. The right kidney, due to its lower position, is more vulnerable,
often being affected.
The hydrostatic pressure from the kidneys, which is an organ filled with
blood, and the particular friability of the renal tissue, are contributing factors of renal
contusions.
Kidney disease is more exposed to contusions by position, or higher volume.
After the production mechanism there are two groups of closed renal trauma:
1. By the direct action of the vulnerable agent to the abdomen, to the
thoraco-lumbar wall or, more rarely, to the spine. Renal contusions appear
from traffic accidents.
2. By indirect mechanism - sudden deceleration, falling from great height by
standing or sitting. The most common lesions by this mechanism are those of renal
pedicle. While the body has stopped suddenly, the kidney and other parenchymal
viscera (filled with blood - "heavy") tend to continue the movement, leading to the
rupture of the pedicle. Renal trauma is usually associated with lesions of other
hollow viscera or parenchymal, being actually about polytrauma.
Pathology. Lesions interest two components of the kidney.
1. Parenchymal lesions are hemorrhagic and ischemic.
a) Subcapsular hematoma. When the renal capsule is intact, after a minimum
superficial fissure, single or multiple, or when deep lesions are produced, interested
in parenchyma, associated with or without calyx and renal pelvis lesions, hemorrhage
2. Urogenital apparatus trauma
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Fig. 2.1. Different types of renal contusion. A -
partial sissure; B - kidney explosion, C -
subcapsular hematoma with external fissure, D
fissure that opens in the colecting system; E -
fissuree open in the renal pelvis F - subcapsular
hematoma limited to the cortex fissures.

is followed by an accumulation of subcapsular blood, making subcapsular hematoma
(fig. 2.1.). Subcapsular hematoma may or may not be associated with hematuria, as
the excretory pathways are affected or not.
b) Perirenal hematoma. When renal capsule is affected, blood flows
perirenal, making a perirenal
hematoma. Associated parenchymal
lesions may be discrete (single or
multiple fissure), with direction to the
organ hilum, always associated with
bleeding. Sometimes parenchymal
lesion is more serious and it is
associated with damage to the capsule
and excretory pathways, making c)
renal rupture (Fig. 2.1.). Depending
on the intensity of the trauma occurs
d) crushing or e) kidney explosion
sometimes associated with pulling
from the pedicle, the worst aspect
lesions (Fig. 2.1.)
2. Pedicle lesions - the
most common renal pedicle is
detached in block at the hilum,
parenchymal lesions and excretory pathways are associated.
Sometimes tears by pulling the renal artery or vein may be total, causing a
massive retroperitoneal hemorrhage, with the formation of a voluminous
retroperitoneal dissecting hematoma, rapidly progressive, associated with collapse,
hemorrhagic shock and death by rapid and massive bleeding. When the vulnerable
agent is less intense, renal pedicle fractures can be partial, causing vessel
thrombosis, or scar stenosis, with post-traumatic arterial hypertension. Hematuria
does not accompany the isolated lesions of the renal pedicle.
3. Intrarenal excretory pathway lesions (calyx, basin) are rarely isolated
explaining the urine going in the retroperitoneal space, often associated with fissure
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or parenchymal rupture, being accompanied by hematuria of variable intensity.
Usually, however, hematuria is massive, leading even to acute urinary retention by
clots.
4. Associated lesions. Parietal peritoneum ruptures are more common,
fractured ribs (ribs 11, 12), fractures of the transverse apophyses of lumbar vertebrae,
pelvis fractures, contusions of the abdominal organs (liver, spleen, pancreas,
stomach, intestine, etc. ). Perirenal fat is the place of a rising blood forming perirenal
hematoma.
CLINICAL MANIFESTATIONS
Case history should highlight the conditions in which the trauma was
produced, the nature of the vulnerable agent, traumatic consciousness, etc.
Sometimes these data can not be supplied by the injured.
Clinical signs are general and local.
The general symptoms vary depending on the severity of lesions, during the
first hours after the accident are general signs of traumatic shock: pallor, arterial
hypotension, tachycardia, low pulse, slightly depressed, cold sweating, agitation,
dizziness, or coma.
Local signs:
pain is sometimes violent, sometimes of a lower intensity. The location of
pain is usually in the lumbar region, sometimes in the flank or
hypochondrium. There is no proportionality between the pain intensity and
the importance of renal lesions.
Hemorrhage. The kidney is a highly vascular organ. Any injury causes
bleeding. After the way that blood is flowing from the place of contusion it
can cause hematuria, when the blood enters the main excretory pathway.
Perirenal hematoma occurs when blood flows around the kidney, bringing
kidney fat. Internal hemorrhage occurs when blood leaks into the peritoneal
cavity through a fissure in the parietal peritoneum, usually posterior.
Hematuria may be absent in situations where the ureter is blocked by a clot,
or ruptured, and in cases where renal pedicle is pulled.
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Fig. 2.2. IVU renal trauma

Inspection reveals sometimes skin lesions, bruising localized into lumbar
region, bringing valuable information about where the vulnerable agent acted and
sometimes even on its intensity.
Palpation of a consistent formation in flank or lumbar, associated with
muscular defense is very likely to be a retroperitoneal urohematoma, whose
evolution will be observed clinically and in ultrasound at short intervals. Clinical
examination must detect associated lesions: skeletal, visceral, thoracic, but primarily
abdominal. A renal concussion can lead to muscular defense, or even a localized
abdominal contracture retroperitoneal urohematoma, it is sometimes very difficult
to distinguish from a localized peritonitis.
LABORATORY EXPLORATIONS. It is harvested from the emergency
room: hemogram, hematocrit, renal function tests, blood glucose, coagulation. The
decrease in hematocrit values to the values initially found means persistent bleeding.
IMAGING INVESTIGATIONS
KUB X-ray) - informs on the status of the skeletal system x-rays (ribs, hip
bones, spine), the presence or absence of psoas shadow (lumbar hematoma), the
presence of pneumoperitoneum.
IVU is made in emergency before any patient with macroscopic hematuria,
in shock, but with systolic arterial tension values above 70 mm Hg or in case of
palpable lumbar hematoma inform the morpho-functional status of the contralateral
kidney and also provides information
on the traumatized kidney. Thus, the
kidney can be normal morpho-
functional, something that does not
exclude renal trauma with a very
important renal hematoma.
Sometimes, one can observe an
extravasated of a contrast agent
intraparenchymal (interstitial
hematoma), or perirenal
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Fig. 2.3. CT right renal trauma
(retroperitoneal hematoma). The kidney can be non-functional (renal artery rupture,
obstructed urinary tract by clots, or when the injured kidney is compromised
morpho-functional previous to trauma) (Fig. 2.2).
Chest X-ray inform about the integrity of the ribs, allows assessing the
existence of pneumothorax or of hydrothorax (hemothorax).
Computer tomography (CT) - is the
most important paraclinical investigation in
cases of renal trauma. It sets the renal pedicle
integrity, renal rupture lines, the size of
retroperitoneal hematoma. It gives information
on the morpho-functional state of the opposite
kidney and on the intraperitoneal abdominal
organs. (Fig. 2.3).
Renal arteriography is less used since the CT entered in current use. It is a
very accurate investigation, which gives the most accurate informations on the renal
pedicle and on the vascularization of renal parenchymal trauma. Reveals the
presence of aneurysms, arteriovenous fistulas, arterial thrombosis and posttraumatic
arterial stenosis.
Ultrasound - unlike the radiological investigations mentioned before, it is a
purely morphological method of investigation. It provides important details on the
integrity of renal parenchyma, the presence of subcapsular or perirenal hematoma
and their size. It is available at the bedside whenever the situation requires, being a
valuable investigation for determining the development of the hematoma and thus in
the therapeutic attitude tracking. Also it informs about the state of other abdominal
parenchymal organs (liver, spleen, pancreas). Instead it does not provide a large
range of information or the accuracy of the CT and arteriography of the renal pedicle.
Doppler ultrasound increases the accuracy of the ultrasound about the damage of the
renal pedicle.
EVOLUTION
In most of the cases, the evolution is favorable with spontaneous
disappearance of hematuria, the return to normal of the heart rate, arterial tension
(AT) and the stabilization limits of lumbar hematoma. Sometimes the evolution is
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severe, bleeding continues and lumbar hematoma increases in size, requiring
emergency surgery for the purpose of hemostasis (renal suture, partial nephrectomy
or nephrectomy). Sometimes, in a variable interval, between 8 days and 2 months,
when everything seemed to come into normal, signs of a major internal bleeding
appear, with signs of hemorrhagic shock with or without abundant hematuria, by
kidney rupture. Emergency surgery is required.
COMPLICATIONS
Bleeding occurs as a perirenal hematoma with a two-stage evolution, or as a
total hematuria.
Early infection of the urinary tract. Late complications are: posttraumatic
hydronephrosis, after a interstitial hematoma is formed, with progressive dilatation
and renal parenchymal destruction. Urohematic cyst, posttraumatic hydronephrosis
and arterial hypertension of posttraumatic renal origin that is caused by renal vascular
lesions, such as arteriovenous aneurysm.
DIAGNOSIS
Renal contusion diagnosis relies on case history (information on the
circumstances of the accident) and on the cardinal symptoms (hematuria and pain).
In addition, the lesions associated with other viscera must be specified (abdominal or
thoracic), which almost always coexist. To specify the type of renal injury and to
determine the prognosis and therapeutic attitude in conditions of renal contusions,
described radiological explorations and ultrasound are indicated. From the beginning
it should be noted that at 3-6 months after trauma, an ultrasound and an urography
examination will be performed to assess the progress of the perirenal scar and / or
retroperitoneal, with secondary effects on urinary paths and on renal pedicle.
TREATMENT
Statistics show that 80% of the renal contusions receive a conservative
treatment consisting of:
compulsory bed rest;
shock removal when necessary;
monitoring of vital functions and of the development of renal trauma;
pain relievers;
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preventive antibiotics;
Perfusions for balancing volume and electrolyte and for diuretic effect.
When with all the above measures the hematuria persists and / or perirenal
hematoma increases and it is associated with signs of anemia and the general
condition declines, the question of surgery appears, which should be conservative.
Nephrectomy is required only in cases of irreversible kidney damage, or where vital
necessity requires. The access path is represented by a lobotomy or a laparotomy
which allows the treatment of any associated abdominal injuries. Surgery consists of:
evacuation of retroperitoneal urohematoma;
simple fissure, unique, is sutured with wires in X, polar localized lesions can
be followed by partial nephrectomy. Large lesions, explosive, pediculare
lesions, that are not easily rebuilt require nephrectomy;
ensuring a safe hemostasis;
effective lumbar drainage
The patient will be followed from 6 months to assess the degree of functional
recovery and the occurrence of late complications, which may require secondary
surgical therapy.
II. URETER CONTUSION
It is an exceptionally rare lesion because usually the ureter, with its small
volume, the elasticity and the mobility, runs from the vulnerable agent. Rarely, by
association, the abdominal viscera may be affected. Treatment is always surgical and
it is aiming to restore the continuity of the ureter and treatment of abdominal organs
lesions involved.
III. BLADDER INJURIES
The bladder is located on the pelvic floor, behind the symphysis pubis. Bones
and pelvis muscles give good protection.
Bladder injuries are more common in men and can be divided into open
(wounds) - more frequent during the war and closed (tearing, contusion, perforation),
produced by an external agent and commonly associated with fractures of the pelvis
bone. Iatrogenic bladder injuries result frequently after gynecologic interventions or
endoscopic urological operations (resection of bladder or prostate).

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Fig. 2.4. Median antero-posterior section,
bladder and urethra male. 1 - abdominal
muscles, 2 - bladder, 3 - peritoneal
cavity, 4 - rectum, 5 - prostate, 6 pubic
area, 7 - urethra.
CLOSED TRAUMA
ETIOPATHOGENESIS
1. Determinants - Vulnerable agents act directly or indirectly:
a) Direct - when the vulnerable agent acts on the inferior abdominal level, the
bladder is projected posterior on the sacrum, whose resistance causes a counter-
stroke.
b) Indirectly - by fall - lesions have a
complex mechanism: shock force tends to
move the bladder in the direction of action;
in return, the bladder is immobile because of
fixing means. If the energy of these forces
exceeds the strength of the wall, it breaks.
2. Contributing factors:
endocavitary hyperpressure - liquids
are not compressible, so the
hyperpressure produced is
transmitted in all directions, giving the bladder wall in its weak points (Fig.
2.4);
the degree of bladder filling a full bladder is directly exposed to shock.
Bladder wall thinning yields in areas with low elasticity;
areas of low resistance - superior and posterior wall of the bladder;
pathological states of the bladder cause serious lesions: bladder stasis,
infection, tumors, diverticulitis, old scar lesions; alcoholic patient bladder,
diabetic, cirrhotic, neurological bladder, etc.. Perforations occur after
diagnostic or therapeutic endoscopic maneuvers.
PATHOLOGY
Closed bladder trauma can cause tears, contusions and perforations.
Contusion - usually single, rarely multiple, have irregular borders. When
placed in the bladder dome, there is a possibility of involving the parietal
peritoneum which covers the bladder at this level, making a direct
communication between the bladder and the peritoneal cavity. In contrast,
lesions of the other bladder walls are subperitoneal.
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Fig. 2.5. Subperitoneal rupture of the bladder. a Filling cystography extraperitoneal
extravasated contrast agent; b - scheme.
Perforations like ruptures, they can be intra- and extra-peritoneal; single or
multiple; punctual or with irregular edges.
Bladder explosions make multiple fractures, with irregular borders, that
accompany the perivesical hematoma.
SYMPTOMS
Bladder injuries are often associated with other visceral injuries and with
fractures of the pelvis. As the most frequently encountered, they will be pesented
below.
1. Subperitoneal bladder injuries (fig. 2.5):
intense hypogastric pain, after light fractures;
perivesical hematoma (in pelvisubperitoneal space) which is perceived
as a tumor on palpation and rectal palpation, with muscular defense.
Sometimes can occur even muscle contracture;
signs of traumatic shock and / or bleeding (pallor, cold sweat,
tachycardic pulse, weak, with hypotension);
micturition is common, painful, with bloody urine. "The rush" of urine
in the perivesical space makes a false urine retention.
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Fig. 2.6. Intraporitoneal rupture of the bladder. A -
IVU with intraperitoneal extravasated contrast agent; b
- scheme.

2. Intraperitoneal bladder
injuries (fig. 2.6):
hypogastric pain after
trauma plus peritoneal
irritation signs;
abdominal pain located in
the hypogastrium or
generalized, especially
when urine was
previously infected;
limited muscle contracture in hypogastrium or generalized;
on rectal palpation the fluid accumulated in the peritoneum an be found, this
exam is very painful due to peritoneal irritation
signs of septic shock, usually;
malaise, nausea, vomiting.
In the forms with uninfected urine the clinical panel is more dimmed. Urinary
signs point to the suffering bladder. Hematuria is often macroscopic, overall,
associated with dysuria, urinary frequency and bladder tenesmus when the solution
of continuity is high, urine flows entirely in the peritoneal cavity, making the picture
of urine rentention without bladder globe, no urine in the first 24 hours can simulate
anuria.
DIAGNOSIS
The place of action of the vulnerable agent, pelvic lesions, endoscopic
maneuvers made recently, have an indicative value for the diagnosis. Diagnosis is
based on trauma history that cause urinary symptoms.
KUB X - ray highlights consecutive bone trauma injuries (fractured pelvis,
spine);
IVU shows morpho-functional integrity of the kidneys and ureters, bladder
injury will be highlighted on the cystogram or on the clich of urographic
cystography, by perivesical extravasation of the contrast agent;
Retrograde cystography is the most important investigation. The of antero-
posterior and oblique x ray incidence will reveal perivesical extravasation of
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the contrast agent, or peritoneal cavity; sometimes it can be seen in the
parietal-colic niches. Uretro-bladder catheter by which the dye was
introduced will be clamped, and then compare the amount of contrast agent
introduced to that obtained by removal of the catheter. In the subperitoneal
bladder ruptures a variable amount of liquid is recovered, while in the
intraperitoneal bladder ruptures a small quantity of fluid is recovered, or not
at all;
Ultrasound shows perivesical fluid accumulation, pelvisubperitoneal or in the
peritoneal cavity, when bowel loops are observed in the fluid in the peritoneal
cavity;
Instrumental investigations involves a risk of infection;
Laboratory exploration - reveals anemia, haemoconcentration,
hidroelectrolyte disorder and hematuria.
TREATMENT
If diagnosis is not certain, before any suspicion, exploratory intervention is
necessary.
Therapeutic measures at emergency are aimed for shock and hemorrhage
treatment
Contusions and perforation heals on uretro-bladder catheter for 7 days,
involving an anti-infective and an anti-inflammatory therapy.
Treatment of subperitoneal bladder ruptures require surgery with bladder
opening and suturing of the lesion. Bladder drainage of the uretro-bladder
catheter 7-10 days and prevezical drainage.
Peritoneal cavity exploration it is mandatory to discover and treat any visceral
injuries. Antibiotic therapy and hidroelectrolyte rebalancing measures are associated.
Treatment of intraperitoneal bladder rupture requires surgical exploration on
emergency of peritoneal cavity and the bladder. Cystorrhaphy of the bladder
wall, and lavage of peritoneal cavity. Bladder drainage of the uretro-bladder
catheter.
Treatment of bone lesions will be done by trauma specialists and by
orthopedic specialists.

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Fig. 2.7. Urethra rupture above urogenital diaphragm. a - scheme urinoma and
hematoma subperitoneal extent b - Digital rectal examination reveals the prostate
located above compared to the normal position.

IV. URETHRA TRAUMA
Their incidence is higher in men. After their location they classify in:
posterior urethral injuries,
anterior urethral injuries.
2. POSTERI OR URETHRAL I NJ URI ES
The most common posterior urethral injuries occur in the membrane segment
level which crosses the urogenital diaphragm. At this level the membranous urethra
can be broken by shear.
ETIOPATHOGENESIS
The most common causes of posterior urethral injuries are road accidents,
work and sport accidents. A smaller number of causes are iatrogenic lesions during
endoscopic maneuvers with diagnostic or therapeutic purposes. Vulnerable agents
act:
directly, by kicks or falls on a hard body, or as a result of exploratory or
therapeutic maneuvers (cystoscopy, urethroscopy, surveys, urethral dilation,
etc.).
indirectly urogenital diaphragm muscles are inserted on pubic posterior
branches, which makes in the bone fractures with displacement, membranous
urethra to be broken by shear to the prostatic apex (Fig. 2.7).
PATHOLOGY
Most urethral trauma are closed (fractures, perforations), rarely open trauma
are observed (wounds). Iatrogenic injuries are usually perforations.
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Ruptures can be complete (involving all the circumference of the organ and
moves the urethral ends) or incomplete (involving only one part of the
circumference).
Perforations can involve all layers of the urethra (total), or only one layer
(partial).
SYMPTOMS
The symptoms are: perineal pain, total hematuria, dysuria, especially in
incomplete ruptures or complete retention of urine (bladder globe).The urethrorhagia,
quasiconstant sign and traumatic and hemorrhagic shock signs.
IMAGING INVESTIGATIONS
X-ray of the pelvis is mandatory. In several incidents, it highlights pelvis
fractures.
IVU gives data about superior urinary status.
Retrograde urethrocistography - usually the constrast agent enters the
prostate-bladder perineal space in complete ruptures, while in the incomplete
ruptures dye enters the bladder and then opacifiers it.
Ultrasound reveals the bladder globe in the complete ruptures of the urethra;
perineal ultrasound reveals perineal hematoma. For the infection risk
exploration tools are contraindicated.
DIAGNOSIS
To any patient with pelvis fracture which can not urinate, posterior urethral injury
is presumed. Highlighting the globe bladder is an addition to diagnosis, and if it is
missing is assumed that there is also a bladder lesion usually involving the
peritoneum. For the avoidance of doubt urethral catheterization with a soft catheter is
made:
When the urethrovesical catheterization follows easily the urethral damage is
unlikely, but can not be excluded;
Catheterization flows with difficulty, the injury is certain, especially if there
isnt a history of strictures;
When the catheterization can not be performed there is an urethral rupture
with movement of urethra ends.
Imaging tests mentioned before confirm these assumptions.
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COMPLICATIONS
They are mainly represented by: urethral strictures, erectile dysfunction and
incontinence of urine.
TREATMENT
State of shock therapy;
Ensure the urinary drainage by cystostomy, to resolve the eventual bladder
lesions if they are found. Cystostomy will be maintained approximately three
months.
Reconstruction of the urethra (urethroplasty) is performed after 3 months,
provided that the perineum to be flexible (the perineal hematoma is
completely absorbed).
Sometimes urethroplasty takes place in one time, on emergency, when bone
fractures and large perineal hematoma does not occur. After the dissection of
the two urethral ends and their resectuion into healthy tissue, it is sutured
together with absorbable wires, on a modeled urethrovesical catheter.
Cystostomy, is made for urethroplasty, is suppressed after clearing the urine,
usually after 4-5 days, and the urethrovesical catheter after 3-4 weeks, after
which the patient will resume urinating.
Internal optic urethrotomy (IOU) is followed by less well over time results in
post-traumatic strictures, when this intervention can be made. Sometimes
drilling scleral scar tissue from the injured area is necessary.
2. ANTERI OR URETHRAL I NJ URI ES
The anterior urethra extends from the urogenital diaphragm to meatus and it
has three segments: bulbar, perineal and penile.
ETIOLOGY
The most common anterior urethral injuries occur by dropping riding on a
hard body, the urethra is traumatized between this and pubic symphysis. Other
mechanisms are blows in the perineum (sports, conflicts) or bending of the penis in
erection. Anterior urethra can be injured during catheterization, dilations or
introduction of foreign bodies in erotic purpose.


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Fig. 2.8. Posterior urethral injury below
urogenital diaphragm with scrotal
hematoma

PATHOLOGY
Anterior urethral injuries are closed (contusion, rupture, perforation) and open
(wounds).
Contusions are injuries resulted by crushing the urethra through the
mechanism described above, without interrupting the urethral duct.
Ruptures are total, when they involve all layers of the urethra, urethral lumen
communicates directly with the periurethral zone and partial, when one or
two urethral tunics are involved. Thus, they can be internal (involving
mucosa and spongy), interstitial (involving spongy) and external (involving
spongy and fibrous).
Perforations are total or partial: internal or external.
SYMPTOMS
Bleeding from urethra is a
symptom seen in all cases and it is
installed immediately after the accident.
Dysuria is intense, reaching up to the
complete urine retention. Living pain
appears in the time of the accident, located
locally and generally in the perineum.
Periurethral hematoma, by blood and
urine accumulation, causes the appearance
of a perineal swelling more or less painful,
, not exceeding cranial urogenital
diaphragm (Fig. 2.8). Through rectal
palpation pelvic structures are normal. Through contact with septic urine, hematoma
may become infected, causing abscess or phlegmons.
DIAGNOSIS
It is based on history of recent trauma, the presence of abrasions, local
bruises and appearance of evocative symptoms. Retrograde uretero cistography
shows the place of trauma and contrast extravasation, which means ureteral injury.
COMPLICATIONS
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Heavy bleeding after the lesion of spongy body stops by compressive
bandage. Local infections, manifested as abscesses and periurethral phlegmon,
requires surgical approach, multiple incisions and drainage, under the protection of
suprapubic urinary derivation (cystostomy). Urethral strictures at trauma place are
common complications that are resolved through optic internal urethrotomy (OIU).
Surgical reconstructions are relatively rarely required.
TREATMENT
a) The contusions of the anterior urethra, the ruptures and the perforations
followed by a light and transient urethrorrhagia, without mictional distress, does not
require complementary treatment. General treatment: pain relief, antibiotics and
unspecified anti-inflammatory, being sufficient.
b) Urethral ruptures with urohematic effusion, which may involve the
scrotum, perineum and the anterior wall of the hypogastrium, requires multiple
drainage, cystostomy of derivation on emergency. Suture of the urethra may be
applied in case of emergency if the two ends of the urethra can be easily found and
the bleeding can be contained. Otherwise, urethroplasty will be applied after 3
months from the accident, following total resorption of the perineal hematoma.
All these interventions require protection with antibitics in effective doses, if needed
more antibiotics can be administrated. There will be also administrated hemostatics
and nonspecific anti-inflammatory drugs. Further development of urethral trauma is
dominated by the sequelae apperance, posttraumatic stenosis scaring. Rebel stenosis
to dilator treatment has OIU indication and finally urethroplasty.
V. PENILE INJURIES
They are represented by strokes, sudden flexion, especially in the erection
and accompanied by ruptures of the cavernous body and spongy with hematomas
more or less extended. Lesions acompanied by large hematomas can become infected
or fibrous, with consecutive erection distress. In less serious injuries cold local
applications and anti inflammatory drugs can resolve the lesion. In cases with major
hematoma is indicated surgical exploration with evacuation of hematoma, hemostasis
and suture.
The wounds usually meet in campaign conditions. The superficial ones
require simple interventions, the extended ones require complex interventions.
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Scaring of the cavernous body can usually leave the imposibility of erection or
distress.
V. INJURIES TO THE SCROTUM AND TO THE SCROTUM
CONTENTS
Lesions are represented by contusion, ruptures or crushes. Healing can occur
spontaneously, under medical treatment: cold local applications, anti-inflammatory,
antibiotics for prophylaxis, in case of limited lesions. Extended wounds and lesions
require large ablation. Open superficial wounds of the scrotal wall can be solved after
the local cleaning and by per primam suture. Testicular trauma is usually a rupture of
the albuginea. It is often associated with funicular vascular lesions. Usually it shows
large hematoma of hemiscrot. Treatment consists of surgical exploration, evacuation
of hematoma, hemostasis with the preservation of the testicle, or orchiectomy in
lesions older then 6 hours. It is associated with antiallergenics, anti-inflammatory
drugs and antibiotics.
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OVERVIEW
Non specific infections are frequent and raise remarkable problems in the
form of serious lesions, sometimes irreversible, which they produce at the level of
the renal parenchyma or the excretive system. Consequently, the treatment of these
infections is sometimes very difficult and may put the urologist in extremely delicate
instances. Urinary infections appear at all ages. During the first 3 months 75% of the
new born children suffer from them, and then up to 1 year old the number of cases
seriously decreases to 11%. During pre-school age the urinary tract infections (UTIs)
are predominant with females, being usually grafted on a disorder of the urinary
system. During adult age the frequency of the bacteriuria and of UTIs increases with
females, especially while pregnant, more specifically in the second half of the term.
Bacteriuria appears with men over 70 years old with an incidence of 3 4 % while
being connected to obstructive symptoms of the lower urinary tract.
EPIDEMIOLOGY
The pathogens mostly responsible are the Gram-negative germs: Escherichia
Coli, Pseudomonas aeruginosa, Klebsiella, Enterobacter, Proteus; more seldom the
Gram-positive cocci occur: Staphylococcus aureus, Enterococcus.
Out of the numerous groups of E. Coli and Proteus bacteria, only a few are
pathogen at the level of urinary system. Membrane antigens (K) and surface antigens
(H) allow the pathogenic stems to fix on the urothelial cells and ascend from the
bladder to the renal parenchyma. Hence, under certain conditions, some of them
known, some others unknown, the germs hosted by the urinary system end to affect
the renal parenchyma or excretive system, determining several types of UTIs. The
pathogens may penetrate the urinary tract through the following ways and means:
The ascendant way (urogenous), more frequent with women due to the short
urethra and to the proximity to the perineal-anal region, facilitates the
contamination of the urinary system. The ascension of the germs to the
bladder is facilitated by the vesicoureteral reflux. With men, the frequency of
3. Non-specific infections of the
genitourinary system
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UTIs is incomparably lower due to the length of the urethra and to the
antibacterial properties of the prostates secretions.
Hematogenous way. Out of numerous extraurinary infections, germs get into
the blood. If they are pathogens for the urinary system and moreover, if they
find favorable field (general and local predisposing factors), they may cause
urogenital infection, mainly at the level of parenchyma organs (kidneys,
prostate, testis).
Lymphatic way. This is a fairly rare propagating means of the infection. The
starting point is usually an inflammatory disorder of a proximal organ (colitis,
cervicitis, prostatis).
Iatrogenic way relatively frequent nowadays due to the endoscopic
treatment and diagnosis methods, it is the result of an innappropriate
instrumentation of the urinary system. A series of saprophite germs that
sometimes may become pathogens are thus introduced up to the bladder or
the ascending urinary tract.
Local predisposing causes are related to the urogenitary system:
Existence of a continuity solution at the level of urothelium (calculi,
ulcerated tumours, subsequent lesions).
Disorders in the physiologic flux of evacuating urine: obstacle, compression,
spasm, inflammation, which accomplish different degrees of urinary stasis.
The urinary stasis is the most frequent and important local predisposing
factor.
Deficiency of defence mechanism of the bladder under the condition of
urinary stasis (sub bladder obstacle, neurogenous bladder) and of the
consecutive congestion of the bladder mucosa it increases the parietal
permeability and alters the mucoproteic structure of the mucosa.
Vesicoureteral reflux. It plays a significant role in making UTIs chronic. The
vesicoureteral reflux occurs in acute cystitis due to the oedema and
congestion of the mucosa of the ureter orificeand determines a functional
insufficiency of the vesicoureteral junction.
General pathologic causes: endocrine or neurovegetative disorders, diabetes,
systemic diseases, colitis, chronic constipation etc. all constitute general factors
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that favour and have an important role in the occurrence and chronicization of the
UTIs.
Knowledge of ethiopathogenic mechanisms of UTIs is necessary for an accurate
diagnosis, as well as for an appropriate therapeutic conduct.
PATHOLOGY
It has been well known that staphylococcus has a peculiar affinity to the
parenchyma and the Coli bacteria to the urinary tract. The causes of these germs
behaviour are unknown.
The infection may either directly approach the renal parenchyma or get
propagated down the urinary tract. When it is gets up to the renal parenchyma, the
lesions may be inflammatory (pyelonephritis) or supurative (pyonephritis) and may
result in the more complicated perinephritis; in case the infection persists,
pyonephrosis of the sclero-atrophic kidney represents the terminal stages of the
pyelo-renal infections.
DIAGNOSIS
It is difficult to put a diagnosis sometimes due to the varying character of the
symptoms or some other times to the poor symptomatic pictures. The settlement of a
diagnosis of a urinary infection must contain the following steps:
Knowledge of the source of infection. Its discovery needs a close
interdisciplinary cooperation (urologist, gynaecologist, general medicine
etc.).
Confirmation of the urinary infection. This is the decisive stage in the
diagnosis of an infection.
The urinalysis shall highlight the leukocyturia, the presence and type of germs. The
Addis test (minute leukocyturia) is a quantitative confirmation of the pyuria.
The negative result of the urine culture urinalysis is interpreted as follows: if the
leukocyturia and germs are not present in the urinary sediment sample, the urinary
infection may be excluded; if the leukocyturia has an increased value and/or on the
urinary sample a significant number of germs appear, the negative result of the
urinalysis cannot infirm the infection, and the urinalysis must be repeated.
The positive result of the urine culture shall be interpreted as follows:
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1. Under 10,000 germs/ml the result is negative ( sample ingathering
germs);
2. between 10,000 and 50,000 germs/ml, the urinary infection is very
highly probable;
3. over 100,000 germs/ml, the urinary infection is sure.
A persistent leukocyturia with negative result of the urine culture urinalysis
(sterile pyuria) imposes additional investigations in order to identify the Koch
bacteria.
The favouring causes of the urinary infection shall be discovered within a
complex urologic examination. Especially with children congenital malformations
shall be searched, while with aged persons the adenoma or prostate cancer, the
inflammatory urethral strictures etc. shall be focused on.
Additionally to the local favouring causes, the general predisposing factors
must be discovered: diabetes mellitus, neuroendocrine disorders, constipation etc.
The consequences that infections may have upon parenchyma must also be known.
The most serious repercussions of urinary infections are eventually on the renal
parenchyma, as the stasis and the infection are the two major circumstances that
contribute to the malfunction of the kidney.
TREATMENT
The hygienic- dietetic treatment is recommended especially in case of acute
forms and consists in rest, hydration (oral or parenteral), diet low in salt and
condiments.
The symptomatic treatment: antialgics (Algocalmin, Piafen, Fortral),
spasmolitics (Papaverine, Scobutil), sedatives (Plegomazin), nonspecific anti-
inflammatories (Diclofenac, Indometacin, Fenilbutazone), antipyretics (Antipirine,
Piramidon, Paracetamol etc.).
The treatment of local predisposing factors is mandatory, is often the most
important and consists of: high urinary derivation, ablation of a calculus or of a
prostate adenoma, solving a urethral stricture through urethrotomy, etc. Similarly
important is the correct treatment for the equilibration of a diabetes mellitus or for
gynaecopathies with persistent urinary infections as side effects. In acute stages
instrumental explorations must be avoided.
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The antimicrobial treatment. In the case of urinary infections with no stasis,
entitled medical, the antimicrobial treatment is on top of all treatments; in the case
of urinary stasis infections, entitled urologic, the objective is to remove the
obstructive factor which is associated with the antimicrobial treatment. The urinary
infection is usually produced by only one germ as rarely does a combined infection,
produced by associated germs, occur.
CHOICE OF MEDICATION
An antibiotic or a urinary chemotherapeutic must contain the following
conditions:
Appropriate microbial spectrum. The antimicrobial treatment must be
applied focused, according to the antibiogram. In case of acute infections
treatment must be started urgently, before having the result of the antibiogram, and
consists in administering a wide spectrum antibiotic, usually cephalosporin.
High urine concentration in active form. The antibiotic or urinary
chemotherapeutic must be eliminated through the kidneys in active form and have
optimal urinary concentrations. Up to a creatinine level of 1.5 mg%, all these
medications are administered in normal doses; when the levels are higher, in case of
renal failure, the doses shall be adapted in close relationship with the creatinines
level or clearance, by administering the so called urinary doses.
Optimal activity depending on the urinary pH. Neglecting to keep the
urinary pH at a correct level, depending on the medication taken, represents one of
the failure causes with non-specific urinary infections. Urine is acidified with the
help of food diet or with administration of diluted phosphorous acid (1%) 3x40
drops/day, Metionine or Vitamin C, and the alkalinization is obtained with Na
bicarbonate 6-8 gr/day or Uralyt U, Blemaren N or vegetarian diet.
The optimal antimicrobial effect is obtained under the following values of urinary
pH levels, depending on medication:
Sensitive to very acid pH (pH 5-6): Negram, Nitrofurantoin, Peniciline
G, Oxaciline;
Sensitive to acid pH (pH 6-6,8): Ampiciline, Carbeniciline, Colistin;
Sensitive to neuter pH (pH 7): Cephalosporine, Rifampicine, Neoxazol,
sulfamide retard;
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Sensitive to alkalin pH (arround 8): Eritromicine, Tetracicline,
Streptomicine, Kanamicine, Gentamicine.
Nephrotoxicity and general toxicity as reduced as possible. An ideal
urinary antibiotic must completely lack renal toxicity. Short term treatments or
treatment with sub-doses are performed (Kanamicine, gentamicine, Colimicine).
Combinations of antibiotics. In current medical practice a single
antimicrobial agent is being administered within one treatment. Combinations are
used only in cases of serious evolution and in combined infections with germs
sensitive to several antibiotics or chemotherapeutics. When antibiotics are correctly
administered, their combinations reduce the danger of bacterias resistance and have
an increased efficiency.
A. CHEMOTHERAPEUTICS
I. SULFAMIDS
They have bacteriostatic action; out of the non-specific infections of the
urinary tract they and are mostly prescribed in case of acute and chronic cystitis.
Sulfamids were the first chemotherapeutics systematically used for the prevention
and treatment of bacteria infections with humans. They have an important role in
treatment of the non-complicated UTI. They are contraindicated in case of hepatic
medical conditions or allergies to sulfamids.
1. Neoxazol. It has bacteriostatic action on Coli bacteria but is not effective against
Proteus bacteria, Pyocyanic bacteria ans other negative Gram germs. It is rapidly
digested and is eliminated slowly through urine in active form under conditions
of acide pH. The attack dose is of de 6-8 g/day in the first day (3- 4 tablets/6
hours), and then 2-4 g/day for 7-14 days.
2. Sulfametin. It is a sulfamid with extended action. It is not effective against
Proteus bacteria, Pseudomonas and other negative Gram germs, but it is effective
against positive Gram cocci, Chlamydia, Neiserria and protozoa (Toxoplasma). It
is contraindicated in the last 3 months of pregnancy. The attack dose is of 2
g/day for 3 days (2 tablets/12 hours), and then treatment is continued with 1
g/day for 14 days.
3. Trimetoprim. They are antagonistic to the 4-Aminobenzoic acid and interferes
with the metabolism if the folic acid. It is metabolised by the liver and eliminated
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through urine in the form of active metabolites. It has a broad spectrum on
negative- and positive- Gram germs. The dose is of 2x2 tablets/day. It has a
bactericidal or bacteriostatic action, depending on the type of the germ.
II. METRONIDAZOL
It is a synthetic derivative of nitroimidazol, which has an important role in the
treatment of infections with anaerobe germs, as well as in the treatment with
protozoa (toxoplasma). It is active for all anaerobe germs, with bactericidal action,
hence is administered to all patients that have infections with anaerobe germs. It is
well absorbed in the digestive tract and this is why it is orally administered in the
form of tablets, too.
The dose is of 3x1 tb/day. Parenteral administration is done only in serious cases.
Side effects: cephalea, gastrointestinal disorders and neurotoxic effects (dizziness,
ataxy, pheripheral neuropathy).
III. URINARY ANTISEPTICS
II. Nitrofurantoin it is a chemotherapeutic agent with short action, determining
rapid renal elimination and high urinary concentrations. The dose is of 4x1 tb/day
(400 mg/day) for 14 days. It is contraindicated in case of kidney failure.
III. Nalidixic Acid it is a bacteriostatic agent with main action on negative Gram
germs. The dose is of 4x2 tb/day (4 g/day) for 7 days. it is not used with
sucklings. It is contraindicated in case of renal failure. Similarly to
Nitrofurantoin, it causes digestive disorders.
IV. Methenamine. It is rapidly absorbed by the intestine and excreted through urine.
With acid pH it forms formaldehyde with antibacterial effects. The dose is of 4x1
tb/day (4 g/day). It is effective in the chronic forms of urinary infections.
B. ANTIBIOTICS
1. Penicillin with broad spectrum
Ampicillin, Carbenicillin, Methicillin, Oxacillin. They are effective against
positive- and negative- Gram germs, except for Pseudomonas, Klebsiella, some
stems of Proteus and Enterobacter. A series of aminopenicillins (Azlocilllin,
Mezlocillin, Piperacilin) have broad spectrum and are effective against
Pseudomonas aeruginosa.

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Cephalosporins
1
st
generation (C
1
G) (Cefalonium) seldom used, they have an inferior
bacterial spectrum compared to the current agents belonging to new generations.
2
nd
generation (C
2
G). They are frequently used: Cefoxitin, Cefotetan,
Cefamandole, Cefuroxime (Zinacef) against positive Gram germs, but also
against negative Gram germs such as Enterobacter. A series of germs are resistant
though: Clostridium perfringens, Pseudomonas aeruginosa.
3
rd
generation (C
3
G). Despite their broad spectrum against negative Gram
germs, their effectiveness against positive Gram germs is inferior to that of the
cephalosporins in the first 2 generations. Out of this generation the most well
known are Ceftazidime, very effective against Pseudomonas aeruginosa,
Ceftriaxone (Rocephin) and Ceftazidime (Fortum), also effective against P.
aeruginosa.
4
th
generation IV-a, (C
4
G) are Cefepime (Maxipime) - administered in
parenteral manner 1-2 g/12 hours, and Cefpirome the same posology. They are
very sensitive towards Pseudomonas aeruginosa, some stems of Enterobacter and
Serratia.
2.Aminoglycosides are a series of semi-synthetic antibiotics with large spectrum
against negative Gram bacteria. The most used antibiotics belonging to this series
are: GEentamicin, Tobramycin and Amikacin. The group also includes Streptomycin,
Neomycin and Kanamycin. The aminoglycosides are protein synthesis inhibitors and
interferate with the mARN carriage. This mechanism explains the bactericidal action
of these drugs.
They have a high level of concentration in the renal cortex. They are excreted
through glomerular filtrate, attatining efficient urinary concentrations.
The antibiotics belonging to this category of medicines are effective against
Enterobacter, Pseudomonas. They are ineffective against anaerobe germs and have
low action over Gram positive cocci.
Their side effects are ototoxic by destroying the vestibular and cochlear
sensors. They are nephrotoxic through accumulation, after 5 7 days, hence they are
not administered in case of renal failure.
The dose is of 3x80 mg/day with adults, 3x40 mg/day with children.
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The newest aminoglycosides are: Netilmicin (Netromycin); Isepamicin 8-15
mg/ kg body; Spectinomycin (Trobicin).
3. Glycopeptides - Vancomycin and Teicoplanin. They are bacteriocidal against
Staphylococci (aureus and and epidermidis) and bacterostatic against Faecalis
Staphylococcus. They are effective against Enterococci and Clostridium perfringens,
but are ineffective against Gram negative bacteria. They present long half life (70-
100 hours). They are administered either IM or IV (phlebitis may be caused).
4.Aminosides. Netilmicin is used especially in combinations of antibiotics. .
5.Quinolones. Ciprofloxacin, Ofloxacin, Norfloxacin, Levofloxacin and Pefloxacin
are DNA inhibitors. They are effective against Gram positive cocci and Gram
negative aerobes, including Pseudomonas and some Mycobacteria. Elimination is
done via liver and kidneys. They are little bonded to proteins; they are well spread in
the renal parenchyma and reach high concentration levels even in the prostatic
parenchyma. The dose is of 1 g/day (2x500 mg IV or per os.).
6.Macrolides. Chloramphenicol, Erythromycin, Lincomycin and Clindamycin have
an excellent digestive absorbtion and hence are ofted used in ambulatory treatments.
Erythromycin is both bactericidal and bacteriostatic, depending on the blood
concentration. These antibiotics bond well in the intracellulary liquid and have a
good penetration in the prostate. The intravenously administration may cause
phlebitis. They are effective, Erythromycin especially, against Staphylococcus
aureus, Haemophilus influenzae and Neisseria gonorrhoeae. Clindamycin is different
from Erythromycin as it has great effectiveness against some anaerobes (CI
Perfringens). They are protein inhibitors at the level of bacetrial ribosomes.
Macrolides are metabolised by the liver and eliminated through urine. The
adverse effects may be: medullar depression, cutaneus eruptions and diarrhea,
disturbance of equilibrium in microbiota (bacterial flora).
7. Tetracyclines have a broad spectrum bacterostatic effect against Gram positive-
and Gram negative- germs (except for Pseudomonas and Proteus). They are not
administered in the second term of pregnancy and in children up to 6 years. The new
generation is represented by Vibramycin (Doxyciclyne).
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8. Carbapenems. Antibiotics such as: Imipenem, Meropenem, Ertapenem etc.
belong to this class. The first is administered in a dose of 0.5 g/6 hours(2 g/day), and
the second 0.5 g-1 g/8 hours.
Carbapenem are a -lactam antibiotic with broad spectrum used
intrevanously (perfusions). characterized by a powerfull bactericidal action of larger
spectrum of any other known antibiotic. It is resistant to the bacterial -lactamase
enzymes, which confers effectiveness against a large number of germs, mainly:
Pseudomonas aeruginosa, Staphylococcus aureus, Enterococcus phaecalis and
Bacteroides fragilis usually resistant to other antibiotics.
NON SPECIFIC INFECTIONS OF THE ASCENDING URINARY
TRACT
PYELONEPHRITIS
Pyelonephritises represent infections with non specific bacteria with
simultaneous action on both the renal pelvis and the renal interstitium (the space
formed by a connective network separating the uriniferous tubules from the
glomeruli). Practically there are no isolated pyelitises as the inflammatory
processes act simultaneously and constantly on the mucosa of the renal pelvis and
the interstitium. Pyelonephritis is one of the main causes of renal failure. The
medical condition may be mono- or bilateral and, depeding on its evolution, it may
be acute or chronic. Bacteria penetrate the kidney via one of the ways described.
ACUTE PYELONEPHRITIS (APN)
The disease may appear at any age. It is more frequent with females,
especially during pregnancy. It often appears as a complication of the excretory
system, with or without obstruction, or the pathogens may graft on an existing renal
lesion.
PATHOLOGY
The kidney is augmented, may be decapsulated easily, the mucosa of the
renal pelvis is congested, edema marked. The kidney has a smooth, lightly
granulated surface on which little yellow abcesses are noticed. Sectionally, both
medullary and cortical, multiples microabcesses are present. Microscopically,
inflammatory infiltrates with polynucleus neutrophils and abcessed area are revealed.
The tubules contain leukocytes and pus.
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SYMPTOMS
The debute may be sudden onset of fever, shaking chills, degenerated general
state, bilateral lumbar pains irradiating towards hypogastrium, oliguria and
oligoanuria. Pollakiurria, pyuria, smarting pains when urinating are other symptoms
that join lumbar pains; they are less intense in cases of less brutal debut. The renal
pains are weak but still clear enough to assume the renal origin of the infectious
syndrome. Cephalea, asthenia, fatigue, nausea, vomiting are also associated.
Laboratory examinations: urinalysis reveals pyuria and bacteriuria, microscopic
haematuria. The leukocyturia at different times shows an important increase of
leukocytes.
The peripheral blood sample identifies leukocytosis with polynucleus
neutrophils, increased ESR and the haemoculture may be positive.
The bacteriologic test is done directly on the sample with Gram staining on
the germ. The antibiogram urinalysis identifies the germ and tests its
resistance to antibiotics.
The renal functional tests reveal early and constant degenerations of the renal
function. These changes remain for weeks or even months after apparent
cure.
Imagistic investigations
The echography reveals a kidney that is increased in size, with high
parenchyma index (inflammatory process) having a more transonic image
(congestion and edema). The central echogen complex has normal volume and
aspect. When the acute pyelonephritis appears on superior obstructive uropathy,
litiasic or non litiasic, the echographic examination shall reveal dilation of collecting
system and of the ureter and possible echogene images with shadow cones (calculi).
KUB x-ray reveals the renal shadow increased in volume unilaterally or
bilaterally, possible radioopaque calculi.
IVU (intravenous urography) secretion present bilaterally, weker intensity
on the affected part. The ureter also is hypotonic and may be completely opaque up
to the bladder. In case of acute pyelonephritis that develops on a kidney with
ascending obstructive uropathy, the IVU reveals stasis in the ascending urinary tract
and the obstruction, which may be a radioopaque or radiolucent calculus.
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POSITIVE DIAGNOSIS
It is based on the patients antecedents, on the clinical examination and shall
be confirmed by the laboratory and imagistic investigations above mentioned.
DIFFERENTIAL DIAGNOSIS
The acute pyelonephritis shall be differentiated from other general infectious
diseases, of the surgical abdomen, of the renal suppurations and the suppurations of
the perirenal tissue.
TREATAMENT
General and symptomatic. Rest in bed, diet, no condiments, vitamin therapy;
analgesics and antispastics for pain relief (Algocalmin, Piafen, Papaverine, Scobutil).
Medication. The antimicrobial treatment shall be immediately begun the
moment the patient gets hospitalized. A broad spectrum antibiotic is administered,
usually a cephalosporine, until the result of the antibiogram urinalysis is obtained.
Thereafter, the antibiotic or chemotherapeutic substance that is most effective against
the germ is administered, either with or excluding the cephalosporine, until fever
lowers and the urine becomes sterile; the treatment shall then be continued with
sulphamides for 2 3 weeks.
Surgery. If the acute pyelonephritis appears on an ascending obstructive
uropathy, the obstruction shall be removed (the favouring factor of the acute
pyelonephritis): calculus, prostate adenoma, urethral stricture, pyelo ureter junction
syndrome etc.
As far as the efficiency of treatment is concerned, the following instances may
appear:
Healing after 6 months from the treatment end the urocultures remain
sterile.
Relaps of infection after a few months after the treatments end the
infection with the same germ relapses.
The persistence of the infection during the treatment reveals either the
resistance of the germ to the antibiotic or an insufficient dose of the antibiotic
administered.
Re-infection: after a period of sterilization the infection of the urinary tract
with a different germ occurs.
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CHRONIC PYELONEPHRITIS
It is a non specific, chronic microbial inflammation of the renal pelvis and of
the renal interstitium with a persistent infection, on the basis of a congenital disorder
which represents the cause of the perpetuation of the infection. Very often though the
obstruction has been removed and there is no stasis any longer, the chronic
pyelonephritis persists.
PATHOLOGY
In chronic pyelonephritis the kidney presents variable atrophy. It has a
granular aspect with irregular scars. The capsule is adherent, the kidney being
difficult to decapsulate, especially at the level of scars. Microscopically a difuse
inflammatory infiltrate composed of lymphocytes is observed; the scarry areas
present marked sclerosis and glomerular hialinizations. The arteries are thickened,
hialinized, with reduced or obturated lumen.
Pyelonephritis xantogranulomatosa is a particular form of the chronic
pyelonephritis occurring more often after chronis supurated inflammations and
lithiasis.
The kidney is increased in volume and has an adherent capsule; sectionally, the renal
parenchyma presents areas of yellowish colour, sometimes with pseudotumoral
aspect, with abcesses on pyelocaliceal level. Microsopically, a lympho-plasma
infiltrate may be noticed, and occasionally cholesterol crystals surrounded by
gigantic cells pertaining to a different mass.
SYMPTOMS
The chronic pyelonephritis develops in 3 acute stages or may be chronic from
the very beginning. The clinical picture is polymorph and non characteristic. General
symptoms appear in the first year: asthenia, anhemia, cephalea, fatigue, feverish
condition. As far as the urinary system is concerned, the symptoms are of uneasiness
or pains in the lumbar region, disorders of urination (smarting pains, pollakiuria).
The followings may also be associated: digestive disorders, anhorexia, constipation,
alternationg with diarrhea and abdomen swelling after eating.
Within 50 60% of cases the HTN is present. The evolution is prolonged,
interrupted by periods of calmness overcrossed by feverish strokes. In late stage the
symptoms of chronic pyelonephritis are those of the chronic kidney failure.
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The laboratory tests are the same as with the acute pyelonephritis;
additionally, changes pertaining to already installed chronic renal failure appear: in
creased values over normal of the blood urea and creatinin, acidosis, anhemia).
Renal function tests reveal disorders of dilution and concentration and pathologic
values of the tubular clearance.
Imiging tests
Echography shows a kidney reduced in volume, with irregular convexity and
diffusely delimitated, especially in the advanced stages of the illness. The
parenchyma index is reduced, the parenchyma is more echogenic due to the
parenchyma sclerosis processes that are characteristic to the chronic inflammatory
process. Images of calculi may also be revealed in the pyelocaliceal system. When
there are no obstructive conditions (usually lithiasis), stasis is not identified.
Otherwise (lithiasis, congenital malformations etc.) the echography highlights stasis
and the dilation more or less emphasized of the excretory system. The echography
may reveal vesical diverticules or calculi, secondary to a subvesical obstruction
(BPH, postate cancer, urethral strictures); moreover, if the investigation continued, it
reveals the prostate cancer as well as its sizes and volume. The urethral strictures
also may be revealed by the echography, as well as their number and location.
KUB x-ray- reveals possible radioopaque calculi.
IVU offers information that is more or less accurate related to the degree of
the renal insufficiency. In case of chronic renal failure with high levels of urea and
creatinin, it has no indication whatsoever. Yet, in case the renal insufficiency is not
very severe, IVU may reveal a series of pyelocaliceal changes that are the results of
the parenchyma retraction and calyceal hipotony: oblated calices, caliceal bubbles
that are deviated and modify the pyelocaliceal fan.
The retrograde urethrocystography reveals the subvesical obstruction and its
consequences and/or a potential vesico-ureteral reflux.
Renal biopsy lesions with chronic pyelonephritis are few, delimitated at the
beginning, with normal intercalated parenchyma; hence the diagnosis of chronic
pyelonephritis cannot be excluded when renal biopsy shows a normal parenchyma.
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DIAGNOSIS
It is based on the antecedents of the patient (renal lithiasis, BPH, numerous
strokes of acute pyelonephritis) and on the clinical picture. Varying functional
pictures are met with chronic pyelonephritis, which makes interpretation of the
laboratory tests difficult, especially as far as functional tests are concerned.
The laboratory tests provide information about urinary sediment with
numerous leukocytes, microbial germs, especially Gram negative, wherefrom E.
Coli is the most prevalent. When presence of Sternheimer-Malbin cells outnumbers
10% of the urinary leukocytes, chronic pyelonephritis may be diagnosed.
1. Addis test reveals increased leukocyturia.
2. Urinalysis and antibiogram identify the type of germ and its sensitivity to
antibiotics.
3. Renal function tests identify renal tubular insufficiency.
4. The imagistic investigations and eventually the renal biopsy are important for
diagnosis of chronic pyelonephritis and establishment of its etiology.
DIFFERENTIAL DIAGNOSIS
It is done with any arterial hypertension (HTN) and with anhemias lacking
causes; with chronic glumeronephritis, where haematuria is prevalent and at the
beginning only filtration tests are modified, while tubular tests are modified only
later.
It is also done with renal tuberculosis and renal tumors, especially in case of
xantogranulomatosa pyelonephritis.
EVOLUTION
It is variable. Sometimes the renal function is rapidly compromised during
few months. In the most cases the evolution is slow as the parenchyma that is not
affected may ensure a satisfactory renal functioning.
If there is not HTN, a slow relatively benign evolution of the disease with no
vascular changes may be reckoned.
COMPLICATIONS
The most frequent complications are the cases of pyelonephritis as
complications of renal infections, perinephritis and pyonephrosis, a suppurative
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complication with massive damage of renal parenchyma, when usually obstructive
factors are also associated (stenosis, calculi).
TREATAMENT
It is able to cure the chronic pyelonephritis or at least to stop its evolution and
prevent acute strokes.
Hygieno- dietetic treatment: light diet rich in liquids, change of urinary pH
through acidification.
Medication
Killing pains: antialgics and antispastics.
The antiinfection treatment is started with the antibiotic or chemotherapeutic
agent that the germ is most sensitive to, perhaps a combination of antibiotics for 10 -
1 5 days.
When treatment is efficient the leukocyturia should decrease and the
urinalysis findings get negative. After treatment with antibiotics, it is started
treatment with the chemotherapeutic that the germ has been found to be
sensitive to.
Treatment of general or local favouring factors. The factors that maintain
stasis in the urinary system must be treated: congenital disorders, lithiasis, urethral
strictures, prostate adenoma etc. Treatment of HTN.
PYELONEPHRITIS IN PREGNANCY
It appears mainly between the 5
th
and the 7
th
months of the preganancy, more
frequent at women with more than one birth deliveries. The normal clinical form is
not severe and is cured after normal treatment with antibiotics. The more serious
forms appear in the first half of the pregnancy and may be complicated by
septicaemia. The favourable causes are: hormonal hypotony of the excretive system,
hormonal congestion of the urothelium and the mechanic compression of the uterus
of the pregnant woman.
SYMPTOMS
Symptoms are less significant at debut of the condition, but while the disease
develops, fever, lumbar pains, pollakuria, smarting pains, pyuria and bacteriuria
appear.
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Haemoculture is usually positive. Sometimes the severity of the condition is
due to the renal failure and arterial hypertension, the infectious syndrome being less
serious.
TREATMENT
Treatment is the same as in the case of acute and chronic pyelonephritis, but
needs more precautions.
Preventive treatment consists in periodical examinations aiming at finding
of possible proteinuria and oligo-symptomatic bacteria.
Curative treatment antibiotics and chemotherapeutics selected on the
basis of tibiogram, but without including medication with teratogenous effect:
Tetraciclin, Chloramphenicol. The degree of severity of the condition may cause
pregnancy interruption or premature delivery.
PYONEPHRITIS
It is a purulent inflammation of the renal parenchyma with 2 ethiopathologic
possible forms: pyonephritis staphiloccocus metastasis and pyonephritis
complication of an infection of the ascending urinary tract.
PYONEPHRITIS STAPHYLOCCOCUS METASTASIS
ETIOPATHOGENY
The pathogen is represented by the Staphyloccocus aureus, which gets to the
kidney via blood circulation. The starting point is usually a primary focus of
cutaneous infection (furuncle, pyodermitis, panaritium and abscess), seldom
osteomyelitis. Between the apparition of the infections focus and the occurrence of
renal suppuration there is a period of 3 5 weeks, sometimes longer.
PATHOLOGICAL ANATOMY
Three different anatomopathological forms of pyonephritis are known:
disseminated millet size abscesses, large abscesses and renal antrax (carbuncle).
From the pathogenic point of view, the carbuncle represents the septic necrosis of a
part of renal parenchyma belonging to a region irrigated by a lobular artery that is
obstructed by a microbial embolism. Sectionally, the lesion has the form of a
triangle with the angle in the depth of the renal parenchyma whereto it is connected
through an arterial vessel. The carbuncle is separated from the healthy parenchyma
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by a clivage plane that allows its enucleation as a benign tumor. In the moment of
enucleation the arterial vessel, initially embolized, bleeds.
SYMPTOMS
It clinically manifests with fever and pain. The fever is increased and
persistent (suppurative process). The curve is irregular, in plateau, or wavy. The pain
manifests in the lumbar area, is spontaneous or caused and has a varying intensity.
Local examination reveals lumbar region sensitive to palpation. Giordano sign is
present.
Laboratory tests
Urine is clear, with no pathological elements, as long as the suppurative
lesion does not communicate with excretory tracts. The urinanalysis findings are
sterile in the same conditions above mentiones. Haemoculture sometimes reveals
Staphyloccocus aureus. The leukocytosis with polynucleus neutrophils is revealed in
the peripheral blood picture. ESR has increased values.
Imagistic investigations
Echography. In the millet size abscesses the echographic examination is not
conclusive. Perhaps it could provide information about a pole that is increased in
volume with a nonhomogenous structure parenchyma. In the large abscesses forms
the echographic examination highlights a transonic area of variable sizes at the level
of abscessed part and normal echographic structure in the rest of the image. In the
case of carbuncle it is revealed also an area where the echographic structure of the
parenchyma is modified towards non-homogenity: areas that are more transonic
alternate with areas having a more echogenic structure.
KUB x ray does not provide important information for the diagnosis.
IVU especially in cases of renal carbuncle but also in those of large abscess,
images similar to those in cases of tumour are identified: calices that seem
elongated, curved, compressed, deviated. In cases of millet size abscesses the
image of the renal cavity system does not get modified.
Retrograde ureteroscopy provides a better image that that given by the IVU.
CT discovers the intra-renal modifications caused by the inflammatory
process and remaining encapsulated, more or less iodophil, depending on the
intensity of the distructive process. Also, the inflammatory perpendicular
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adenopathy is revealed; the latter is sometimes difficult to differentiate from a
tumour adenopathy.
Arteriography seldom prescribed, it reveals an area that has no blood
vessels in the zone of the carbuncle or large abscess.
Renoscintigraphy reveals that the radioisotope is not fixed into the affected
area.
Pulmonary radiography reveals the hypomobility of the diaphragma in the
affected part.
DIAGNOSIS
In order to put a diagnosis it is very important how it is interpreted a feverish
condition whose cause does not seem obvious; this generally appears with yourng
patients with variable lumbar pain, with clear urine and who has had as antecedents
(in the course of latest weeks) a cutaneous infection (furuncle, panaritium or other
staphyloccocus infection) with hyperleukocytosis and signes of renal tumour
provided by the IVU. In the clinical contest above mentioned the echography, which
cannot reveal a tumour, may nevertheless set the question over a non specific
inflammatory process, a pyonephritis, probably caused by a staphylococcus.
DIFFERENTIAL DIAGNOSIS
The medical condition must be differentiated from other forms of pyelorenal
infections, from neighbouring suppurations and renal tumour processes.
In case of acute pyelonephritis pyuria and bacteriuria are always present, but
IVU does not reveal dezorientation of the collecting system;
In case of acute colecystitis the disease history is characteristic; the
radiological and echographic investigations clarify the diagnosis.
Renal tumour - febrile form the urine has no pathological elements and the
diagnosis is rendered by the imagistic investigations.
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EVOLUTION. PROGNOSIS
Pyonephritis may be cured or may get complicated with a perinephretic
phlegmon or, more rarely, with septicaemia. In rare cases the kidney is completely
destroyed by multiple disseminated supurative centers. The prognosis may be
provided depending on the clinical form and the early start of the treatment.
TREATAMENT
Antibiotherapy (oxacillin, cephalosporines) administered correctly and
especially in early stages of the disease may cure pyonephritis with millet size
abscesses even without after effects. The antibiotics treatment is associated with
antialgics, antipyretics.
The failure of medical treatment imposes a more energic therapeutical
attitude; in the case of renal abscess or furuncle open surgery is indicated from the
beginning. In these cases renal decapsulation permitting opening and drainage of
abscesses or enucleation in the case of renal carbuncle are followed by healing.
With renal abscess the following may be beneficial: percutaneous puncture
wherefrom pus is aspirated, followed by creating a percutaneous trajectory in the
abscess cavity and elimination of purulent contents and then installation of a NP
balloon catheter, with double circuit. The next days this bag can serve for washing
the abscessed cavity with antibiotics. The ballon catheter is removed after 5 days.
Administration of combination of antibiotics with broad spectrum in the course of
the next days is mandatory.
PYONEPHRITIS- COMPLICATION OF AN INFECTION OF THE
ASCENDING URINARY TRACT
With this ethiological form of pyonephritis, the infection of the renal
parenchyma represents the complication of a canalicular infection of the urinary
tract. Hence, neither this form of pyonephritis is a self standing medical condition,
but a complication of a urinary infection already existing.
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ETHIOPATHOGENY
The pathogen is not specific: most frequent E.. Coli, satphyloccocus, Proteus
or associated microbial flora are encountered.
The disease appears as a result of acute or chronic pyelonephritis and
especially as a complication of a vesical-prostate-urethral infection. It represents the
frequent complication of the disectasia of the bladder neck, in the stage of vesical
distension, of the vesical or ureterovaginal fistulas, of ureteral orifice invasive
bladder tomors and ureteral stasis.
The parenchyma is attacked either canaliculary (pyelovein reflux,
pyelocanalicular or pyelointerstitiary, vesico-ureteral reflux) or via blood circulation.
In cases of patients with vesical distension (prostate adenoma) pyonephritis is often
bilateral, extremely serious.
PATHOLOGY
The inflammatory process is prevalent in the medullary area, the suppurating
clusters spread radially, starting from the papilla, in the form of yellowish striations.
The lesions develop further towards diffuse suppurated nephritis or sclerosis chronic
nephritis.
SYMPTOMS
Clinical symptoms: lumbar pains, fever, shivering, vomiting, cephalea,
anhorexia all occurring as a consequence of a pyelonephritis. The kidney is
enlarged, causing pain when palpated, the renal lodge is sensible, Giordano
manoeuvre present.
Laboratory tests: the urine is cloudy (pus and blooc cell). The uroculture is
infected. Hyperleukocytosis and haemoculture usually positive.
Paraclinical investigations: are the same as described in the case of
Pyonephritis metastasis staphylococcus; they must additionally identify the
favouring urinary medical conditions.
The evolution of this pyonephritis is extremely serious and may cause death
within few days; others have a slower evolution, causing damage of the kidney
through diffuse suppurated nephritis (septic kidney), pyo- or nephro-sclerosis. The
whole kidney accommodates disseminated abscesses and the perirenal fatty tissue is
congested and edematous.
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TREATMENT
The treatment consists in: administration of antibiotics, which at early stages
may stop the evolution of the suppurative process at the level of the kidney;
treatment of the urinary condition accountable for the disease: congenital
malformation, prostate adenoma, urethral stricture etc. and ensuring an efficient
urinary drainage. In the cases of renal abscess, the treatment consists in lombotomy,
incision, evacuation and drainage. In the severe cases, nephrectomy is the only
therapeutic method for unilateral lesions.
PERINEPHRITIS
Perinephritis denotes the suppuration of the perirenal connective and fatty
tissue. It is secondary to suppurative processes of the kidney, most frequently to
pyonephritis or pyonephrosis. More seldom, it may be a consequence of a
pyelonephritis or of trauma or surgical perirenal haematoma. There is no primitive
perinephritis. Its frequency has considerably reduced in the antibiotics era but still
remains as option in making a diagnosis on the symptom of prolonged high fever.
ETHIOPATOGENY
The accountable microbial germs are those characteristic to non specific renal
inflammatory processes. Germs penetration is possible either through direct
extension (pyonephritis, pyelonephritis, pyonephrosis) or via blood starting from a
cutaneous or prostatic septic cluster etc.
PATHOLOGICAL ANATOMY
The primitive renal lesion is one of the two original lesions of perinephritis:
pyonephritis and pyonephrosis. Perinephritis may appear under three forms:
1. Sclerolipomatous form sclerosis lesions associated with an exaggerated
proliferation of the perirenal fat tissue.
2. Suppurated form or perinephric phlegmon represents the suppuration of the
connective and fatty tissue around the kidney. Depending on its evolution, three
stages may be differentiated: edematous infiltration, localized or diffuse suppuration.
3. Chronic form- wooden phlegmon: the perirenal fat accommodates sclerotic
reaction.
Suppuration is usually located on the posterior side of the kidney.
Reported to the kidney, suppuration may have other locations too:
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Superior polar phlegmon;
Inferior polar phlegmon;
Prerenal phlegmon.
Retrorenal phlegmon
Suppuration may extend to the posterior abdominal wall and then penetrate
through the latters weak points: Grynfeltt quadrangle and triangle of Petit almost
reach under teguments.
Rarely the perinephric phlegmon may penetrate in the thoracic cavity through
the lumbar hiatus; similarly, the inferior phlegmon, as above mentioned, or the
posterior one, penetrate in the femoral triangle (of Scarpa) or through the sciatic
cavity, and thus reach the gluteal muscles.
Perinephritis must be differentiated from the inflammation of the perirenal
fatty tissue of Gerotas fascia, secondary to a suppuration of the abdominal visceras
(colon, vermix etc.)
SYMPTOMS
Perinephritis is preceded by the symptoms of the causative disease. There
usually appears only one symptom: fever. Clear urine with no pathological elements
determines sometimes that the possibility of renal infection be eliminated.
Discovering of cutaneous infection in the patients antecedents represents the key in
the correct interpretation of the feverish condition. Hyperaemia that is not joined by
other symptoms corresponds to renal parenchyma stage.
Obvious local inflammatory symptoms appear late, the phlegmon already
being located thoroughly, and depend on the phlegmons place.
Retrorenal phlegmon is characterized by parietal signs: painfull lomb,
somtime with muscle contracture; sometimes congestion and edhema of
lombar tegument is noticed (the folds of the underwear and bedclothes are
impregnated on the tegument).
Superior polar phlegmon- clinically it is revealed by thoracic symptoms:
pain, hypomotility of the corresponding hemidiaphragm, pleural reaction.
Thoracic radiography confirms the hypomotility of the corresponding
hemidiaphragm.
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Inferior polar phlegmon: pain in the flank, vicious conduct of the thigh
(psoitis): external flexion and rotation.
The anterior phlegmon gives symptoms of peritoneal irritation and may be
misinterpreted for any acute abdominal syndrome.
DIAGNOSIS
The anamnesis discovers a staphylococcus infection in the past few weeks,
fever, lumbar pain, immobility or hypomobility of the diaphragm.
Laboratory tests
Hyperleukocytosis with polinuclears.
Increased ESR
Urinalysis: with no pathological elements or pyohaematuria (complication of
a pyonephrosis)
Positive urineculture Staphyloccocus aureus or germs of non-specific
urinary infections, generally Gram negative germs.
Imagistic investigations
Echography provides information related to the renal pains, signs of renal
abscess or modification that may raise the suspicion of renal carbuncle;
sometimes it reveals pyonephrosis. It also identifies the location of the
phlegmon, which appears as a transonic area with polar placement on the
anterior or posterior part of the kidney.
Pulmonary radiography reveals the hypomobility of the diaphragm in the
affected side.
KUB x-ray reveals a lack of the kidneys contour and the external margin of
the psoas. Lumbar scoliosis with concavity on the affected side.
IVU identifies the modifications caused by the renal pains; when it is
pyonephrosis, the kidney is silent from the urographic point of view.
CT examination confirms the information obtained within US.
Lumbar puncture under echographic supervision- if it is a posterior
phlegmon, inferior polar or even superior polar, when puncture findings are
positive (pus is extracted), the diagnosis of perirenal phlegmon is confirmed.
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TREATMENT
Medical treatment: antibiotics, non specific anti-inflammatory medication
may heal some forms of pyonephritis, especially the edematous forms. Shortcoming:
by modifying evolution it often hinders accurate diagnosis and extends the evolution
of the medical condition.
Surgical treatment is mandatory when lumbar puncture extracts pus and
when, after medical treatment, the echographic examination reveals intensification of
the abscess in the known locations. It consists in lombotomy, evacuation of the pus
and drainage of lumbar region. The cause of the abscess shall also be solved: renal
carbuncle, renal abscess or pyonephrosis. If from the urographic point of view the
contralateral kidney is normal, nephrectomy shall be performed, as the pyonephrotic
kidney is morphofunctionally compromised.
PYONEPHROSIS
Pyonephrosis represents suppuration of the pyelocaliceal cavities and of renal
parenchyma joined by the latters damage. The pyonephrotic kidney of increased
volume, with unequal consistency, with no parenchyma is transformed into a bag of
pus spread into cavities via septa, where calculi may exist as cause or consequence of
pyelorenal infection. There is always a perirenal reaction involved (sclerolipomatous
perinephritis).
ETHIOLOGY
There are no specific germs; E. coli is the most frequently met, but many
times it appears as a germ of secondary infection.
PATHOLOGICAL ANATOMY
The kidney is enlarged, with irregular surface and expanded cavitary system.
The renal parenchyma is atrophic, thinner, with wide sclerotic areas. The renal
pedicle is surrounded by a mass of sclerolipomatous tissue.
Microscopically, the kidney presents an extremely marked process of
sclerosis, being replaced by a scarry fiber tissue where hyalinized glomeruli and
atrophic tubes persist.
SYMPTOMS
The main clinical symptoms of pyonephrosis are: fever, pyuria, malaise,
lumbar pains in the affected part, one larger kidney when palpated, lumbar muscles
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contraction and Giordano sign present. Pyonephrosis is an extremely serios condition
due to its septic character. Even if the disease is unilateral, the septic retention has
large impact on the global renal function, oligoanuria and ARF being frequently
associated to the septic process.
DIAGNOSIS
Within anamnesis the following antecedents of the patient are important to
consider: lithiasis with spontaneous elimination of calculi or surgeries for their
removal; fever, shivering strokes, malaise, vomiting, nausea, one large and paiful
kidney at palpation.
The urinalysis reveals pus in the urine and the urine microscopy identifies the
germ (or germs) causing suppuration. The presence of ordinary germs does not
remove the possibility of tuberculous origin of the pyonephrosis, which may be
infected with usual germs. The haemoculture during shiveringmay identify the germ.
The KUB x-ray shall reveal the enlarged renal shadow; sometimes renal or
urethral calculus is discovered the cause of pyonephrosis.
With IVU the pyonephrotic kidney is dumb; still, the urography is
compulsory, as it provides information about the other kidney.
Renoscintigraphy shows the absence of the radioactive substance in the side
of the pyonephrotic kidney and provides information about the other kidney. With
infected hydronephrosis and pyelonephritis with septic retention it reveals the value
of the affected kidneys parenchyma, being a good method in differential diagnosis
with pyonephrosis.
Within cystoscopic examination purulent discharge from the affected kidney
through ureter orificeare noticed.
Withind retrograde ureteropyelogram undertaken before surgery the
expansion of renal pelvis and calices is observed in case of infected hydronephrosis
or the characteristic aspect of pyonephrosis: large irregular volumed cavities
communicating through orifices of the narrow caliceal canes, sometimes with
hydroair levels; at ureteral level it is often irregular, expanded or filiform.
PROGNOSIS
The essential elements of the life prognosis are: the state of the other kidney
and the patients resistance. The increased values of urea and cretinin encountered at
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these patients sometimes reveal global renal insufficiency as the pyonephrotic kidney
has an inhibitory effect on the other kidney. The values of urea and creatinin come
back to normal after pus is drained or the pyonephrotic kidney is removed.
TREATMENT
The only treatment of pyonephrotic kidney is nephrectomy provided that the
other kidney and the general health condition of the patient allow this surgical
intervention. In the serious forms when the quo ad vitam prognosis is severe,
nephrectomy may be preceded by temporary nephrostomy for drainage of pus;
nephrectomy is performed after the general health condition of the patient improves.
The pre-surgery treatment in acute forms is short termed as obtaining re-
equilibrium aims at reducing the surgery shock. Simultaneously the antimicrobial
treatment is started, as well as the treatment for electrolytes and acido-basic balance.
In cases of hyperazotemia and malaise, haemodialysis improves biological
data and the general health condition of the patient and so allow for performance of
nephrectomy.
NONSPECIFIC INFECTIONS DESCENDING GENITORINARY
SYSTEM
CYSTITIS
They are infections with no fever, except for pancyctitis (vesical gangrene)
as a result of the localization of nonspecific infection at the level of urinary bladder.
ETHIOPATOGENY
There are multiple ethilogic forms, out of which the most frequent are the
bacterial forms as infections with Gram positive and Gram negative germs. As far as
their frequency is concerned, the following are the parasite origined forms
(trichomoniasis) and mycotic (Candida albicans). Some chemical substances in high
levelled concentrations in the urine determine apparition of acute haemorragic
cystitis: sublimate poisoning, methylic alcohol, flutamide, urothropine (the local
irritating effect of formaldehyde). Cytostatics, roentgen therapy or cobalt therapy
may bring about serious acute cystitis.
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With females, acute cystitis is prevalent in ascending urethral tract and is
most frequent with sexually active women. The local favouring causes are: short
urethra, vicinity with perineal region (septic ares) and inflammations of the uterus
and its annexes. The onset factors are: cold, humidity and sexual intercourse. At
climacterium period, cystitis occurs due to hormonal deficiency (estrogenic) which
causes trophic disorders of the trigonal mucosa.
With males, cystitis is most frequent with old people and is secondary to a
sub-vesical obstruction. With children it is usually related to obstructive
malformations of the descending urinary tract.
PATHOLOGICAL ANATOMY
Depending on the character of the exudates, the acute cystitis may be:
catarrhal, fibrinopurulent, diphteroid, hemorrhagic and gangrenous. At the beginning
oedema with hyperaemia of the mucosa appears, followed by its ulceration. The
ulcerated areas are covered by fibrin- based membranes or false purulent membranes.
Microscopically lymphatic infiltrates with neutorphils are revealed.
In chronic forms the wall of the urinary bladder is thickened. Mucosa is
sometimes eroded with polypoid formations that are prominent in the bladders
cavity. The vesical wall presents an interstitial fibrosis and infiltrates with
lymphocytes and plasmocytes.
1. ACUTE CYSTITIS
It manifests through polakiuria, pyuria and pain. It may be joined by haematuria
and dysuria. Polakiuria appears due to reduced capacity of the urinary bladder.
Pain has variable intensity, generally intense enough; it is present with urination
and gets exaggerated at its ending.
Pyuria is intense or discreet and haematuria may be total or present only at
urinations ending, with character of terminal haematuria, which in general is not
abundant.
Fever appears with pancystitis or after a complication of cystitis, as a result of
vesical-urethral reflux (oedema, congestion of mucosa at the level of ureteral orifice)
and of consecutive pyelonephritis.
Clinical examination. Rectal or vaginal examination provides information
related to the internal genitary organs. Sometimes a large and painful kidney is
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revealed at palpation, as well as vesical stasis, periurethral, epididimary or prostate
inflammations. The existence of urethral, vaginal or prostate secretion imposes direct
examination on sample or culture.
Urinalysis - leukocyturia (sediment, Addis-Hamburger test), urine culture
identifies the germs and the microscopic urine antibiogram identifies the germs
sensitivity.
Echographic examination revelas prostate adenoma, vesical lithiasis etc.
and/or vesical residue.
Radiological examination is compulsory. KUB x-ray and IVU reveal
medical conditions that are the direct causes of cystitis.
Instrumental manoeuvres are contraindicated with acute phases of cystitits.
TREATMENT
The general principles pertaining to urinary infections must be complied with:
chemo or antibiotics- therapy with high levelled urine concentration: sulphamids,
urinary antiseptic (Nitrofurantoin, Negram); out of antibiotics quinolons are
preferred.
Alcohol and condiments are contraindicated; light diet and highly hydric
ingestion are recommended, as well as warm baths and heat application on the
hypogastric region. Antialgics and antispastics are necessary
The local and general favouring causes must be solved for healing and
prevention of recidivations.
2. CHRONIC CYSTITIS
It is a chronic infection of the urinary bladder caused by non specific germs. It
may be the consequence of acute cystitis, of other disorders of the urinary tract that
maintain the infection through stasis or of an adjacent genitary infection.
Pathological anatomy. The persistence of vesical infection in the acute phase
brings about chronic cystitis which is different from the acute cystitis through the
character of the inflammatory infiltrate. In early stages of chronic cystitis the vesical
mucosa gradually becomes edematous, congested and friable and may get ulcerated.
In advanced stages of chronic inflammation, the submucosa is infiltrated with
fibroblasts, lymphocytes and plasmocytes. The vesical wall gets thickened and
develops fibrosis.
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Symptomatology is the same with acute forms. The symptomatic triad of
cystitis is: polakiuria, pyuria and pain.
Treatment may be effective provided that it cures the local and general
favouring factors.
ACUTE URETHRAL SYNDROME
It consists of dysuria and polakiuria. A series of vesical or urethral symptoms
associate (hypogastric or retro-pubis pain, dysuria, stinging and burning sensations
after urination). Uroculture is sterile with these women.
Causes maybe numerous: existence of a colpitis, a pretty large stenosis of the
urethral meatus, prolaps of urethral mucosa, vulvular injuries, pre-menstrual or
climacterium hormonal modifications, ovarian insufficiency (bilateral anexectomy).
Some women with insignificant pyuria and bacteriuria usually have
uretrocystitis and shall be treated with usuala antibiotics or chemotherapeutics. Some
others have positive urocultures for the germs that may be sexually transmitted: these
women and their partners shall betreated with antibiotics that have broad spectrum
against Chlamydia trachomatis (Tetracicline, Erithromicin, Klacid), or against
Neiseria gonorhaeae. There is a reduced number of women that have neither pyuria
nor identificable pathogenic germs and do not respond to the antimicrobial treatment
they probably have vesical functional disfunctions.

I. NON SPECIFIC INFECTIONS OF THE MALE GENITARY TRACT
NON SPECIFIC PROSTATITIS
Prostatitis includes both infectious inflammatory conditions of the prostate
(acute and chronic bacterial prostatitis) and non bacterial inflammatory conditions of
the prostate (nonbacterial prostatitis) and prostate painful conditions (prostatodynia).
The criterion of this classification resides in the examination of the prostatic
fluid/secretion obtained through prostate massage (expressed prostatic
fluid/secretion).
The urine and the expressed prostatic secretion obtained are divided into
several fractions:
The first urinary fraction (FU
1
) represents the first 10 ml of urine; it represents the
urethral bacterial protective lining.
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The second urinary fraction (FU
2
) represents the sample of the middle urinary
stream and translates the high vesical or urinary origin of the infection.
The expressed prostatic secretion is obtained as a result of prostate massage, after
collection of FU
2
and may identify the germs within cultures, as well as,
microscopically, the presence of pus.
After expressed prostatic secretion is collected, the patient urinates another 10 ml
of urine FU
3
. As FU
3
contains also expressed prostatic secretion, this fraction
receives prostatic significance when expressed prostatic secretion is not obtained
through prostatic massage.
I NTERPRETATI ON OF FI NDI NGS
The urine in the bladder must be sterile in order to differentiate urinary
infection from prostatic infection through comparison between the number of germs
in the urethral fraction (FU
1
) and the number of germs in the prostatic (expressed
prostatic secretion and FU
3
). In case of urethral infection, the number of germs in
FU
1
is much higher than the number of germs in expressed prostate secretion or in
the FU
3
. On the other hand, in case of prostatic infection, the expressed prostatic
secretion and the FU
3
contain more germs than the FU
1
and FU
2
.
If the urine in the bladder is infected, all urine fractions shall contain a larger
number of germs and so the sample cannot be interpreted but after the urine is
sterilized.
The study of the ejaculated fluids (culture, sediment, spermogram) may
reveal potential participation of the seminal vesicles to the infectious prostatic
process and thus clarify over a possible ethiology of sterility.
1. BACTERIAL PROSTATITIS
A) ACUTE BACTERIAL PROSTATITIS
ETHIOPATHOGENY
Acute bacterial prostatitis is usually caused by aerobe Gram negative germs
(E.Coli, Pseudomonas aeruginosa). As per some authors, enterococci (streptococcus
faecalis) and other Gram positive germs are less accountable.
The local favouring causes that are most often encountered are the sub-
vesical obstructive lesions: urethral strictures, prostate adenoma, as well as the
endoscopic maneuvers for diagnosis or therapeutic reasons.
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PATHOLOGICAL ANATOMY
When it is about urethrogenic penetration means, the infection spreads in
retrograde manner from the urethral mucosa, thorugh the tubes of the prostatic
glands to the prostate glandular acini, causing apparition of microabscesses. In a
more advanced stage, the microabscesses get united in large abscesses which remain
on a single lobe or encapsulate the whole gland.
Haematogenic means. From an infection focus at distance (sinusitis, dental
granuloma etc.) blood transports the infection, which invades at first the interstitial
tissue, then locates in the glandular tissue, causing abscess in a prostate that is
apparently healthy or bearing a prostate adenoma.
DIAGNOSIS
Clinical symptoms:
General symptoms: fever, shivering, malaise, myalgia, arthralgia, pain in the
perineal or pelvic region.
Urinary symptoms: pollakiuria, dysuria, stringing sensations with urination,
cloudy urine. The congestion of prostate causes sometimes acute retention of urine.
Also, initial, terminal or more rarely total haematuria may be encountered.
DRE is extremely painful, sometimes impossible to undergo. The prostate is
enlarged and very sensible. Sometimes one may feel at the level of one lobe a
fluctuation which means that the abscess is forming.
Laboratory. Leukocytosis - left deviation of the leukocyte formula.
Urinalysis presence of pus. Urine culture identifies the germs and their resistance.
The prostatic massage is contraindicated: on the one hand because of the patients
pains, on the other hand because it may cause bacteraemia.
Echographic examination: in the stage when the abscess is formed, the
supra-pubis echography and especially the transrectal US reveal and accurately
locate the abscess (transonic well determined area in one of the lobes or
encompassing the whole gland).
The instrumental methods of examination are contraindicated with acute
prostatitis. In case of complete urinary retention, the bladder shall be drained
through a Foley catheter or, more correctly, through a minima cystotomy that shall
be maintained until healing of acute prostatitis.
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DIFFERENTIAL DIAGNOSIS
The abscess of Cowper gland. The pain is felt in the perineum close to the medial
line in a Cowper gland.
Granulomatous prostatitis cannot be differentiated in acute stage from a bacterial
prostatitis. In its chronic form it is difficult or impossible to clinically differentiate
from a prostate cancer. The diagnosis cannot be made but histopathologically.
EVOLUTION
The evolution is usually favourable under antibiotics treatment.
Complications appear in case of treatment that is incorrectly prescribed or undergone
too late.
Prostatic abscess. Fluctuation area in the prostate which is very painful
during DRE. It usually opens spontaneously in the urethra and more rarely in the
perineum.
Bacteriaemia, septic shock may appear with at patients with comorbidities.
Acute epididimitis may be associated or secondary to acute prostatitis.
Acute cystitis usually joins acute prostatitis.
TREATMENT
Being an acute inflammatory bacterial process caused by Gram negative
germs, aminoglycosides are usually administered: Gentamicine or Tobramicine -
3x80 mg before eating, combined with Ampiciline 4x2 g I.V or a cephalosporine.
Favourable results are obtained also with the help of fluorquinolones: Ciprofloxacin,
Levofloxacin (Tavanic).
Rest in bed, antialgics, non specific inflammatory medication, hydration,
light diet with no condiments.
The urinary retention that may appear shall be solved through a minimal
cystotomy.
In case the prostatic abscess is already formed, the general therapeutic
measures are identical. Additionally rectally or perineally puncture or incision shall
be performed in order to drain the abscess.



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B) CHRONIC BACTERIAL PROSTATITIS
ETHIOPATHOGENY
The chronic bacterial prostatitis, as the acute one, is caused by the aerobe
Gram negative germs. Aseries of Gram positive cocci are also accountable
(streptococci, staphylococci). Rarely does chronic prostatitis have Chlamydia or
Ureaplasma as pathogenic agents. In majority of cases it is associated with infection
of seminal vesicles (prostate-vesiculitis).
The infection penetration means is the same as with acute bacterial prostatitis.
Moreover, chronic bacterial prostatitis appears as consequence of incorrectly trated
acute bacterial prostatitis.
PATHOLOGICAL ANATOMY
The inflammatory reaction is less intense and placed within the gland, as
compared to the acute forms. It is noticed a lymphoplasmacellular inflammatory
infiltrate at peri- and intra- levels of the prostate acini and in the stroma, which
causes the increase in volume of a part of or of the whole gland (chronic
hypertrophic prostatitis). When the inflammatory process is partial but disseminated
into the whole gland, the chronic nodular prostatitis is diagnosed.
DIAGNOSIS
Clinical symptomatology is usually non-characteristic. Some patients are
completely asymptomatic and diagnosis is made only because they have an
asymptomatic bacteriuria accidentally discovered; most of the patients have irritative
symptomatology (urgent need to urinate, pollakiuria) and less obstructive (dysuria).
Patients also accuse pains in different regions of the perineum with radial spread in
the inguinal, retropubic or hypogastric regions or in the gland.
Psychosomatic disorders are present with the majority of patients: insomnia,
neurasthenia, sexual disorders (painful erections and ejaculations with
hemospermia).
DRE: prostate with variable volume, even or nodular consistency.
Laboratory the test of fractioned uroculture provides the exact diagnosis:
in the expressed prostatic secretion more then 10 leukocites on the microscopic
sample are identified, which represents a doubtless sign. When there is a secondary
cystitis, in the FU
2
fraction pyuria and bacteriuria are identified.
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Imagistic investigations. Echography may reveal more echogenic areas in
the prostate (fibrosis) in the case of nodular prostatitis, or even echogenic areas with
shadow cones (prostatic calculi). Radiology: retrograde uretrocystography- except
for some uretroprostatic conditions (urethral strictures, prostate adenoma etc.) that
are local favouring factors, it reveals the presence of prostatic pathological cavities
communicating with the urethra.
Endoscopic exploration discovers lesions of chronic urethritis, coliculitis
and purulent secretions permeating from the orifices of prostatic canals.
EVOLUTION
Chronic prostatitis may develop into fibrosis of the prostate parenchyma and
sclerosis of the vesical tube.
TREATMENT
Antimicrobial treatment does not often succeeds in removing the germs
from the prostate because most of the antibiotics and chemotherapeutics do not reach
an optimal prostatic concentration. The following are used: Eritromicin,
Clyndamicin, Vibramicin, Tetracicline and Quinolones (Ciprofoxacin,
Levofloxacine). Anti-inflammatory medication shall be associated, as well as warm
bath and microenemas with antipirine.
Surgical treatment. Some of the cases of chronic prostatitis located besides
the urethral wall may be opened and drained into the urethra. Thus the favouring
factors shall be solved too: urethral strictures, stenosis of urethral meatus etc.
2. NON BACTERIAL PROSTATITIS
ETHIOLOGY
This is the most frequent form of prostatitis. The cause is unknown. Males
with non bacterial prostatitis have an increased number of leukocytes in the
expressed prostatic secretion but germs cannot be identified. The efforts to identify
different pathogenic agents (anaerobes, Chlamydia, Trichomonas, protozoa or
viruses) were generally unsuccessful.
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PATHOGENESIS
The ethiology and pathogenesis of non bacterial prostatitis are not known.
The histopathological modifications resemble the ones encountered in chronic
bacterial prostatitis.
SYMPTOMS
It is non characteristic and overlaps the symptomatology of chronic bacterial
prostatitis. Urethral secretion lacks and the DRE is not conclusive.
LABORATORY
The test of the urine fractions identifies pus and absence of ordinary germs in
the expressed prostatic secretion and the FU
3.
Sometimes, with the help of special
techniques, Chlamydia trachomatis, Ureoplasma urealyticum and viruses may be
identified.
TREATMENT
When ethiologic agents are identified, giving the right treatment is not
difficult to do; in the cases when germs are not identified, the supposition of
prostatitis caused by Chlamydia or Ureoplasma must be made. Eritromicin or
Doxyciline is administered for 14 days as they are effective against Chlamydia or
Ureaplasma.
3. PROSTATODYNIA
It seems to be a neuro-vegetative disorder in the male genitary system with no
organic lesions. The infectious cause can be removed through the test of urine
fractions, where cultures are negative and there are no leukocytes in the expressed
prostatic secretion and the FU
3
.
DIAGNOSIS
The symptoms resemble the ones of prostatitis. The patiens accuses painful
sensations of different intensity, from a simple discomfort to unbearable pain,
appearing in perineum, hypogastric region or renal pelvis. Irritative urination
disorders are associated: urgent need to urinate, pollakiuria especially related to cold
and disorders of sexual appetite and potency. There are cases when patients accuse
prostatorrhea or spermatorrhea during excretion.
DRE reveals a prostate of normal volume or lightly increased and the
sensitivity of the whole gland. By prostatic massage a serous and abundant fluid is
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obtained (retention). Psychomotor disorders are also present: irascibility, insomnia,
neurasthenia and fatigue.
DIFFERENTIAL DIAGNOSIS
Differentiating from the chronic bacterial prostatitis is possible with the help
of fractioned urocultures test. The anal-rectal syndrome encompasses the presence if
hemorrhoids, anal fissures and fistulas, as well as lesions of proctitis revealed by
proctoscopy.
TREATMENT
It is recommended to avoid cold and humidity, alcohol and condiments.
Sedatives. Non specific anti-inflammatory medication (Phenilbutozone,
Indometacin). Alpha blocking agents seem to have good results (Tamsulosin 4
mg/day). The treatment with antibiotics is useless, abusive and not efficient.
II. NON SPECIFIC INFECTIONS OF THE EPIDIDYMIS
Due to the fact that specific epididymitis (tuberculosis and gonococci) play
nowadays a secondary role, the most encountered cases of epididymitis are those of
non specific epididymitis.
The highest incidence is with young sexually active males and with patients with
sub-vesical obstructive medical conditions. The first are associated with urthritis and
usually have Chlamydia trachomatis as ethiologic agent (sexually transmitted
epididymitis). Non specific bacterial epididymitis associated with UTI and bacterial
prostatitis belong to the second category of patients; most often they are caused by
Enterobacterias or Pseudomonas aeruginosa.
ACUTE EPIDIDYMITIS
ETHIOPATHOGENY
The infection reaches the epididymis through several ways:
Ascending (deferential) way: the most frequent, it starts from the posterior
urethra or prostate, wherefrom the pathogenic germs, due to the increased pressure
during urination, may penetrate the ejaculating channels and along the vas deferens
reach the epididymis.
Lymphatic way (perideferential network) is also involved.
The hematogenic way implies a focus at distance whose ethiology is usually
staphylococcus; yet, this way is rare.
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The local favouring factors are: pre-existent urethroprostatitis or subvesical
osbstructive conditions (prostate adenoma after enucleation or transurethral
resection; ejaculant ducts communicate directly with prostatic lodge), prrevious
urethral strictures etc.
PATHOLOGICAL ANATOMY
The epididymis is swollen and has increased consistency. The infection
usually starts at the tail of epididymis and then extends to the whole organ.
Sectionally numerous little abscesses are noticed. A reactive hydrocele might be
encountered (vaginalis reflects the pathology of epididymis). Microscopically an
inflammatory infiltrate with neutophils is encountered.
SYMPTOMS
The pain is extremely intense, at first localized and then irradiated along the
whole sperm cord, inguinal duct to the iliac fosa.
Fever and shiverings are associated with a rapid increase in volume of the
epididymis. The hemiscrotum is increased in volume, with congested, edematous and
warm teguments. When suppuration appears, the teguments become plae, thinner and
fluctuating and the abscess may open spontaneously on the posterior side of the
scrotum.
DIAGNOSIS
The sudden onset and characteristic symptomatology sometimes associated
with urethral secretion with sexually active young males, with males having urethral
stricture or having undergone surgery for prostate adenoma orientates the diagnosis
towards acute epididymitis.
The urinalysis and urine culture identify or remove the possibility of
infection with ordinary germs.
Echography the epididymis is increased in volume, presenting transonic
echostructure (congestion and oedema) or with small dispersed transonic areas
(microabscesses). Some other times a large transonic area is revealed (already
formed abscess). The whole testis and epididymis may be encompassed in a
transonic cavity (reactive hydrocele).
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DIFFERENTIAL DIAGNOSIS
2. Tuberculous epididymitis in its acute form it has identical symptomathology.
The presence of specific antecedents, acide sterile pyuria and positive baciloscopy
help making a diagnosis. The presence of b. Coli in the cultures on specific
environments reinstates the diagnosis.
3. Testicular tumours. The testicular tumoural mass is clearly distinguished from
the normal epididymis. The inflammatory signs of the scrotum and sperm cord are
usually absent. The echography reveals the testis that is enlarged in volume, usually
with non homogenous structure or a hypoechogenic area surrounded by healthy
tissue. Some other times transonic areas within tumoural mass may be discovered
(tumoural necrosis).
4. Spermatic cord torsion. With sudden onset, during the night, the epididymis is
placed in front of the testis, at first, and then forms a unique and very sensitive mass.
The testis is raised towards the internal orifice of the inguinal duct. The smooth
raising of the scrotum is followed by calming down the pain in case of epididymitis
and accentuating pain in case of spermatic cord torsion (prehn sign). Doppler
investigation identifies the absence of pulsations of spermatic artery in torsion. The
echography is not specific as the echographic aspect of the affected testis resembles
the one in the case of orchiepidedymitis.
5. Acute orchitis. The echography is not specific but may identify the increase in
volume of the testis and epididymis, which have a more transonic aspect due to the
inflammatory process. The inflammation of the epididymis and testis may be joined
by a reactive hydrocele; this is also visualized within echography.
EVOLUTION
In acute stage the resolution of the inflammation of the epididymis is
achieved with a consequent induration at the level of the tail of epididymis or of the
whole organ. The abscess forms end in fistulas with characteristic locating on the
posterior side of the scrotum.
TREATMENT
The inappropriate or inefficient treatment brings about the chronicization of
the infection. Bed rest is compulsory for 10 15 days. Pain is killed by
administration of antialgics and by infiltration of the sperm cord with Xiline 1%.
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Local cold applications are very important (ice bags): on the scrotum that has
precviously been raised in fixed in position. Non specific anti-inflammatory agents
are beneficial too (Phenylbutazone, Indometacin, Diclofenac).
Antibiotherapy: Tetracicline, Doxyciline, Ciprofloxacin, Levofloxacine or
other quinolones present high chances to heal due to the optimal diffusion in the
acute inflammatory process.
Surgical treatment is indicated when abscesses are formed or opened and
consists in orchiectomy.
CHRONIC EPIDIDYMITIS
It represents the irreversible result of an acute epididymitis that has been
incorrectly treated. Chronic epididymitis is characterised by fibrosclerous reactions
with total or partial induration of epididymis and occlusion of tubules. When the
process is bilateral this constitutes a cause of sterility.
Clinically the only syndrome is diffuse pain that the patient feels at the level
of that hemiscrotum, giving a sensation of uneasiness. The epididymis and the sperm
cord are thickened. Non specific inflammatory lesions of the prostate or urethra may
be present.
US - the epididymis has variable volume non- precisely delimitated from the
testis and hyperechogenic image due to the sclerosis process. Sometimes it may be
visualized a secondary reative hydrocele.
DIFERENTIAL DIAGNOSIS
Tuberculous epididymitis from the palpatory point of view it is very similar
to chronic epididymitis; the two medical conditions are impossible to delimitate
exclusively on the basis of clinical investigations. Palpation of seminal vesicles on
the same thickened side, acide sterile pyuria and baciloscopy are essential to make a
diagnosis of the tuberculous epididymitis.
Testicular tumours. Careful bimanual palpation differentiates a normal
epididymis from a testis that is enlarged in volume and weight and has the specific
organ sensibility lost.
TREATMENT
The chronic inflammatory tissue with the fibrosclerosis processes hinders the
diffusion of antibiotics in the inflammatory process. Treatment of a potential UTIs or
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of an existent prostatitis is recommended. In case symptomathology persists,
epididyctomy may be performed and thus the histopathological examination which
can make a doubtless positive diagnosis.
IV. NON SPECIFIC INFECTIONS OF MALE URETHRA
ACUTE URETHRITIS
ETHIOPATHOGENY
In case of iatrogenic infections (endoscopic maneouvers for making a
diagnosis or for theraphy), the accountable germs are the known Gram negative and
Gram positive ones. The sexually transmitted urethritis (non-gonoccocal) is caused
by Chlamydia and Mycoplasma.
The non specific urethritis is usually the consequence of ascending infections
but may have prostate as starting point, when the formation mechanism is
descending.
PATHOLOGICAL ANATOMY
In case of acute form the mucosa is congested, edematous and may present
ulcerations. Periurethritis is frequent with severe forms and the periurethral abscesses
may appear immediately or too late. The periurethral glands are interested too.


SYMPTOMATHOLOGY
The acute non specific urethritis manifests similarly to the gonoccocal
urethritis through abundant purulent urethral discharge joined by urination disorders
(pollakiuria, urgent need to urinate, burning sensations at urination). The urethral
meatus is congested, edematous.
Laboratory examinations. The native sample identifies Trichomonas and the
Gram staint identifies the non-specific germs. In the absence of above mentioned
microroganisms and of Candyda albicans, the ethiology of urethritis is virotic;
Chlamydia and Mycoplasma should be considered as possible ehiological agents.
In acute stage the instrumental examination of urethra and of other segments
of the urinary tract is contraindicated.
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DIFFERENTUAL DIAGNOSIS
The microscopic examination of the urethral secretion differentiates the various
ethiological forms from urethritis.
COMPLICATIONS
B. The periurethral abscess usually appears as a result of instrumental
maneuvers performed in acute stage.
C. Epididymitis, prostatitis and cystitis appear as a result of the ascending
extension of the inflammatory process.
TREATMENT
Chemotherapy or antibiotherapy focused as per the ethiology and
antibiogram findings. The sexually transmitted urethritis (nongonoccocal) is treated
with 2
nd
generation tetraciclins (Doxyciline). Erithromicine is another efficient
antibiotic. The mycotic urethritis is treated with antifungics (Stamicin, Nistatin). The
trichomoniazic urethritis is treated with Metronidazol and Fasigyn. Intermittent
smooth catheterism with catheters of thin calyber may be performed in case of acute
complete urine retention, or, more correctly, an a minima cystotomy with
temporary character should be made.
CHRONIC URETHRITIS
It is the consequence of acute non specific urethritis that has been treated
inappropriately. Some other times it is the result of a sexually transmitted non-
gonoccocal urethritis.
ETHIOPATHOGENY
The pathogenic agents are identical with those encountered at acute urethritis.
PATHOLOGICAL ANATOMY
The purulent discharge is less abundant and the urinary symptoms are more
alleviated. The urethral mucosa is slightly granular. The infection extends to the
prostate and seminal vesicles; at the level of urethra, urethral strictures may be born.
DIAGNOSIS
The urethral secretion and symptoms are a lot more reduced as intensity, as
compared to acute forms.
The laboratory examination may reveal the germs described within the acute
form.
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Radiological examination the retrograde urethrocistography usually identifies
the favouring factors: anomalies, strictures etc. with location in the urethra.
Urethrocystoscopy reveals the inflammation of urethral mucosa, diverticular
orifices and urethral stricture. The purulent discharge through the orifices of prostatic
glands suggests prostatitis as consequence of urethritis.
DIFFERENTIAL DIAGNOSIS
Chronic urethritis differentiates on the basis of laboratory tests.
COMPLICATIONS consist of spreading of the urethral infections to the
prostate, bladder and even ascending urinary tract. Locally the most frequent
complications are the urethral strictures and, more rarely, periurethritis.
TREATMENT. The treatment of chronic urethritis is given in
closerelationship to the ethiology.
The primary treatment of urethral strictures consists in internal urethrotom. The
Otis urethrotomy is applied in cases of strictures of the anterior urethra, while for
posterios urethra the internal optical urethrotomy (Sachse) is performed.
PERIURETHRITIS
It represents the inflammatory process of the periurethral tissues. Reported to
its evolution, it may be acute and chronic; reported to the limits of the lesions,
periurethritis may be circumscribed or diffuse.
ETHIOPATHOGENY
Periurethral tissues are infected through septic inoculation. This is favoured
by lesions of the urethra such as: strictures, accidental or surgical plagues, urethral
calculi, permanent urethral catheter etc. Out of all these, mostly strictures cause onset
of periurethritis through chronic suprastrictural urethritis which may complicate in
inflammations of Littre and Cowper glands, in phlebitis of the erectile tissue or in
lymphangitis. Out of these foci the infection may extend to the periurethral tissue,
where it may undertake one or the other form. Germs are usually anaerobes
(Clostridium perfringens, b. fragilis, and b. funduliformis).
THE CIRCUMSCRIBED PENILE PERIURETHRITIS has superficial or
profound urethral origin with starting point in a urethral stricture or in urethritis that,
by extension, has encapsulated the periurethral tissue. The patient has a limited
swollen part on the urethra trajectory. The lesion is associated with fever; it is
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painful, presents fluctuations and opens spontaneously in the urethra or on the skin,
being followed by a urinary fistula.
THE DIFFUSE PENILE PERIURETHRITIS (gangrene of the genitary
organs developing extremely rapid) is mostly encountered with young males. The
penetration orifice is usually represented by the prepuce. The germs are represented
by streptococcus and anaerobe agents.
The disease has an extensive and necrosis producing character. The onset is
sudden, joined by fever, shivering strokes, malaise and cephalea. The prepuce is
edematous, congested; the inflammatory process extends along the penis up to the
scrotum. Thereafter lesions and partial necrosis appear and the general health state is
profoundly alterated. Differential diagnosis is made against the diffuse perirenal
phlegmon that expanded to the penis.
Under correct antibiotics treatment the tissues undergoing necrosis are
removed; healing is obtained with vicious scars that need plastic surgery.
Out of pulmonary complications death may survene.
TREATMENT consists in antibiotherapy in profound incisions along the
penis; continuous washing showers and locally administered antibiotics are
undertaken. Antigangrenous serum is also administered.
DIFFUSE PERIURETHRAL PHLEGMON is the most severe form of
periurethritis. It occurs with patients that have organic medical conditions (diabetes,
CKF). The infection is rapidly spread towards scrotum, penis and pubis; crepitations,
lesions and sphacels. One should also mention: high fever, shivering strokes,
profound alteration of general health condition, sleepiness, obnubilation.
Treatment is given in emergency manner: cystotomy, wide opening of the
phlegmon, drainage, oxygenated water, Rivanol. Wide spectrum antibiotics.
Metronidazol, anti-gangrenous serum, support of the general health condition of the
patient. If the patient remains alive, plastic surgery of the penis and treatment of the
urethral strictures shall be done thereafter.
BALANOPOSTHITIS
It is an inflammation of the glans penis and of the prepuce.
ETHIOPATHOGENY. The pathogens are represented by the Gram positive
and Gram negative germs; rarely it may be caused by fungi.The lesions are favoured
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by stagnation of secretions as consequence of precarious hygiene or of neglected
phimosis.
It is manifested in pruritus and burning sensations and further on the prepuce
gets edematous and painful. The purulent secretion is discharged through the
fireskins slot. The medical condition may cause, especially with children,
balanopreputial adherence.
TREATMENT
With cases that are not severe local hygiene with camomile infusions or disinfecting
substances: silver nitrate, mercuric oxide, Rivanol, hydrogen borate are necessary; if
these fail, circumcision (postectomy) is necessary.










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The frequency of tuberculosis (TB) is quite high in the world, causing
annually 3 million deaths , 3-4% of which with urogenital tuberculosis.In Romania,
the incidence is somewhat constant ( 3/100.000 in 1970 compared to 5/100.000 in
1994). Renal tuberculosis incidence is the highest between 20-40 years, is rare in
children and uncommon in the elderly.
In Europe, the incidence in Western countries was 12.9% in 2000, while in
central Europe it was on average three times higher.
In Romania, since 1950, tuberculosis incidence decreased after the
introduction of treatment with tuberculostatics, reaching in 1987 the figure of
53,2
0
/
000
. Thereafter the incidence gradually increased, reaching 142,2
0
/
000
in 2002.
In 2003 there was a stagnation that was maintained in 2004.
The incidence of AIDS represents an increasing incidence of tuberculosis
(Corbett 2002, 2003). Worldwide, about 11% of new cases of tuberculosis in 2000
occurred in patients infected with AIDS.
PATHOPHISIOLOGY
Urogenital tuberculosis is the location of a general disease, it is not an organ
disease but a system disease. Separate studies of tuberculosis in each of the
urogenital organs are required by educational needs.
Renal tuberculosis is always secondary and it has an evolutionary cycle
beginning from the Koch Bacillus entering the body, to chronic phthisis is installed.
Koch Bacillus (KB) enters the body during childhood, or adolescence, and only
exceptionally in old age. The way to enter the body is airborne (by inhalation) or,
more rarely, gastrointestinal (Calmette).
Genital tuberculosis in man may be secondary to urinary tuberculosis, or it
represents hematogenous metastasis tuberculosis with the starting point of a lung or
extra pulmonary outbreak.

4. Specific urogenital infections (urogenital
tuberculosis- GUTB)

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TBC INFECTION CYCLE (Ranke Scheme)
1. The first period, or the period of invasion occurs in a non-sensitized body
when the first localized tuberculous infection occurs usually in the lungs (95% of
cases), where "primary complex" is performed: inoculation chancre in a pulmonary
alveolus, lymphangitis and satellite adenopathy.
Rarely primary lesion may be intestinal. A lesion of primo-infection of the
urogenital has never been observed.
This is the stage characterized by a state of hypersensitivity (allergic), due to
the absence of specific resistance. Usually, the ganglio-pulmonary complex is
scarring by calcification or seclusion.
The secondary period - is manifested by bacillary dissemination.
Mediastinal lymph nodes fail to form an effective block in the way of KB and they
escape into the pulmonary circulation, then in the general circulation. This is the
beginning of the bacillemic phase in the tuberculous infection cycle, where KB
dissemination occurs KB from the primary focus, either by blood (bacillemia) or
lymphatic (embolic). Hematogenous metastases occur in the lungs, located pleural
or apical.
When released into general circulation, bacilli can colonize, giving
extrapulmonary tuberculosis locations that characterize the secondary period. In the
order in which they appear, they are: serous, osteo-articular, ganglion, skin. Renal TB
occurs at the end of secondary period. Its appearance is not excluded in the early
stages of this period.
The tertiary period - manifests by extensive tuberculous lesions, fibro and
ulcero-caseous, which characterizes phthisis, locating disease to a single organ, most
commonly in the lung (the period of decline).
In conclusion, renal localization takes place haematologically, with two
phases of clinical anatomical evolution: parenchymal phase (closed) and ulcero-
caseous phase (open). The renal TB, once open affects all segments of the urinary
tract. Initial renal lesion affects urinary and then genitals.
Other authors state that urinary tuberculosis (UT) and genital tuberculosis
(GT), in man, are two independent hematogenous determinations, having common
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origin with the primary complex. Both have a parenchymal phase and evolve
simultaneously or separately.
PATHOLOGY
Renal tuberculosis. Initial renal tuberculosis lesions (follicle and
granulation) are based in cortical. Their characteristic is their spontaneous tendency
to heal by scarring. This stage is named renal parenchymal TB (closed).
In a few cases, necrotic lesions occur, extending in the "oil patch" to the
medulla. In this poorly vascularized area, with increased hypertonia, the tendency of
scarring lesions no longer takes place and the evolution is made to the canaliculi,
lymphatic and continuity, causing papilla invasion with fistulization in calyces. It is
the second stage of renal parenchymal TB (open), when ulcerative lesions in the
parenchyma opens in the urinary. The following segments are affected:renal pelvis,
ureter, bladder, urethra, prostate and genitals. Tuberculosis spreads downward in
urinary and upward in genitals (Cayala).
The evolution of lesions is the result of interpenetration of two processes in
tuberculous inflammation: caseous necrosis, a specific process with destructive
tendencies and sclerosis, a non-specific reaction of the connective tissue. In the renal
parenchyma, prostate, testis, inflammation is manifested by caseous process of
tubercle follicles, leading to the formation of caverns and tuberculous abscess.
Instead, at the level of urinary tract, specific inflammatory process moves through
two phases: the infiltration and sclerosis.
Renal pelvis tuberculosis the inflammatory process affects all tunics,
transmitting to the tissue surounding renal pelvis, forming a pyelitis with
sclerolipomatosis stenosis peripyelitis.
Ureteral tuberculosis has two specific locations, at the pielo-ureteral
junction (PUJ) and at the juxtavesical ureteral level, where the specific inflammatory
process produces infiltration and stenosis, with upstream dilation of the duct.
Bladder tuberculosis. The initial lesions (granulation and ulceration) are
reversible at the beginning. In advanced stages they extend in depth, involving the
entire bladder wall. There is a sclerosis of the detrusor and it withdraws (small
organic bladder). Retraction is due to the moving part, trigone is usually respected;
rarely the trigone also retracts. Detrusor sclerosis leads to terminal ureters alteration,
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stasis and expansion upstream, the renal function declines gradually and uremia is
installed.
Prostatic tuberculosis. Regardless of the gateway (urinary or
hematogenous), KB causes the appearance of periacinar granulations, that by
conglomeration and parenchyma is forming caverns, whose content is fistulising in
the urethra. They represent outbreaks of sowing for the seminal vesicles, epididymis
and testis.
Epididymal tuberculosis, the most frequent location of GT is in the head.
Epididymal TB lesions have the appearance of "crest of a helmet." The lesions
evolve subacute or chronic. Evolution is to caseation.
Testicular tuberculosis is usually the result of the extension by continuity of
the epididymis and exceptionally, it is due to direct hematogenous seeding. Evolution
is made by caseation or abces, with non systematic fistulisation.
SYMPTOMS
Closed renal tuberculosis stage is oligosymptomatic or asymptomatic in
cortical period. In medullar lesions phase, when tubercle granulations or follicles
have a tendency to caseation, there are general signs of bacillary impregnation: low
grade fever, asthenia, fatigue, headache, loss of appetite, night sweats. Laboratory:
elevated ESR, positive PPD test. Urine is clear with normal sediment or with
leucocyturia and microhematuria. Urine analysis may reveal a persistent albuminuria.
Isolated b.K. presence in urine constitutes, in some cases, the only manifestation of
closed renal TB.
In open renal tuberculosis stage (urinary TB) signs are not specific. In the
foreground, there are the symptoms of tuberculosis cystitis (urinary frequency at
night, in the second half of the night, which becomes daytime, pain on urination and
sterile pyuria). Urinary frequency can be very intense (urination in small intervals),
simulating even incontinence.
Renal symptoms are rare.
Total hematuria is an early sign, but rarely of renal lesions. In late stages of
disease, it is terminal and has bladder origin.
Lower back pain, dull and transient is often reported.
The kidney shows hydronephrosis or pyonephrosis TB.
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AHT or hyperazotaemia (advanced bilateral lesions).
Male genital tuberculosis has two forms: superficial GT (TB epididymitis)
and deep GT (prostatic TB).
Epididymal TB may be chronic from the beginning (unipolar or bipolar
nodules, rarely affects the whole epididymis); sometimes is masked by hydrocele;
subacute with pain and feverish and acute with living pain, fever and local signs of
inflammation. Acute or sub acute form eventually becomes chronic.
Chronic from the beginning or secondary can fester. KB is isolated from pus.
The vas deference may be enlarged and beaded. According to Legueu's aphorism,
"any patient with genital tuberculosis had or will have a renal tuberculosis," an
isolated chronic epididymitis, even without clinical signs, bacteriological or IVU,
unless a complication of a urinary infection, should be considered with a high
probability as being of specific origin.
Prostate-seminal tuberculosis - male genital apparatus is caught entirely,
not only testicle or epididymis. Gil Vernet demonstrated the primordiality of prostate
localization of tuberculosis, where inflammation reaches to catch the pipes.
Propagation is achieved not only canaliculi but also lymphatic. This explains the
bilateral lesions in the reproductive tract, the prostate is a "turntable" of genital
crossroads.
Digital rectal examination does not regularly reveal the lesions, prostate may
be normal, sometimes may present isolated nodules, or is entirely scleral. Scleral
prostate contributes to the bladder neck sclerosis. Seminal vesicle can be palpated, it
is enlarged and hardened.
DIAGNOSIS
It is not easy, because genitourinary tuberculosis (GUTB) can evolve slowly,
torpid, without typical clinical manifestations.
Diagnosis is based on careful history check up, highlighting the history of
tuberculosis and any urinary infection rebellious to treatment. It combines a careful
clinical examination of respiratory, bone, urinary, genital and ganglionic system.
Essential for diagnosis is KB isolation from the specific lesions.


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Laboratory investigations
Urine studies. A characteristic for GUTB is pyuria, acid and sterile. Sometimes
microscopic hematuria is present. B.coli can be identified in 20% of cases, causing
recurrent urinary infections. Pyuria is explored by the Addis test, it is normal in
parenchymal phase (2000 leukocytes / minute), reaching significant values without
reaching figures over 100.000/minut as for nonspecific infections.
KB presence - To highlight it, the procedure is 3-5 urine sampling, which
are seeded on Lowenstein-Jensen medium and inoculated into mice. Direct
bacilloscopy - Ziehl-Nielsen stain: KB is an acid-alcohol resistant germ. This
method is the fastest and the cheapest, KB can be confused with Smegmei
bacillus (also acid-alcohol resistant).
Cultures on special media, although they are read only after 5-6 weeks, have
the advantage of determining the type of bacillus, and especially
tuberculostatics sensitivity.
ESR is moderately increased;
PPD test - intradermal injection. It develops an inflammatory reaction at the
injection site after 48-72 hours, if it has at least 10 mm in diameter, it is
considered a positive test. This means that the patient was infected with
tuberculosis, but does not mean that it has active tuberculosis;
Exploration of the renal function - global renal function in unilateral lesions
is preserved;
Investigations
Cystoscopy - specific lesions are granulations surrounded by a red halo,
located around the ureteral orifice on the affected side, or in the bladder dome.
Ulcers, the result of flaking grains have the same base and may be synchronous with
granulations;
Radiological exploration is essential and indispensable for both diagnosis
and for monitoring treatment outcome.
a) KUB X-Ray - identify renal contour changes (decreased by renal TB
atrophy, increased irregularly in TB pyonephrosis), or ureteric , bladder, duct
defferent and seminal vesicle calcification. It can also detect the existence of a Potts
disease.
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Fig. 4.1. Renal tuberculosis - different aspects to urography. a tbs
stenosis at the calyx orifices, b - upper polar caverns (1.2) and pelvis
stenosis, c UPJ stenosis, d - UPJ and pelvis stenosis, e thorne
calyx by exclusion of secondary calyx, f - upper polar caverns g
calyc stenosis, h - cavern and thorne calyx (i), and - leather stenosis
dilated pelvis, j - caverns of papilla (1, 2, 3), k - pionephrosis,
ureteral TBC, l - pionephrosis TBC
b) IVU - show morpho-functional changes caused by urine and it founds
alterations caused by tuberculosis process in the genitourinary system.
Pyelocaliceal
modifications - there
are three types of
isolated or combined
lesions: stenosis,
dilation, ulceration
and caverns (fig.
4.1.).
Stenosis
consists in the
narrowing of the
calyx or renal pelvis,
due to healing by
sclerosis. The tubes
appear thinned, or
even disappear, when -"exclusion" of that cavity or "amputation", when calyce is not
visible.
Above stenosed areas, cavities progressively expand, calyces are rounded and
calyce "bubbles" appear. Their edges are regular or festoon, ulcerated, where small
tracks open leading to a cave located in the parenchyma, which is filled non
homogeneous, unlike the dilated calyce (fig.4.1).
By the complete closure of a calyceal rod, the exclusion of superjacent cavity
appears, and the calyce ends in "Spike". For this spin the renal pelvis, ureter and the
rest of calyce retract, being the image of "Wilted Flower". When the renal pelvis has
stenosis, and the rods of main calyces are also stenosed at their opening in the renal
pelvis, the calyce is dilated; the image is "daisy flower".
There are cases of early lesions, in which the calyce rod may have a normal
aspect, but the papilla-calyx area is eroded, festooned - "calyx caries". When the
destructive process is advanced pyonephrosis, with compromised renal function,
contrast material is no longer eliminated; the kidney is "urographic silent".
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Fig 4.2. Ureter TB
Ureteric Changes. Often in order to have
a better opacification, higher doses of contrast
agent are required. The ureter usually appears
with modified peristaltic, dilated or thickened,
rigid, with stenosed areas, which give a
moniliform appearance (Fig. 4.2).
Changes in the bladder - in the early
stages hypertonic bladder is "tense", but still
with relatively normal capacity. The hemibladder
of the affected part is contracted (Freudenberg's
sign), it is not filled with contrast agent (Constantinescu sign), the median axis of the
bladder is directed toward the diseased part, pulled by ureteral stenosis and shortened
(Mussiani sign).
Small bladder with detrusor sclerosis, which is maintaining the ability based
on the trigone (unaffected) - "trigonal bladder", " urethralisation of the bladder ",
when the bladder capacity is so small that the bladder increases it, due to posterior
urethra that widens.
Retrograde ureteropielography, (RUP) is more invasive, is less often used,
when the kidney is silent in urography or in case of stenosis of the distal extremity of
the ureter.
Descending pieloureterography the kidney is punctured by percutaneous
renal puncture. By the puncture needle the renal content can be aspired, for various
tests, including detection of KB, and then introducing the contrast agent the kidney
and ureter can be observed. It is a less invasive investigation compared with RUP.
Vas deferens graphy shows deferens obstruction, seminal vesicles dilated,
with anarchic aspect and filling defects. It gives specific aspects of "leaf eaten by
caterpillars", "bottle washing brush," etc..
Retrograde urethrocystographyis used rarely, in order to highlight
stenosing lesions of the posterior urethra, and of geodes and prostate tuberculosis
caves; it emphasizes the outline of the bladder and a possible vesicoureteral reflux.
Angiography is rarely used.
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Isotopic investigation does not provide additional data for renal function
tests and for the radiological studies that were mentioned.
Bladder biopsy is contraindicated in acute tuberculosis cystitis; it can bring
important data for diagnosis of GUTB.
Ultrasound - has a limited diagnostic value, but it is a useful investigation in
order to track disease progression.
Computed tomography it is used mainly in the diagnosis of replacement
images of space and to detect pathological prostatoseminal aspects.
DIAGNOSIS
The only accurate exam is bacteriological examination, highlighting KB by
direct bacilloscopy, on specific culture media and by inoculation in guinea pigs.
Since clinical features given are only suggestive: pyuria important, sustainable,
recurrent, in the absence of a certain maintenance cause (stones, congenital anomaly,
subvesical obstacle, diverticulitis), it should be considered as being of tuberculosis
origin. Pyuria, with all the features must be interpreted as specific origin, only in the
clinical context.
The elements offered by radiology are evocative, but not a certainty. The
result of bacteriological examination is crucial.
Histological examination also is not a certainty, histological lesions are
possible to be tubercular, but it is not sure.
DIFFERENTIAL DIAGNOSIS
It is made with numerous urination problems, the clinical context and the
results of laboratory investigations are crucial.
EVOLUTION, PROGNOSIS
Today GUTB, due to tuberculostatic treatment, is presented in mitigating
forms, least progressive and destructive. Bladder lesions prognosis and recent
epididymal lesions is relatively good, they retrocede spontaneously or under
treatment.
TREATMENT
GUTB Treatment is based on a reliable diagnosis, with a certain positive
bacteriological result, and on a functional and lesion balance, clinically and
especially radiologically established. The treatment is medical in all stages of
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disease; surgery is addressed to destructive forms converted under medical treatment
(excision surgery) and sequels, so-called "cure disease" (conservative surgery).
MEDICAL TREATMENT is the essential treatment in therapeutic GUTB,
because tuberculosis is a general disease of the body, medical therapy is indicated in
all forms of the urogenital location. This is the basic tratment and it is aimed at
healing, stabilization and lesion preparation for a possible radical or conservative
surgical treatment.
The means to monitor the effectiveness of treatment are: clinical (improvement and
disappearance of urinary disorders, improving the general condition, etc.), laboratory
(decrease or normalization of Addis test values) and radiological, urography and
ultrasound particularly, identifying a series of morphological elements, etc.
Hygienic-dietary treatment. Food should be varied, hyperglucidic and
hypercaloric. Alcohol and spices should be suppressed. Hospitalizing patients is
mandatory for biological control and radiology.
General tonic treatment includes a vitamin complex consisting of vitamin C
for anti-inflammatory effect in active lesions; Vitamin D, associated with Ca
preparations: anti-inflammatory, healing and vitamin B6, which increases the
tolerance of tuberculostatics.
Tuberculostatic treatment. The correct conditions for tuberostatics
chemotherapy are: a) improving the sensitivity to b.KB antibiotics, b) knowledge of
the efficacy of doses, toxicity and side effects of drugs, c) chemotherapy is usually
associated, targeted and prolonged, d) drug intake certainty e) control treatment.
Tuberculostatics are divided into three groups (Table I):
Tuberculostatics I
(major)
Tuberculostatics II Tuberculostatics III
Isoniazid (INH) Cycloserine
Linezolid
Rifampicin Ethionamide
Macrolides: e.g.,
clarithromycin
Ethambutol Capreomycin
Arginine
Pyrazinamide Amikacin and
kanamycin

p-Aminosalicylic
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acid (PAS)
Table I. The main tuberculostatics

Attack treatment lasts 2-3 months, daily, and it consists of the combination
of three drugs. Lattimer proposed the association of INH, rifampicin and ethambutol.
After Gow, the most active combinations are those associated with: INH, rifampin
and pyrazinamide, or rifampicin and pyrazinamide.
The doses administered are: INH -300 mg / day, rifampicin 450-600 mg / day,
ethambutol 900-1200 mg / day, pyrazinamide 1000-2000 mg / day.
Isoniazid and Rifampicin are bactericidal and bacteriostatic (it acts on
division and metabolism). Pyrazinamide acts efficiently in the acidic environment,
entering into macrophages, where the germs can withstand. Ethambutol has a weaker
action of sterilization. After three months, a physical examination is mandatory: IVU,
tests (urinalysis, Addis test) and KB (3 samples).
Stabilization treatment. The most active combinations are pyrazinamide
with rifampicin or rifampicin with INH; INH and ethambutol combination can be
also used. The duration of treatment is 3-6 months.
Consolidation treatment covers other 6-9 months. Only one tuberculostatic
is given, usually INH.
Other drugs associated with tuberculostatics can be also administrated,
corticosteroids in order to mitigate the reaction of sclerosis (particularly to reduce the
reaction of sclerosis at terminal ureter and bladder).
During pregnancy, the treatment administrated in normal doses does not
cause birth defects in fetus. Similarly, during lactation, the doses reaching into breast
milk are small, in a normal therapy.
Tuberculostatic treatment discontinuation may be decided only by laboratory
tests (urinalysis, Addis figure), the absence of bK in urine and radiological
(parenchymal lesions, especially of pipes, evaluating sequelae).
SURGICAL TREATMENT
Surgical procedures are divided into: radical interventions (for excision) and
reconstruction.
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Excision surgery (radical). In principle, during the attack phase of the
tuberculosis treatment, operation does not occur. At this stage, may benefit from
surgical treatment only certain destructive forms with the silent kidney in urography
(pyonephrosis, ulcerative caseous tuberculosis, mastic kidney, etc.). after a specific
treatment of 14-21 days; in these cases will be performed nephroureterectomy
(Burghele).
In the consolidation phase, surgery is more often used, in front of a non-
functional kidney, or ureteric stenosis, which in development stifle and compromise
kidney function. In the localized lesions to one renal pole, containing calcifications
and limied dysfunction, partial nephrectomy is indicated.
Reconstructive Surgery (Plastic). The healing process of tuberculous lesions
(healing by sclerosis) determines at the ducts level of the urogenital system a number
of serious disabling diseases that can compromise kidney function, known as
"healing disease" or "second disease".
Bladder sequelae - small tuberculous bladder is usually treated by
enterocystoplasty to increase bladder capacity with digestive segments of ileum,
colon, etc.
Ureteric stenosis in the distal portion requires, after the length of pelvic ureter
stenosis from the bladder, uretero-vesical reimplantation (juxtavezical stenosis), or
bladder flap (Casatti-Boari) in ureteric stenosis in a few cm of the bladder,
reimplantation into psoic bladder or entero-urethroplasty with the ossified ileal
segment in lombo-iliac ureter stenosis.
At the kidney level, in the renal pelvis stenosis, ureterocalicostomy is
performed. A speleotomy or partial nephrectomy will be performed in the caves from
the kidney parenchyma.
TREATMENT. Surgery is always accompanied by the tuberculostatic
treatment. Epididimectomy or orchiectomy is recommended in large fibroid or
fistulising lesions.
After clinical recovery and end of treatment, the patient requires a long
follow through treatment because TB relapses are not excluded.



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The lithiasis of the human urinary system is a disease known ever since
antiquity, around 5000 B.C.
The first document related to this disease is a mixed calculus (uric acid and
calcium phosphate) discovered on an Egypian mummy dating back to year 4800 B.C.
Hippocrates explained it by way of calcarous water indigestion, and in Rome,
Galenus made the connection between tophi and uric acid calculi.
In the Middle Ages, on the one hand because of the negative influence of the
Hippocratic oath (I will not cut to remove gravels, even with pacients affected by
such a disease) and because of the increase of responsibility, lithotomists almost
disappeared.
The renal lithiasis is currently frequent in developed countries, with an
incidence of 0,1% of the population. Geographic distribution is uneven. It is an
endemic disease in South Eastern Asia, Middle East, India, etc, whereas in Southern
Africa it is a very rare, practically unknown, disease.
ETIOPATHOGENESIS
Of the attempts to explain lithogenesis, many etiopathogenic theories came
out, some discordant or even contradictory. Urinary lithiasis is a disease caused by a
number of intricate etiopathogenic factors, which act simultanously or alternatively,
with a multitude of proptious causes. Of the multitude of factors explaining the
etiopathogenesis of lithiasis, there are 4 more or less exact theories trying to account
for the apparition of urinary calculi:
Crystallization theory: a solution is over-saturated when it contains a bigger
quantity of substance than it is normally possible to be dissolved. There are two
additional conditions: excessive elimation of salts from the urine and the decrease of
the urinary volume. Urine is an over-saturated crystalliod substance, the result of the
concentration fuction of the kidney; it is in equilibrium and it does not precipitate
and therefore calculi will not appear. Excessive elimination of salts leads to an over-
concentration, which in conjunction with the decrease of the urinary volume (the
4. Lithiasis of the urinary tract
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solvent) disturbs the equilibrium of the solution (the urine), which becomes unstable
and thus the conditions for the precipitation of the urinary constituents are created.
The matix theory. The crystals lay on an organic matrix made up of serum and
urinary proteins: alpha-1 albumines and 2-globulines, glycozoaminoglycans, A
matrix substance, mucoproteins, B matrix substance, etc. It is a fact that all calculi
have the organic matrix in commun.
The theory of the precipitation nucleus. According to this theory, the
formation of calculi is initiated by the presence of an external particle or of a crystal
in the over-saturated urine. This is the element which creates the conditions for
urinary precipitatious constituents and their subsequent growth.
The theory of urinary crystallization inhibitory elements. Magnesium, zinc,
pirophosphates, citrates, a series of mucoproteins, proteoglycan, ribonucleic acid,
chondroitin sulphate etc, inhibit the crystalliation in the urine. Low concentration or
absence of such substances in the urine lay the conditions for calculi crystallization
and formation.
Favourable factors: There is a series of risk factors with various action mechanisms
among which over-eating, especially too much meat eating habits (uric lithiasis);
vegetarian diet (phosphate lithiasis). Sedentary lifestyle, obesity, hormonal lack of
balance, metabolic status of the patient usually with a genetic cause, reduced liquids
ingestion, are known risk factors. Geographical and climate factors also play a role.
Metabolic disorders. A number of metabolic disorders (hypergycemia,
hypercalciuria, uricozuria, cystinuria) have a lithiogenic etiologic implication.
DISORDERS OF THE CALCIUM METABOLISM
Primary hyperparatyroid it produces extra parathyroid hormones. It is met
with less than 5% of the lithiasis patients and it is caused by a hyperplasia or by a
parathyroid adenoma. Hypersecretion of parathyroid hormone produces an increase
of resorption of calcium in the bones, a reduction of the tubular re-absorption of
phosphorus (in the distal tube) and an increase of the re-absorption of calcium in the
distal tube. This is followed by hypercalcemia. Finally a hypercalciuria and a
hyperphosphaturia are produced against the background of a hypophosphatemia and
hypercalcemia.
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Overdose of D vitamin brings about an increased intestinal absorption and an
enhanced resorption of the calcium in the bones. Hypercalcemia leads to
hypercalciuria in the end.
Prolonged immobilization (after trauma, fractures, stroke etc) leads to
demineralization of bones, consecutive hypercalcemia and hypercalciuria.
Absorbative and renal idyopathic hypercalciuria
Absorbative hypercalciuria is the result of an enzyme disorder related to the
intestinal calcium transfer.
Renal hypercalciuria is an enzyme disorder related to the re-absorption of
calcium at the level of the renal tube. In these two forms of hypercalciuria, the serum
calcium is normal.
DISORDERS OF THE OXALIC METABOLISM
Secondary hyperoxaluria is caused by the increased intestinal absorption of
oxalic acid. In the intestine, the oxalic acid is mostly linked to calcium and
consequently, it cannot be absorbed at this level in this form. In the end part of the
ileitis there is an extra quantity of free fat acids which fix calcium. A bigger quantity
of free oxaic acid is thus created which is absorbed and eliminated afterwards
through the kidneys (hyperoxaluria).
Primary hyperoxaluria is a renal enzyme metabolic disease followed by the
excessive elimination of the oxalic acid which evetually becomes a malign recurrent
calcium oxalate lithiasis, especially with children, followed quickly by the the
installation of renal insufficiency.
DISORDERS OF THE URIC ACID METABOLISM
Normal uric acid level is 700-750 mg/24 hrs.
Primary hyperuricozuria is a metabolic disorder consisting of an over-
production of uric acid which lays especially at the level of small articulations,
making up the clinical overview of the gout. Still, only 10% of these patients have
hyperuricozuria.
Secondary hyperuricozuria is a a more frequent form, a consequence of an
excessive amount of purines (over-eating), or the consequence of an increased
consumption of alcohol. Sometimes hyperuricazuria is brought about by a massive
distruction of the bodys proteines (consumptive diseases tumors, after treatments
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with cytostatics). An important detail is the presence of a simultaneous disorder of
the uric acid metabolism with patients accusing calcium oxalate lithiasis. The
mechanism could consist of the blocking action the uric acid has against
proteoglycan (which inhibits crystallization).
METABOLIC DISORDERS OF THE AMINE ACIDS
Cystine lithiasis is the result of an enzyme metabolic disorder which consists
of amine bibasic acids (cystine, lysine, ornithine, arginine) re-absorption disoder
from the level of the renal tube and the gastrointestinal tract. The results is an
elimination in big quantities of cystine, which, like the uric acid precipitates in an
acid environment, and it leads to cystine lithiasis.
Urinary infection and urinary stasis are important risk factors which
contribute to the apparition of the various types of infectious lithiases, of which the
phosphate-ammonia-magnesium one appears in the presence of the proteolithic
germs (Pseudomonas, Proteus, Klebsieila). These germs have the capacity to divide
the urea in ammonia and CO2. In its turn, the urinary stasis sets the conditions for
infection through urodynamic disorders and aggregation of crystals, an intermediary
phasis of calculi formation.
PATHOLOGICAL ANATOMY
The place of calculi formation. There are several theories related to the place
of the lithogenesis:
Settling of crystals or of the lithogenic elements takes place on the bottom
membrane of the collecting tubes and on the surface of the renal papilla (Randalls
theory). Thus, the Randal plates are formed; they come loose and fall in the pelvis
cavity where, by contact with urinary constituents, the calculus grows bigger.
Carrs theory. The settling of the lithogenic material takes place in the renal
lymphatics which begin clogging afterwards. At a later stage, the bottom membrane,
which separates it from the collecting tubes, breaks and it eventually enters the
urinary channels.
Location rarely intraparenchymal, in the pelvis cavity (minor and major
calyces), renal pelvis, UPJ, (lumbar, iliac or pelvic) ureter, urinary bladder, urethra.
Number they can be single, multiple, and staghorn calculi can totally or
partially occupy the colecting system. The chemical compostion can be determined
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by means of spectrophotometric studies or by crystallography. The presence of
calcium in the composition of the calculi confers radio-opacity; the more intense
radio-opacity, the bigger the concentration of calcium. The crystalographic
classification is described in Tabel II.
The echo of the calculum upon the excretive channels and upon the renal
parenchyma is determined by:
Obstruction urinary channels expand causing renal pelvis dilatation (hydro-
nephrosis), which compresses the parenchyma and it makes it thinner leading to
attrofiation and to the loss of fuctionality of the kidney;
Infection of the urinary channel in the long run it can be responsible for
pylo-nephritis (accute or chronic), pylo-nephrites or pylo-nephroses (final stage of
renal suppurations).
LITHIASIS CRYSTALOGRAPHIC
NAME
HARDNESS
I. CALCIUM
Monohydrate Ca oxalate Whewellit +++++
Dihydrate Ca oxalate Wheddellit +/++
Ca phosphate Hydroxiapatite ++
Apatite carbonate Apatite carbonate +++
Dihydrate Ca carbonate Brushite +++
II. Non-calcium
Uric acid Uric acid ++++
Phosphate-ammonia-
magnezium
Struvite +
Cystine Cystine +++
Tabel II. Crystalographic classification of the urinary system calculi.

SYMPTOMS
Clinically, urinary lithiasis is latent or active.
The latent form is dicovered by chance on the occasion of a systematic
exploration of a general disease or accidentally, on the occasion of a general
examination for other reasons incorporation, employment, periodic examinations
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run in various professions or on the occasion of paraclinical examinations developed
in order to diagnose a disease urine examination, radiologic examination,
ultrasound etc.
The active form. The signs of lithiasis are typical and non-typical.
Non-typical signs reduce lumbar pain, non-systematical with abdominal
projection pain. In other instances (especially with women), the pain is missing, the
sole manifestation being dim, stinking urines, which appears after various treatments
for unsufficiently explored urinary infections.
Typical signs typical renal colic is a very intense, paroxistic pain, usually
caused by a trip, sports etc, which rare appears spontaneously. Most frequently, the
renal colic has a lithiasic etiology, but they are not synomymous. Any obstacle that
suddenly appears on the superior urinary channel (clot, calculus, pus, external
obstacles) can start the renal colic. From a physiopathological point of view, the
renal colic is the result of a hyper-pressure appeared at the level of the superior
urinary channels. Muscular spasm and the distension of the renal capsule, which
accompany it, contribute to the amplification of the pain.
It can be unilateral or bilateral, more intense on one side, at the level of the lumbar
region, with irradiations in flanks and in the respective iliac fossa, as well as at the
inferior level, towards external genitals (testicles and labia) or towards the basis of
the thigh, and never in the inferior member (when it usually is of vertebral origin).
The renal colic can be associated with bladder signs: pollakiuria, bladder
contraction, dim and bloody urine; general signs: agitation, paleness, perspiration,
nausea, vomiting, at times accompanies by abdominal flatulence.
Haematuria is: macroscopic, sometimes with clots, very often started by an
external factor; or microscopic, revealed by a series of investigations: urinalysis or
the Addis test.
The infection has various aspects, from pyuria, accompanied by burning
during urination, to the urinary infection of the parenchymal-type, with fever,
pointing to an accute pyelonephritis or to a lithiasic pyelonephrosis, with a
suppurative perinephritic reaction.
The general manifestations urinary infection, with bacteremia or even with endotoxic
shock, can have a dramatic evolution.
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Kidney faliure:
Accute. It is active in the form of anuria, and it usually appears on a sole
functing kidney (congenitally, functionally or surgically), or in the more rare
situation of bilateral simultaneous obstruction of the superior urinary system by a
calculus.
Chronic, with a slow installation. It usually appears with patients with old
lithiasis history, with bilateral manifestations, where the combination obstruction-
infection has caused extended parenchymal distructions.
DIAGNOSIS
History. The patients living and working conditions have to be known. Also
it is important that the eating habits of the patient be known: meat characterized diet,
hypercalcium diet etc.
The family history is also important for the diagnosis: congenital anomalies,
cystine, uric lithiasis etc.
Thus, information about a series of personal diseases can be obtained:
tuberculosis, bladder-ureteral reflux or urination disorders caused by obstructions at
the level of the inferior urinary system.
Objective examination is an important moment with a view to establishing
the diagnosis of urinary lithiasis: the abdomen will be carefully examined in order to
discover potential signs of peritoneal irritation and to make the most important
differential diagnosis from a peritonitis caused by various factors. The lumbar
regions and the urethral points will be touched and determined pain will be
discovered (the current Giordano sign). External and internal genitals will also be
examinated.
Laboratory investigations
Urinalysis will be made and taken from all patients suspected of having
urinary lithiasis. These investigations can reveal a macroscopic or microscopic
haematuria, pyuria and the presence of germs in the urine. The presence of crystals
will be discovered, which will provide potential indications about the type of the
urinary lithiasis (uric acid, oxalates, cystine etc). The urinary PH gives information
related to its sensitivity to antibiotics and chemotherapy.
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The urea and the creatinine blood level provide information on the global
renal function of a patient with bilateral lithiasis or with lithiasis at the sole kidney.
Imagistic investigations
Ultrasound. It is an important investigation with patients having renal
insufficiency, but also with pregnant women. The calculus appears as a hyper-ecoic
image with a psterior shaddow cone; also, the US reveals the conseqence of the stone
on the urinary tract (the dilatation) and of the kidney (the lamination of the renal
parenchyma).
KUB X-ray. The calculi which contain calcium are visible at x ray. The calculi
made up of uric acid are radiolucent and cannot be identified with this examination.
Apart from the radioopaque urinary calculi, one can see mesenteric lymphatic
ganglonic calcifications, the calculi in the gall bladder, foreign elements and
phleboliths. The renal pelvis calculus on a L-L radiography is projected on the spine,
whereas the biliary calculi are projected in the front of the spine.
The IVU shows the place and the number of radioopaque calculi or confirms
they do not exist in the urinary system; it also objectifies the radiolucent lithiasis
(mantel symptom). Secondly, IVU show the echo of the lithiasis upon the kidney
and upon the colecting system.
Retrograde ureteropylography. It is seldom used, namely when IVU is not
conclusive, from one reason or other, or if the patient is sensitive to the contrast
substance.
Explorations related to knowing the nature of the lithiasis. Blood and urine
investigations have to be made in order to point to high elimination substances which
can precipitate.
Calcium, uric acid, phophorus, cystine etc will be known by blood and 24 hrs-
urine tests. The value of the urinary PH, the density of the urine and the urine sample
will aslso be found out and checked;
Induced crystalluria can provide information on the type of lithiasis;
The analysis of the stones is the most precise method to find out its
composition the chemical analysis and, even more accurately, radiocrystallography
and X-rayed radiomicrography of the calculus, or the spectral analysis of the
calculus.
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ANATOMICAL-CLINICAL FORMS
Ureteric lithiasis. It manifests usually through reno-ureteric colics, very often
associated with total hematurias, associated digestive phenomena: nausea, vomiting,
flatulation. While the calculus goes down along the ureter towards the bladder, the
pains are still colic, but are intermitent and have irradiations towards the inguinal
channel, testicles and the basis of the thigh; with women, the pain irradiates towards
hypogastrium and the big labia. While the calculus gets closer to the urinary bladder,
the obstructive signs described above are associated with bladder irritations
(pollakiuria, bladder tenesmus, urination pain), explained by the common
innervation of the terminal ureter and the bladder trigone.
The diagnosis steps have been already described. We should mention the
possibility to see, by way of US, the calculi in the terminal ureter (ureterovezical
junction, intramural or submucosa). The US is to be done on a full bladder by
applying the cutaneous transducer on the hypogastric area. The pelvic ureter lithiasis
can also be identified by way of transrectal US.
Differential diagnosis poses problems especially in the case of proximal ureter
lithiasis when the digestive symptomatology is louder. In the case of such non-
typical forms, a series of digestive diseases will have to be excluded: gastro-
duodenal ulcer, accute appendicitis, accute pancreatitis, intestinal-mesenteric infarct,
ileus etc.
Bladder lithiasis
The primitive form is rare and it appears especially with children.
Etiopathogeny the cause is low proteine diet and deshydratation in hot, tropical
regions.
The secondary form appears with patients suffering from various obstructive
under bladder diseases: adenoma, prostate cancer, bladder neck sclerosis, ureteral
strictures. It is therefore more frequent in male patients. More seldom, the bladder
calculi have their origin in the kidney, being eliminated through the ureter.
The diagnosis is based on clinical symptomatology: hypogastric pains with ureteral
irradiations, total haematurias with induced character, pollikiuria, urination disorders:
dysuria, interrupted urination, total haematuria or dim urine.
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The paraclinical necessary tests are: KUB x-ray and IVU with a; the US of the
bladder (a full bladder) and cystoscopy under anaesthesia.
Urethral lithiasis
Primitive urethral calculi appear on an obstructive malformation of the
inferior urinary system which brings about stasis and urinary infection and are
usually very rare.
Secondary urethral calculi are more frequent, they form inside the kidneys or
in the bladder and they are comprised in the ureter while they pass through this
region together with the urinary flow only to be eliminated spontaneously. Many
calculi stop at the level of the membraneous ureter, and the majority get stuck at the
level of the anterior ureter.
Diagnosis. The clinical symptomatology is characterized by intense perineum or
urethral pain, followed by complete urine retention, intense dysuria with very weak
urinary stream, even dropping.
Clinical examination can reveal the stone when touching the anterior urethra.
With women, the urethral calculus can be felt by vagina examination.
Paraclinical necessary explorations are: radiography of the bladder, prostate
and urethra, which can highlight an opaque image along the urethra; voiding
cystourethrography or retrograde urethrocystography confirms the presence of the
urethral stone and the urethroscopy allows us to see it.
DIFFERENTIAL DIAGNOSIS
I n the clinical stage the differential diagnosis must be made in spite of the
painful abdominal syndromes. US and radiology of the urinary system must be a rule
in spite of the undetermined painful abdominal symptomatology.
I n the radilogical stage a series of errors are possible:
Errors caused by excess. Radioopaque images identified on the KUB X ray as
calculi can be non-lithiasis intraparenchymal opacities (bacillary calcified wounds,
calcified tumors), or extra-renal opacities (stercoliths, ganglionic calcifications,
billiary calculi). On the L-L X ray (profile) urinary calculi project against the spine
while the biliary calculi project in front of the spine.
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Errors casued by not recognising the lithiasis; the calculus can be too small,
semiopaque or radiolucent. The comparison of the KUB x ray with the IVU ones
leads to avoiding errors.
PROGNOSIS
When the calculus has been eliminated (spontaneously, ESWL) or removed by
various methods (classically, by endoscope PCLN, ureteroscopy), healing can be
final. Recurrance is a rule though in lithiases that have been developed on
malformations of the urinary system or against the background of metabolic disease
(hyperparathyroidis, gout etc.).
COMPLICATIONS
Complete obstruction of the excretion channel on a sole functioning kidney
calculus anuria. Depending on the presence or on the absence of the urinary
infection, which is an aggravating circumstance, with a more reserved prognosis,
there are two clinical forms of calculus anuria:
calculus anuria with uninfected urine usually appears after a typical renal
colic, the patient does not have urinary infection history and does not have
fever;
calculus anuria accompanied by infection is very severe, the patient has fever,
a general bad condition, the major complication being the installation of the
toxic- septic shock;
I nfectious complications. The infection can be located in the channels or it
can invade the renal parenchyma or even the perirenal tissue.
The infection of the excretion channels is more frequent and it persists until
the calculus is removed. The invasion of the renal parenchyma translates into
pyelonephritis (the complication of a urinary infection), pyelonephrosis, and when it
permeates through the perineal fat, the perirenal phlegmon appears.
Cronic kidney faliure.. It is the result of the parenchymal participation in the
inflamation process, of the stasis and of the dillatation of the excretion channels. It is
a chronical renal insufficiency which evolves along several years.
TREATMENT
The treatment of the lithiasis comprises gneral and preventive emergency
measures as well as specific treatment for each type of lithiasis. The treatment needs
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to be adapted per each patient, depending on the composition of the stone, the state
of the kidney affected by lithiasis, the state of the opposite kidney, the value of the
renal function, and on the pathophysiological mechanism of the lithiasis.
EMERGENCY TREATMENT it refers to the complications of the
lithiasis.
Mechanical complications require various measures, depending on the nature of
the complication. The renal colic. Pain can be relieved by getting painkillers: The
neuroleptics intensify the effect of the painkillers, they are antiemetic and reduce the
spasm of the sleek musculature: Plegomazin - 1 phial intramuscular or intravenous,
slowly, dissolved in 10 ml of serum. Opiums may be given only in extreme cases,
after the diagnosis has been established and is certain; they always have to be
associated with antispasm medicine, because the opiums kill the pain but maintain
and strengthen the spasm of the sleek musculature Demerol. Antispasm medicine
shall also be given: Papaverine in the form of pills or solution of 4%.
In case of heavy vomiting, 0,25-0,50 mg of Atropin shall be given i.v., which
apart from the antispasmodic effects, it also diminishes the digestive secretions.
Calculus anuria requires an emergency treatment. Irrespetive whether it is
infectious or not, the best solution is high urinary derivation nephrostomia. Whwn
this intervention cannot be made, a ureteral stent will be set up above the obstacle. If
the obstacle is surpassed, the surgical intervention (PCLN, ureteroscopy,
ureterolithotomy or pyelolithotomy) will be made in several days; alternatively, it
will have to made immediately.
Infectious complications
Accute or chronical pyelonephritis antibiotherapy or chemotherapy, usually
for a longer period in the case of chronical forms and the ablation of the calculus
which partially blocks the channels and which has caused the pylonephritis.
Pylonephrosis requires a massive antibiotics treatment from the very first
moment and possibly permanet emision nephrosomy and subsequent drainage. Then,
taking into account that the kidney is practically distroyed, a nephrectomy will be
made, but only when there are information about the functionality of the opposite
kidney.
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Perinephritis antibiotherapy and surgical treatment, which consists in the
incision and the drainage of the renal loculus. The treatment of the lithiasis, or the
nephrectomy, will be made subsequently
Chronic kidney faliure it is treated by dialysis and possibly transplant.
MEDICAL TREATMENT
General measures
Diuresis treatment. It is supposed to produce a diluted urine with low saline
concentration. Not all patients can take a 6l/ 24 hrs duiresis for sevarl reasons
(cardiac state, high blood pressure, the refuse of the patient etc.), but a 2,5-3l/ 24 hrs
can be made. The important fact is how much is being eliminated and not how much
is being drunk. 2500 ml of (measured) liquid will be drunk every second hour, during
the day, and 500 ml before going to bed.
Alcohol is contraindicated in uric lithiasis patients.
Diet. In principle, a balanced diet is recommended, without useless
restrictions, but also without abuses.
Sedentary lifestyle is to be avoided
Removal of the obstacle in the urinary channel
Special measures. They depend on the chemical nature of the calculus and on
its etiology. The urinary pH in the desired direction shall be modified by urine
alkalizing or acidifiation. The medicine treatment will be customized according to
the various etiological forms.
Calcium lithiases a modrate reduction of hydrocarbonates and cheeses, if
there is a hypercalciuria. Etiological treatment in hyperparatyroid, D
hypervitaminosis, sarcoidosis, avoidance of prolonged immobilization.
The patho physiological treatment is meant to reduce hypercalciuria. When the
absorbative form is active, a low calcium diet and products that inhibate its intestinal
absorption will be recommended, such as: Natrium-cellulose- phosphate, sodium
phytate, etc. In the case of hypercalciuria of renal origin, a low salt diet and diuretics
(Tiazide) are recommended. With patients with calcium lithiasis, but also with
hypouricozuria, it is indicated that Allopurinol (an inhibator of oxidase xanthine)
should be given, because it stops the production of uric acid.
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Uric lithiasis benefits of diuresis treatment with alkaline waters. The diet
will be a low proteine one, but rich in fruit and vegetables. Alcohol will be out of the
question.
Oxalic lithiasis the diet will avoid cacao, chocolate, spinach, a low
carbohydrate diet. The pyridoxine (B5 vitamin) has a good effect. 2g/ day of
orthophosphates as well as potassium salt will be given. If hyperuricozuria is also
present, it is indicated to use Allopurinol and natrium-cellolose-phosphate, in case of
hypercaciuria.
Cystine lithiasis: moderate restriction in using proteines, Metionine (not with
growing children). Increased diuresis. Acetalozamide for inhibating the carbon
anhydrase. Solubilization of the cystine, Tiola, D-penicilamina (it produces
leukopenia). It has recently been discovered that an inhibator of the conversion
enzyme (Captopril) used in the HTA treatment forms compounds which are very
soluble with cystine. Unfortunately, due to its low blood pressure character it can
only be used with patients suffering of cystine lithiasis who have a high blood
pressure.
Xanthine lithiasis in principle, it requires the same measures as the cystine
lithiasis. The administration of alkalizing substances and of Allopurinol leads to the
elimination of the hypoxanthine, which is more soluble than the xanthine.
SURGICAL TREATMENT
In general, with urinary lithiasis, surgical treatment is indicated for all stones
which cannot be eliminated spontaneously, be it open or endoscopic surgery. Today,
the majority of urinary calculi is solved by ESWL. These methods are supposed to be
used with calculi on the superior urinary channels associated with urinary infections
that cannot be treated otherwise, which cause progressive renal parencymal pain, the
obstruction of the main urinary channel and a persistent pain. In most cases, the
surgical treatment has to be applied only after the patients entire metabolic
assessment. In emergency cases, such as a complete obstruction of the main urinary
channel, urosepsis, it is first manadatory to make a urinary deviation by setting up a
urethral stent or by making a percutaneous nephrostomia. The lithiasis is solved
afterwards, after the treatment of the septic state.

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OPEN SURGICAL INTERVENTIONS
The nephrectomy and the partial nephrectomy. The nephrectomy is a radical
intervention by which a compromised morphofunctional organ is removed, as a
consequence of the renal sound of the calculus (the stasis and the infection). Partial
nephrectomy is a radical intervention on a compromised renal pole (1/3 of the
kidney), keeping the other two thirds which are not distroyed. Partial nephrectomy
can remove even more than 1/3 preserving a smaller part of the kidney, when the
situation of the patient requires it.
Pylolithotomy is an intervention meant to remove the calculus from the renal
pelvis, consisting of a limited dissection of the sinus in order to get a better view of
the renal pelvis posterior side. After the extraction of the calculus, the renal pelvis is
sutured with 4 or 5.0 chromated catgut wires (pyloraphy).
Pylonephrolithotomy is a technique used to extract a pelvian calculus which
has some prolongations usually in the inferior pelvis (fig. 5.1. A and B). The
pylotomy on the
posterior side of the renal
pelvis is extended to the
posteriour side of the
inferior renal pole along
the inferior pelvis. After
the calculus has been
removed, both the renal
pelvis and the kidney
will be sutured. (pylography and nephrography)
Anatrophic nephrolithotomy (Smith and Boyce
1967) is recommended in cases of coral-shaped
calculi with pelvis stenosis. It is also indicated in any
situation when the pylolithotomy is practically
impossible (intra-sinus renal pelvis and for recurrent
situations, after previous pylolithotomies, when the
access to the renel sinus is very difficult).
Radial polinephrotomy (Wickham) (fig. 5.2.) It
Fig. 5.1. A and B. Pylonephrolithotomy
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Fig. 5.3. PCNL
is used as a sole procedure or in combination with one of the above-mentioned
procedures. It is a technique usually used to extract pelvian calculi associated with
volumunous calculi in the renal pelvis. Radial incisions are made on the posterior
side of the convex margin of the kidney. After the calculus has been removed
multiple nephrographies are being done.
Bench surgery and self-transplantation is a treatment method with patients
having recurrent lithiasis, with many prior interventions and with renal pelvis and
urethral stenosis after the surgical interventions.
Ureterolithotomy is the extraction of a calculus from the ureter (lumbar, illiac
or pelvic) through a classical surgery. After the discovery and the preparation of the
ureter, the longitudinal ureterotomy is being made, followed by the ureterolithotomy
as such, the operation by which the calculus is extracted from the ureter through the
palgue made by means of the ureterotomy. The intervention is finished by the
ureteroraphy of the ureteral plague.
In the age of the ESWL and of PCLN these interventions have only a historical
interest. However, ureterolithotomy remains an intervention only when ESWL,
PCLN, URSA or URSR fail from one reason or other, or they are couter-indicated.
PERCUTANEOUS NEPHROLITHOTOMY (PCNL)
It has opened the era
of the endourology of the
superior urinary system.
Practically, any stones,
irrespective of its location,
size, hardness, volume or
number, can be solved
endoscopically. The
nephroscope can be
introduced through the nephrostomy path, allowing the extraction of the calculi from
te renal plevis, pelvis or JPU (fig. 5.3.). The ultrasound allows the fragmentation of
the voluminous or coral-shaped renal pelvic calculi and their extraction.
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The advantages of this method consist in the fact that it is possible to remove
a renal calculus through a 1 cm plague, the convalescence is short and the full
recovery of the patient is made in a short while.
The complications and the PCLN morbidity are much reduced as compared to
open surgery. However, severe complications with serious consequences leading to
hemostatic nephrectomy or even death in rare cases are not excluded.
URETEROSCOPY
It is an endoscopic diagnosis and treatment procedure
for various affections of the ureter, among which lithiasis is
the most frequent. Pelvic ureter calculus is treated by means
of ureteroscopy with ultrasonic, electrohydraulic, pneumatic
or laser fragmentation, followed by the extraction of the
fragments (fig. 5.4). Other ureter diseases which can be
solved through retrograde ureteroscopy are the benign
ureteral stenoses, congenital hydronephroses through a UPJ
syndrome. In well selected cases, with a correct operational
indication, ureteral or peilo-pelvic tumours can be removed.
Antegrade ureteroscopy is an endocopic method to solve
calculi in the proximal (lumbar) ureter through the transrenal introduction (through
the percutaneous nephrostomy channel) of the ureteroscope in the ureter; contrary to
the retrograde ureteroscopy where the ureteroscope is being introduced in the
opposite direction of the urine flow, transurethrally in the bladder and from there in
the ureter through the ureteral orifice.
Besides lithiasis, the antegrade ureteroscopy is also used to solve benign
stenoses of the proximal ureter, external fragments (broken stents in the ureter) can
be extracted, and also to solve tumours of the proximal ureter in well selected cases,
with an operational clear indication.
LAPAROSCOPY
The laparoscopic transperitoneum approach, but especially the
retroperitoneum one, can be utilized for pylo-, ureteral and even renal calculi. It is an
alternative to open surgery, for cases when the endoscopic intervention does not
solve the lithiasis.
Fig. 5.4. Ureteroscopy
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BLADDER LITHOTRIPSY
The treatment oft he bladder calculus is endoscopic (lithotripsy) in the first
place. The primary fragmentation of the calculus can be made mechanically (fig.
5.5), ultrasonically, pneumatically, electrohydraulically or by laser, followed by the
extraction of the fragments through the pod of the Punch lithotripsy (mechanical
lithotripsy), after their processing.
In the case of ultrasonic, electrohydraulic, pneumatic lithotripsy, these forms
of energy produce the primary desintegration of the calculus which afterwards is
being processed mechanically by the Punch lithotripsy into fragments that evacuate
through the pod of the lithotripsy along with the stream of the irrigation liquid, or, in
the case of bigger fragments, they are extracted with the working element of the
lithotripsy.
The surgical treatment (cystolithotomy) is used only in the case of
voluminous, multiple calculi, which cannot be solved endoscopically, or in the case
of associations with big prostate adenoma. The intervention consists of
cystolithotomy (the extraction of the calculus from the bladder) and simultaneous
suprapubic adenomectomy. When the prostate adenoma is small, and the open
intervention (adenomatomy) is not indicated, the transurethral resection of the
adenoma will be made (TUR P).
EXTRACORPORAL SHOCK WAVE LITHOTRIPSY (ESWL)
It solves the urinary lithiasis without incision. The shock waves produced by
the electrod are focused and directed towards the calculus through a digitalized
system.
Fig. 5.5. Mecanic bladder lithotripsy (Punch).

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The principle of the extracorporal lithotripsy consists of the desintegration of
the urinary calculi under the effect of the shock waves generated outside the body
and focused towards the calculus. The penetration of the tissues by the shock waves
cause minimum cellular damage. The calculi are desintegrated in small fragments
which can be eliminated spontaneously. The location of the calculus can be set by
ecography or radiology (fluoroscopy). The localization allows the treatment of the
calculi in the superior urinary system, irrespective of their location, if they have
dimensions up to 1,5 cm in diameter.
THE TREATMENT OF THE URETHRAL LITHIASIS
It is a surgical intervention and it consists of the extraction of the calculus or
of the calculi, through external urethrotomy and the surgical correction of the
urethral anomaly (urethral stricture). In some cases (small calculi), the calculus can
move into the bladder, where it can be treated by mechanical lithotripsy (Punch).
Except for ESWL, all above-mentioned interventions are made on a general
anaesthesia with orotracheal intubation or anaesthesia: rachidian or epidural.
CONCLUSIONS
In 80% of the cases, the lithiasis of the superior urinary system has metabolic
causes. The ablation of a renal or ureter calculus represents just an episode of the
treatment. After this, the treatment needs to be continued, more exactly prophilaxis
has to be done.
This episode in the treatment of the urinary lithiasis is done in special centers
in other countries, where, along with the chemical analysis of the calculus, which
leads to better information about its composition, all metabolical blood and urine
explorations are being made to see the metabolic status of the patient.
Based on these investigations, and after a correct analysis of the results, plus
the removal of the risk factors, the prevention of the urinary lithiasis starts to be
undertaken.
The treatment of the urinary system lithiasis consists of several therapeutic
measures (diuresis, eating habits etc) and a metaprophilaxis directly linked to the
nature of the calculus, of the metabolic disorders and of the risk factors.
The introduction of the endoscopic surgery (PCLN, ureteroscopy),
laparoscopy and ESWL in the treatment of the urinary system lithiasis meant a real
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revolution. The ablation of the lithiasis of the superior urinary system can be solved
without a classical surgical intervention in more than 90% of the cases. The
treatment of the lithiasis cannot and must not be confined to this side of the complex
treatment of this disease.
In the future, it is possible that in our country too the patient should be studied
also from a metabolic point of view (after the removal of the calculus, be it
endoscopically, or through ESWL, as a sole therapy, or through an associated therapy
endoscopic surgery + ESWL), in order to pevent recurrent situations by association
of some special targeted measures, depending on the characteristics of the lithiasis.




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Fig. 6.1. Prostate after McNeal a. peripheral zone; b central zone; c
transition zone; d - fibro-muscle stroma



The prostate is a gland with a complex structure made up of acini, stroma and
smooth muscular fibres.
Its development starts in the 12th week of the embryonal life, under the
influence of the testicular androgenes produced by the foetus and it has its origin
mostly in the urogenital sinus, with the exception of the ejaculatory duets,
verumontanum and of the acinus glands of the central region which come from
Wolffs channels.
Having the shape of a flat cone, it is situated in the small pelvis, behind the
pubian symphysis and in front of the rectum and it contains the Prostate urethra. It
usually is 4-6 cm long, 3-4 cm wide and 2-3 cm thick.
On the basis of some anatomical and histological studies, McNeal introduced
the concept of prostate regional anatomy, in 1970 (fig. 6.1.).
Thus, it
comprises a large
peripherical area
and a small central
one, which
together make up
95% of the
volume of the
gland. The
transition zone
(5%), the part
situated exactly near the urethra at the level of the verumontanum, is made up of the
peri-urethral glands and it constitutes the starting point of the benign prostate
hyperplasia (BPH).
The prostate cancer (PC) has its origin in the peripheral region, in around 60-
70% of the cases, in the transition zone, in 10-20% of the cases, and in the central
zone, in 5-10% of the situations.
6. Benign prostatic hyperplasia (BPH)

a
b
c
d
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BPH is a histopathological term, it is the currently accepted name of this
disease, replacing the other names such as: prostate adenoma, peri-urethral adenoma
of the benign prostate hypertrophy.
The prostate adenoma develops inside the gland and since it is impossible to
establish its origin clinically, the name of prostate adenoma seems to be the most
correct one from a clincal point of view. It is a benign tumor, but it is a severe
progressive disease by its high ureter-pielo-renal echo, which, unless it is dicovered
early and treated properly, can lead to renal insufficiency and even death. The first
sign of the progress of the disease is when clinical symptoms become worse and
worse. Sometimes, on a fragment from where the nucleus has been removed or on
other removed parts it is possible to establish the diagnosis of prostate
adenocarcinoma (PC), which, in this case, is a hidden cancer.
BPH inicipent microscopical modifications, which consists of stroma
nodules, can appear around the age of 35 at the level of the gland. Acinus nodules
will form around them in a long process spread over years, until a state of clinically
manifested hyperplasia is reached. Inside the hyperplasia, the nodules vary in size
from several mm to several cm and are mostly made up either of gladular elements,
of fibromuscular elements, or they can have a mixed composition.
The incidence of the disease is similar on all continents (e.g. with 51% of the
men between 60 and 69 years of old), which suggests that the apparition of the BPH
is not linked to environment or genetical factors. It grows with the age and it
practically appears with all men who live long enough.
Systematic studies to allow the assessment of the natural evolution of this
disease have not been made yet. However, some remarks can be made based on data
we have from autopsies, on data obtained after surgical treatments, and on the results
of clinical studies on patients with low urinary phenomena pointing to BPH.
Autopsy studies have shown that BPH is a progressive disease which starts at
around 30. Based on surgical treatment (because there are no well- conducted
epidemiological studies that should give information on the incidence of the
symptoms based on age groups, or on the incidence of the surgical treatment based
on the same criteria), it is estimated that 25-30% of the 50 year old men require
surgical treatment for their BPH in the course of their life.
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An important and still unclarified clinical problem is whether this disease can
stabilize itself over the years, or even an amelioration of the symptomatology. Some
short studies state that with some patients a spontaneous improvement of the
symptomatology is possible. We dont know if this is purely subjective, based only
on a situation where the symptomatology has diminished, or it also has an objective
component due to the decrease of the adenomas volume, or due to the increase of
the contraction force of the detrusor muscle.
ETIOLOGY
The BPH etiology is still unknown. Several hypotheses have been formulated
based on histiological and homoral changes which come along with the age. It is
known that hyperplasia appears if the two following factors are present: 1)
dihydrotestoterone (DHT) and 2) aging.
The importance of DHT in prostate increase is proven clinically with
patients with a genetical deficit of 5-a- reductase, the enzyme responsible
with the transformation of the testosterone in DHT. The affected men have
ambiguous external genitals at birth, but at puberty due to the normal level of
plasmatic testoterone, they become virile, and the erection and the ejaculation
are normal. However, because of the absence of DHT, the prostate remains
undeveloped and will never have hyperplasia. The administration of DHT (at
any age) brings about the normal growth of the gland.
With age, the testosterone decreases becasue the stimulation of the Leydig
cells diminishes and becasue of its conversion in estrogen, in the peripherical
tissues. On the other hand, an increase of the level of 5- - reductase and of
the androgyne recipients in the hyperplasia tissues can be seen. Anyway, the
role the androgenes and the estogenes play in the apparition of the BPH is
complex and too little is known about it. Male subjects castrated before
puberty do not develop a hyperplasia. On the other hand, the castation of
patients affected by a clinically proven disease does not lead necessarily to
the atrophy of the gland. It seems that the estrogens lead to the apparition of
the hyperplasia of the stroma and this, in its turn leads to gland hyperpasia.
Another role in the development of the prostate epithelium is triggered by
more growth factors (FGF, KGF= keratinocyte growth factor, a and b growth
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Fig. 6.2. Urethrocystography: prostatic urethra (PU) is elongated, with aspect of scimitar; at
the bottom of the bladder is observed the shadow of the two lobes of BPH
factors), which act on a paracrine and an autocrine way. All these mediators are
induced by the testosterone.
There is also the hypothesis that the BPH appears as a result of the increase of
the stem epithelium cells, a proliferation which is not followed by apoptosis (= the
genetically programmed death of cells).
ETIOPATHOGENESIS AND PATHOLOGY
The first histiopathological modifications appear in the peri-urethral gland
at the level of the veru-montanum (transition zone).
The stroma nodules are made up of a mixture (in various proportions) of
fibrocims and smooth muscular fibers which can be infiltrared with lymphocytes.
The fibro-adenoma nodules contain various proportions of fibrous tissue and glands
affected by hyperplasia.
Glandular hyperplasia usually gets the form of acinus nodules which can
contain stroma hyperplasia. Hyperplasia glands are usually big and are covered by a
high cylinder shaped epithelium. The nuclei are always normal with no signs of
malignity.
Hyperplasia glands can also get other aspects: a) cyst shape as a result of their
distal obstruction; b) small acini covered by a cubic epithelium; c) transition
epithelium, or d) cribiform aspect (which can mime cribiform prostate cancer).
Like the normal cells of the prostate glandular epithelium, the ones of the
BPH are secretion cells producing PSA, citrate, acid phosphatase and other enzymes
and contain zync (data revealed by histochemical studies).
Summarizing the morphological modifications of the urinary system caused
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Fig. 6.3. Cystoscopy. The aspect of bladder weith trabeculation

Fig. 6.4. IVU. The suffering ureter and
bladder
by the BPH , they are:
Prostrate urethra: along with the increase of the prostate volume, the urethra
above the veru-montanum gets longer, it curves and flattens transversally (the
lateral diameter gets smaller, whereas the prior- posterior diameter gets
bigger. Therefore, the urethra appears under the shape of a scimitar; the
presence of the median lobe sets its scoliosis shape (fig. 6.2.).
The bladder neck is risen, and its orifice becomes a sagittal slit (where there
are two lobes), or it gets the shape of the letter Y when the median lobe is
present too.
The bladder trigone is risen, and behind it a retro-trigon depression is formed;
sometimes a very strong inter-urethral bar appears.
After the detrusor hypertrophia, the bladder takes the characteristic aspect with
trabeculation (fig. 6.3.).
Diverticuli will progressively be
formed; they are a series of inert
non-contracting cavities, real
herniations of the bladder mucous
membrane through the muscular
fibers of the detrusor.
The terminal ureter suffer a series
of morphological modifications,
which constitute the mechanisms
of complication related with
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BPH: a) the comprimation of the intramural ureters through the hypertrophia
of the detrusor; b) slow urine elimination through the ureterl orifices because
of the intrabladder hyperpressure; c) the uretral orifices are opened with a
bladder-ureteral reflux; d) fishing line hook ureters by the lifting of the
bladder trigon, which activates the rise of the ureters terminal segments,
leading to an angular shape at their crossing with the deferential channels
(fig. 6.4.).
PATHPHYSIOLOGY
Because the development of the BPH is slow, its effects on the urinary system
install insidiously. The effects of the physiopathology of the hyperplasia are the result
of the complex interaction of several factors such as:
the increase of the resistance of the prostate urethra against the urinary
flow (be it through a spasmodic mechanism caused by the contraction of the smooth
muscular fibers, or through a compressive mechanism);
the level of the intra-bladder pressure, generated during the urination;
the function of the vegetative nervous system
the existence of some associated diseases (diabetis, alkoholism)
BPH represents a morbid entity only if it entails the obstruction of the bladder
neck and, through the alteration of its aperture during urination, it brings about all
physiopathological modifications from the upper region (bladder, ureters, kidneys),
followed by the consecutive anatomo-pathological modifications which were
described at the respective chapter. From this reason there are patients with BPH.
During normal urination, the bladder neck opens at a pressure of 20-40 cm of
water, whereas as far as the BPH is concerned the inter-bladder pressure before the
opening of the bladder neck reaches 100 cm of water. The obstacle which hinders the
emptying of the bladder (in this situation the BPH) always triggers a high bladder-
ureteral-pielo-renal echo. The first organ suffering from the disectasia is the bladder
and, depending on the degree of the bladder suffering, there appears the consequence
on the superior urinary tract.
The bladder consequence. The presence of the cervical obstacle brings
about the hypertrophy of the detrusor; there appear trabeculation - visible
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cytoscopically, but also on the cystography. These modifications characterize the
fighting bladder and they represent the first phase of the bladder suffering.
The hypertrophy of the detrusor is of interest for the terminal part of the
ureters which it compresses leading to the installation of a upper urinary tract stasis,
which appears urographically under the form of a ureteral hypotonia with the
complete opacification of the ureters from the kidneys to the bladder.
Unless the obstacle is removed, the bladder decompensation, characterized by
the apparition of the bladder residue, will start after a longer or a shorter period. The
patient will no longer be able to empty his bladder; the urinary stasis followed by
distension (a residue bigger than 300 ml) is the main cause of all complications of the
urinary system which appear in BPH.
The decompensation of the bladder musculature becomes gradually more
accute, the contractions of the detrusor are slower and slower, and the abdominal
musculature is needed in order to eliminate small quantities of urine. Bladder stasis
gets bigger and at a certain point the urination becomes impossible; a complete urine
retension is installed.
The upper utinary tract consequence is caused by the difficulties of the
ureter in evacuating the urine from the bladder. Slowly there appears the uretero-
hydronephrosis becasue of the following factors:
the compression of the intra-mural portion of the ureter in the phase of
detrusor hypertrophy;
the pressure of the bladder residue upon the ureteral orifices;
the ureteral orifices under bladder distension aer opened bladder-
ureteral reflux.
The effect on the upper urinary tract is bilateral in the BPH and non-
symetical in prostate cancer. The created pressure and the urinary stasis in the small
pelvis leads to the oedema of the renal parenchyma followed by sclerosis, which will
gradually diminish the renal function. The infection brought about by the stasis or by
a iatrogenic cause leads to a sever pylonephritis with renal insufficiency.
SYMPTOMS
The symptoms of the BPH are obstructive and/ or irritative.
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Obstructive symptomatology appears during emptying the bladder, whereas
irritative symptomatology appears during the filling up of the bladder. Irritative
disorders are caused by a hyper-reflection and an instability of the detrusor muscle.
Obstructive symptomatology is represented by the decrease of the pressure
and of the caliber of the urinary stream because of the compression of the prostate
urethra. They are among the first clinical signs to appear. Disuria, usually present at
the beginning, is characterized by the long (waiting) period needed before urination.
This is caused by the fact that the detrusor can no longer generate very quickly the
pressure necessary for urination; intermitence appears becasuse the detrusor cannot
support the necessary pressure until the end of the urination process. Terminal
dropping as well as incomplete emptying of the bladder have similar causes or are
caused by the obstructive tissue at the level of the bladder neck, which can create a
ball vave effect.
Irritative symptoms, such as nicturia and pollakiuria, have another
explanation. The incomplete emptying of the bladder leads to shorter periods
between urinations; a voluminous BPH triggers pollakiuria especially if it is
developed intra-bladderly (a process which occupies space and reduces the bladder
capacity). The hypertrophiated detrusor has an increased excitability and contracts at
smaller urine volumes. Pollakiuria is more frequent at night because cortical centers
are less inhibated and the tonus of the sphincters is lower. Urination emergency and
painful urination are less frequent symptoms and are caused by the impossibility to
urinate regardless of the intense contractions of the detrusor. Pollakuiria and night
disuria install slowly, with periods when they are improving and periods when they
are aggravating. In this phase, the pelvic congestions caused by BPH lead to frequent
erections.
When the vsical residue appears, the symptomatology becomes more serious:
the pollakiuria is active also during day time, and the disuria becomes total due to the
hypotonia of the detrusor. The patient is forced to urinate every second hour during
the day and night, and the pressure of the urinary stream is very diminished.
Pollakiuria is sometimes accompanied by painful urination, a simulation of
incontinence. In the very advanced phase of the disease, with significant bladder
residue, the sphincter is defeated by the hyper-pessure created in the relaxed and non-
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extensible bladder, by the small quantities of urine produced by the two kidneys
which evacuate in small drops.
Accute urine retension can happen anytime during this disease. The triggering
mechanisms include: prostate infarct, low temperatures, alkohol consumption,
medication, or agonitii adrenergici, pshychotropic causes and long postponement of
urination (out of social reasons meetings etc.).
General symptoms such as fatigue, loss of apetite, somnolence, are typical
for the apparition of renal insufficiency. In his phase, patients have secondary
symetrical uretero-hydro-nephrosis. Moreover, there are symptoms related to the
increase of the abdominal pressure with each urination effort, such as inguinal hernia
and/ or hemorhoids.
Urinary stasis can lead to calculi apparition, when the symptomatology is
manifested through intermittent obstruction, intense pollakiuria, painful urination.
The mucous membrane of the bladder neck is congestive, with important
vascular ectasia at some patients. Their spontaneous errosion, the injuries of these
varix of the bladder neck during the bladder catheterism or during the endoscopical
exams for diagnosis is followed by significant bleeding which can be followed by
complete urine retensions through clots.
In 1993, AUA (The American Urologic Association) introduced a symptoms
scoring based on a questionnaire addressed to and filled in by the patient. The
questionnaire was translated into all European languages and it constitutes today the
most important criterion in establishing the clinical stage of the disease and of the
therapeutical behaviour. It comprises 7 questions, each with 6 answers (put in a
increasing range depending on the seriousness of the symptom), which provides a
scoring from 0 to 5. The final maximum scoring can, thus, be 35. For a final scoring
of 7 it is recommended a close follow up of the patient (the scoring of 7 was chosen
because it covers 83% of the male BPH population). Men with a moderate scoring
(8-20) or severe (>20) need treatments to prevent complications.
CLINICAL PHASES
In the evolution of the BPH, there are three classical clinical phases:
Preliminary disorders phase characterized by night pollakiuria and
moderate disuria, the patient urinates normally during the day;
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Bladder stagnation without distension phase, characterised by night
and day pollakiuria and an enhanced disuria. In this phase, bladder
diverticuli, bladder lithiasis, visical-urinary ebbing can appear;
Bladder stagnation with distension phase, chracterized by the
enhancement of the pollakiuria and the disuria, involuntary losses of urine
through automatic urination and manifested signs of renal insufficency with a
modification of the general state.
Clinical examination starts with the urine examination when it is eliminated.
While the patient urinates the doctor appreciates the degree of the disuria by
watching the characteristics of the stream. Then he shall examine the hypogastric
region. It is important to establish whether the patient has a bladder stasis or not.
When under palpation the bladder globe purcusses (hypogastric mass sound with
cranial convexity), it means that the patient has bladder distension as well.
Under the examination of the belly, the two kidneys can be palpated, in case
of bilateral hydro-nephrosis.
The clinical examination of the penis and of the urethra is important in order
to exclude other bladder obstruction causes such as: penile cancer, urethral meatus
stenosis or phimosis.
In case of the deterioration of the renal function, the patient can have the
clinical known signs of uremia (HTA, tachycardia, tachypnea, uremic fetor, paleness,
neurological signs, dizziness etc).
Digital rectal examination usually emphasizes a big volume gland, with a
sleek surface, well defined, with the medium pitch not so obvious, with an evenly
elastic content (the content varies depending on the hystological type of BPH),
unpainful. The asymetry of the gland is not rare, when one of the two lateral lobes is
more voluminous. It goes without saying that the posterior part of the gland cannot
be touched, and the size of the BPH is under-evaluated when its intra-bladder
evolution is significant.
PARACLINICAL EXAMINATIONS
Laboratory exams such as urine exam and urine sampling identify the
presence of the urinary infection. The presence of the microscopic hematuria
involved the search for an associated pathology such as: tumors at the evel of the
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urinary system, lithiasis etc. The determination of the blood values of the urea,
creatinine and electrolytes as well as the dosage of the prostate specific antigen
(PSA) provide information about the global function of the kidneys and the
metabolic status of the patient. Increased values of the PSA (normal = 3,2 ng/ml) can
indicate the presence of a prostate cancer. The PSA values have to be interpreted
taking into account the other parameters (the volume of the gland, the age of the
patient etc.). The PSA level is less influenced by the rectal touch, which is not the
case with the values of the prostate acid phospahtases.
The objective signs of the BPH comprise the reduction of the urinary flow
through the increase of the gland volume and the presence (the quantity) of the post
voiding residue.
Urodynamics
The rate of the urinary flow is determined by: a) the contraction force of the
detrusor; b) intra-bladder pressure; c) the resistance of the urethra; it can be
determined by uroflowmetry studies. At least two measurements are done, and the
patient has to urinate minimum 125-150 ml (at smaller volumes the real contraction
force of the detrusor cannot be appreciated). Normal men have a medium urinary
flow of 12 ml/ sec and a maximum flow of around 20 ml/ sec. In case the sub-vesical
obstruction appears (so the investigation is not specific for BPH), a medium flow of
6-8 ml/ sec and a maximum flow of 11-15 ml/ sec, or inferiour values, are considered
pathological. About 7% of the men with a proven adenoma have a normal flow, but
they have it by an increase of the intra-bladder pressure up to 100 ml H2O
(determined through cystomanometry = compensatory hypertrophy of the detrusor).
The limit of this investigation is the impossibility to make a differential diagnosis
between the installation of the obstruction and the incapacity of the detrusor to
generate the pressure needed for urination.
The bladder residue can be assessed exactly only by bladder catheterism and
more than 150 ml is considered pathological, which is equivalent with the reduction
of the bladder capacity with one third. It can be assessed as non-invasive and with a
great accuracy. (Ecography is used today instead of the former method which is no
lonegr used).
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Fig. 6.5. Transrectal US.. Normal aspect of the prostate
Ultrasound of the hypogastric area provides data about the volme of the
prostate and of the bladder residue and can tell the existance of an associated
pathology such as bladder lithiasis, bladder tumors or bladder diverticuli.
The assessemnt of the volume of the prostate is importatant to establish the
therapeutical behaviour. Big hypertrophies of more than 60g usually require open
surgical interventions. The dimensions of the prostate are measured frontally (the
breadth and the thickness) and sagittally (hight), and the volume is calculated after
the formula V = 0,5xD
1
xD
2
xD
3,
where D represents the diameters (in mm) of the
three dimensions. The weight in g can be obtained since it is known that the density
of the prostate tissue is between 1-1,05.
Transrectal ultrasound (fig. 6.5.) is much more precise and is used in
special cases too (the need to assess the exact volume, prostate cancer suspicions
etc.)
With the exception of the cases when we have hematuria, radilogical
investigations rise no interest any longer. They dont bring anything new to the
clinical case and they dont have an economical justification. However, out of
teaching reasons, the radiological examination will be briefly presented, although it
has substantially lost its importance.
KUB x-ray reveals bone diseases, tells the size of the kidneys, discovers
radio-opaque calculi, or it can identify a hypertrophiated bladder or, on the contrary,
it reveals a bladder distension.
The BPH aspect at IVU is characteristics; bladder with regular flat
sometimes bilobated margins, i.e. the symetrical deformation of the terminal ureters
under the shape of a fishing line hook (fig. 6.4.). The scope is to put a prognosis
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since it reaveals the echo of the BPH upon the kidneys (late secretion, pielo-pelvic
dilatation, diminished parencymal index), upon the ureters (symetrical dilatation),
upon the bladder (the fighting bladder, the bladder distension, the bladder
diverticuli), and it reveals the cervix-prostate-urethral modifications on the urination
cystographic negative (the yataghan-shaped urethra etc.)
DIFFERNTIAL DIAGNOSIS
The sub-bladder obstruction symptomatology appears in the case of bladder
neurological disfunctions (the neurogenic bladder), the (anatomical and functional),
alkoholism or utilization of some drugs.
Functional obstruction happens when there is no normal coordination
between the contraction of the detrusor and the relaxation of the sphincters (the
dissynergy of the bladder neck).
The diagnosis findings require cystomanometries, followed by the
determination of the bladder and urethral pressures during urination. The patients
with bladder neck contraction or with urethral strictures do not have the irritative
BPH symptoms. The diagnosis is decided by retrograde urethrocystography or by
urethrocystoscopia.
TREATMENT
The concepts in the BPH treatment have been diversified in the last few
years. The moment of starting any type of treatment depends on the seriousness of
the symptoms and on the presence of the complications. The absolute treatment
indications are represented by the severe obstructive symptoms, urine retension and
the apparition of the renal insufficency. Relative indications include a moderate
symptomatology, recurrent urinary infections and hematuria. Many urologists plead
for an early treatment, which should allow the removal of the symptoms, the
amelioration of the life of the patients and the prevention of the secondary effects of
prolonged obstruction.
Watchful waiting is the alternative with patients who have an easy
symptomatology. This includes education, changing of life style, and periodical
monitoring. The patient will be advised to change his life style: the reduction of
beverages consumption especially in the evening, the reduction of the consumption
of alkohol and coffee (prostate irritative elements), treatment of constipation etc. The
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majority of these patients will progress in a longer or shorter while towards an
accentuation of the symptomatology.
The pharmacological treatment was imposed through the
recognition of the two major factors which determine the sub-bladder obstruction
under the BPH: a) a dynamic component due to the contraction of the smooth
muscles of the prostate and of a prostate urethra, a contraction mediated through the
adrenergic receptors and b) a mechanical component, a result of the compression and
of the narrowing of the prostate urethra by the hyperplasia tissue.
The medication therapeutical strategy has the scope to influence the intra-
prostate dynamic forces (muscular tonus) and the static component (the glandular
volume). It is based on the folowing mechanisms: antiadrenergic influence,
antiandrogenic influencs, phytophamaceutical influences, antiestrogen influence
Antiadrenergic treatment. There are two types of adrenergic recipients:
1

and
2.
The recipients in the first cathegory are at the level of the smooth muscular
fibers, and the others in the sympathetic nervous terminations (and are involved in
the intake of the noradrenalin at the level of the synapses). In their turn, the
adrenergic
1
recipients are of three types, as follows
1a
,
1b
i
1c.
The ones in the
first category are mostly at the level of the vessels, which explains the possibility of
the apparition of the low blood pressure with patients with BPH who utilize the
sypatholytic medication. The
1
adrenoceptor sub-type is responsible for the
contractility of the intraprostate muscular cells.
Among the blocking

preparations which act upon the smooth muscular
fibers (the dynamic component) the most frequently used ones are:
doxazosin HCL of l, 2, 4 or 8mg l tb/day
tamsulosin HCL of 0,4 mg 1 cps/day
alfuzosin HCL of 10 mg 1tb/day
Low blood pressure accompanied by dizziness and sight disorders appears
with 30% of the patients, but the adjustments of the dosages allows the reduction of
this percentage to 10. Moreover, they also have a beneficial effect regarding the
reduction of the blood values related to colesterol and triglycerides. Retrograde
ejaculation is met with 1-10% of the patients.
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The antiandrogenic treatment of BPH. The growth and the secretion
function of the prostate depend on the androgen homones. The suprimation of the
DHT is possible through a series of methods: bilateral orchiectomy, steriod
antiandrogens of the Cyproteron acetate type, non-steriod antiandrogens of the
Flutamida type, LH and RH analogies, 5-alfa-reductase inhibitors through 4-
azasteriods (Proscar, Avodart.)
The orchiectomy is a treatment with historic importance for BPH. The
Cyproteron acetate (Androcur) has antiandrogenic effects also in low doses of 50 mg.
The diminution of the bladder obstruction through the diverse effects of the
antiandrogens is hard to assess.
Once the 5-alfa-reductase inhibitors have been developed, a new perspective
in the BPH treatment has opened. They hinder the intracellular metabolization of the
testosterone in 5-alfa-dihydrotestosterone. Finasterid (Proscar) in doses of 1x5
mg/day leads to a reduction of the prostate volume. Dutasterid (Avodart) in dose of
1x0,5 mg/ day has the same effects as the Finasterid.
The effect will install in several months and it consists in the gradual
reduction, by 20%, of the volume of the prostate (a reduction related to the glandular
component and not to the stromal one, so the effect of the preparation is stonger with
voluminous hyperplasia!). This treatment is a long one (it can last for years) and it is
costy, which limits its use to countries with high conomic power. Its utilization leads
to the modifications of the PSA values which requires that its values be determined
before the beginning of the treatment.
The mixed treatment (antiandrogenic and antiadrenergic) of the BPH.
The efficiency of the BPH treatment is much improved if an antoandrogenic is
associated with an antiadrenergic. The most utilized combinations are the ones
between tamsulosin HCL of 0,4 mg 1 cps/ day and dutasterid in a dose of 1 x 0,5 mg/
day.
This medicin combination mixes the effects of the two groups of medication:
efficient and fast amelioration of the symptomatology and the reduction of the
dimensions of the prostate.
Since 2010 this combination of medicine has been available in one pill
Duodart.
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The phytotherapeutical treatment. Many preparations have been
successfully introduced. The action mechanisms are not known, but they can be used
in cases of BPH with a light sympotomatology.
Surgical treatment entails the utilization of open surgery techniques and/
or endoscopic procedures.
Open surgery implies the digital cut of the nucleus of the adenoma
(adenomectomy) through a transbladder approach suprapubic (the Fuller-Freyer
technique) retropubiac (the Millin technique), in the case of big BPH. The perineum
approach ralated to the adenoma is very limited today, basically abandoned. It is used
only with big adenoma, of over 60 g.
The endoscopic treatment is the most frequently used (currently
considered the gold standard therapy with which the efficiency of the other
endoscopic treatments is compared) is the transurethral rezection of prostate (TURP).
The principle of this procedure consists in the rezection of the adenoma tissue
on the transurethral way by using a rezectoscope and an electrocautery which
generates high frequency cutting currents for the rezection or of coagulation for the
haemostasis. The TURP morbidity is of 18%, and the mortality is under 0,2%. The
immediate post-operation complications depend on the volume of the rezecated
tissue and thus on the duration of the intervention, as well as on the rezection
technique. One of the most serious complications is the TUR symdrome. The
irrigation fluid used under hydrostatic pressure during the resection is absorbed in a
small percentage in the circulation. Usually, 1-2 l are resorbed in about 40 min. If the
resection duration is longer or if the venous sinuses are open since the beginning of
the intervention, the absorption of the fluid increases. A fluid overcharge with
hydroelectrolitical disorders and hemolysis (if water is used which is hypotone as
an irrigation element) is produced. Hyponatremia under 120 meq/ L leads to the
apparition of the cerebral oedema and to convultions. The apparition of this
syndrome has an incidence of 2%. Prevention measures include over-pubian
drainage, the utilization of rezectoscopes with double current, the administration of
diuretic medicine after 30-40 min since the start of the rezection and the fast ending
of the intervention in case of early opening of the venous sinuses. The treatment
consists in the correction of the natremia and in administrating Manitol.
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In the case of small adenoma, the utilized endoscopic technique should be the
transurethral incision of prostate (TUIP). The practice consists in two electric
incisions at 5 and at 7 hrs, which start from the ureteral orifices and stop at
verumintanum or a median incision at 6 hrs. The results are similar with the ones of
the TURP, but the retrograde ejaculation is less frequent (only 17% as compared with
37% in the case of TURP), which makes this method to be recommended to younger
patients.
The other endoscopic methods use either other sources of energy, such as
LASER, or high frequency radio waves (TUNA= transurethral needle ablation), for
the ablation of the adenoma tissue, or other treatment principles such as the
dillatation of the prostate urethra with special balloons, or the setting up of stents in
the same region.
Thermotherapy and hyperthermy consist in the warming up of the prostate
tissue to various temperatures with the help of ultrasounds coming from a sound put
on the rectum (HIFU). The results obtained are inferiour to TURP; another major
disadvantage of these methods is the impossibility to get tissue for the
anatomopathological examination.
Another endoscopic method which gains a lot of popularity is the EWAP
(electrovaporisation of prostate). The rezectoscope is provided with a special loop
which through the high temperatures obtained at its surface vaporize the adenoma
tissue. The results and the intervention time are similar to the classic rezection but
the blood losses are much reduced.
The most recently introduced technique, TURis, utilizes a special rezection
loop in the shape of a mushroom and which, when getting in contact with the
prostate tissue, turns it into plasma. The rezection is made in a salty solution (for
prevention of the postTUR syndrome), the bleeding is minimum, and it can be used
for the big adenoma as well. The disadvantage of the absence of the tissue for the
histopathologiccal examination can be surpassed by using a bipolar rezection loop
before, during or at the end of the TURis.
CONCLUSIONS
The prostate is a gland belonging to the male genital system which
contributes to the volume of the ejaculation through its excrine secretions. Just like
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the testicle, the prostate is influenced in its development and growth by a strict
hormonal control which ends at puberty. The maintenance of the gland, cell renewal
and prostate secretion by the glandular epithelium cells depend on a number of
factors which are only partially known at the moment. The dihydrotestosterone
(DHT), which appears in the prostate cells through the transformation of the
testosterone enzymes, has a key role in these processes.
Out of unknown reasons, after the fourth decade of life, the prostate suffers a
new growth impuls which, together with older age, leads to a detectable and
measurable growth of the gland. This benign hyperplasia of the prostate tissue is
called benign prostate hyperplasia (BPH), because it is about a real multiplication of
the tissue. With about 50% of the older men, it produces typical urination disorders,
and with about 25% it leads to surgical urological treatment.
There isnt a direct corelation between the dimensions of the BPH and the
seriousness of the obstructive and irritative bladder emptying disorders. Thats why it
means that a complementary triggering role is played by other factors. The
decompensation of the higher urinary channel or the accute urine retension often lead
to a clinical diagnosis followed by an intervention, even though the disease has been
there for several years. In other cases, there is no obvioius obstruction; however, the
patients complain about irritative urinations which many times are very difficult to
treat. In these cases, it is necessary to have a positive, correct diagnosis which should
comprise, beside the obstruction degree, the subjective symptoms of the patient,
which are much more difficult to assess.
Against this background, the urodynamic investigations have a decisive
contribution regarding the diagnosis and the therapeutical indication of all the lower
urinary obstructive syndromes.
When taking any therapeutical decision we have to take into account the
change of the patients life.




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Statistically, it is the most common cancer of men (exceeding the lung and
colon cancer) and it represents 32% of all cancers. Its occurrence is correlated with
the natural phenomenon of aging. It is very rare in men under 40 years, but it reaches
its maximum frequency in the eighth decade of life.
We have to mention that the incidence of occult cancers (shown in autopsy) is
much higher than those manifested clinically. The latter ones are characterized by a
large variability in their natural evolution (and therefore the potential for metastasis),
leading to various controversies regarding appropriate therapy attitude, depending on
the evolution of the disease. Therefore, the treatment that may evolve from a simple
monitoring to aggressive surgery (total prostatectomy) depends on the age of the
patient, grading and the clinical stage and last but not least on the protocols and
therapy possibilities of each medical center.
INCIDENCE
The incidence, namely the rate of morbidity / year / 100.000 population
ranges from 1.3 in China, 3.4 in Japan and 30 in Germany. In the U.S.A, this rate is
60 in the white population and 95 in the black population. In Europe, it is the second
cause of death after lung cancer and bronchitis, approximately at the same level with
colorectal tumors. In Germany, there are 40.000 new cases / year. 40-60% of men of
70 years suffer of prostate cancer, mostly well-differentiated, of small dimensions.
These prostate cancers found incidentally at autopsy are known as latent prostate
cancers. Prostate cancer grows slowly; the doubling time of tumor mass is 2-4 years.
The increased incidence of occult cancers may be explained by the fact that
this cancer may occur in advanced ages, and as it grows slowly, it does not manifest
clinically, as the individuals die from other morbid causes associated.
ETIOPATHOGENESIS
Epidemiological studies emphasize the involvement of factors in the etiology
of PC:
Genetic predisposition (if a sibling or parent suffers of PC, the risk of PC is at
least double);
7. Prostate cancer (PC)
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Hormone causes (the involvement of steroid hormone is clear because PC
does not occur in eunuchs; cancer cells depend on hormones and increase
rapidly in the presence of androgens; castration causes a dramatic regression in
the evolution of cancer. Neoplasia occurs in the active prostate glands, not in
those inactive by age). On the other hand, in patients with prostate cancer we
may notice aberrations in the steroid metabolism;
Environmental and diet factors (the second and third generation of Japanese
living in America have the same incidence of PC as the rest of the population,
while in Japan it is only 10% of the incidence in the U.S.);
Local infections (due to the direct relationship between prostate gland and
urethra, it is possible that some viral or venereal infections to be involved in
prostate cancer; these data are controversial).
PATHOLOGY
According to the studies of McNeal, the prostate, a gland, is divided into
several areas (fig. 6.1), into the rectum, related to its anterior part, is found in the
peripheral area, the origin for 75% of all prostate carcinomas.
In less than 5% of cases, prostate cancer originates in the central area, which
is located around ejaculation channels, which open at the level of the seminal
colicullus. Around the proximal urethra, the transitional area is found, the place of
origin of BPH. About 20% of all prostate cancers occur in this area.
Prostate glands have their own channels that open in the seminal colicullus
channels that are covered with cubic epithelial cells. Around the prostate gland, there
is a stroma rich in connective tissue.
In 98% of the cases, prostate cancer originate in the glandular epithelium, and
the remaining of 2% originate in the epithelium of the tubes of the prostate gland.
Very rarely we may also find sarcomas, which originate in the stroma of the
glandular tissue, especially in young people.
Local-regional evolution. Prostate cancer grows in the direction of the apex
of the prostate gland. Following the development of the prostate cancer, the prostate
capsule is infiltrated, the perineural spaces being particularly affected at the entry and
exit of the nerves. The capsular penetration and seminal vesicles are signs indicating
locally advanced prostate cancer.
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Fig. 7.2. Limphnode groups interested in PC
Metastasis. The most comon metastasis of prostate cancer are at the lymph
node and bone.
The obturator lymph nodes represent
the first station. In case of radical
prostatectomy, they are the lymph nodes
indicating the lymphatic invasion or its
absence. The pre-sacral and inguinal lymph
nodes are the next lymph node stop, then the
common iliac lymph nodes and then
paraaortic lymph nodes (fig. 7.2). The
mediastinal and supraclavicular lymph
nodes are subsequently infiltrated.
Hematogenous metastases are
usually found at the level of the skeleton
(osteoblastic metastases), they are found in 85% of the patients dying of this
condition.
Visceral metastases are rare; the lung, liver and adrenal glands may be
involved. Generally, hematogenous metastasis follows the lymph metastasis. Most
PC develop heterogeneous and multicentric.
The "grading" system most commonly used is the Gleason system, which
notes from 1 to 5, based on glandular appearance (and not smear!), two most
frequent focal tumors. The score resulted is interpreted as follows: 2-4 well
differentiated, 5-7 moderately differentiated, 8-10 poorly differentiated. It is one of
the most important clinical indicators for assessing PC prognosis. The stage of the
PC staging is determined according to the TNM system of UICC.
TNM staging system
T - tumor
T
x
- primary tumor cannot be identified
T
0
- no primary tumor
T
1
tumor not clinically apparent
T
1a
- tumor found incidentally at histological examination, representing <5%
of the tissue obtained through TURP
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T
1b
- tumor discovered incidentally at the histological examination,
representing > 5% of the tissue obtained through TURP
T
1c
- impalpable tumor, identified by biopsy (elevated PSA)
T
2
tumor localized in the prostate
T
2a
the tumor occupies half or less of a lobe
T
2b
the tumor occupies more than half of one lobe, but not both
T
2c
the tumor occupies both lobes
T
3
extracapsular extended tumor
T
3a
- extracapsular (unilateral or bilateral) extension with microscopic bladder
neck invasion
T
3b
the tumor invades the seminal vesicles
T
4
the tumor is fixed or invades the adjacent structures others than the seminal
vesicles: external sphincter, rectum, elevator muscle of the anus or pelvis.
N - Lymph nodes
N
x
- the lymph nodes cannot be evaluated
N
0
- no metastases in the regional lymph nodes
N
1
metastasis in regional lymph nodes
M - Metastasis
M
x
- the existence of metastases cannot be evaluated
M
0
- no distant metastases
M
1
- distant metastases
M
1a
- metastasis to lymph nodes other than the regional lymph nodes
M
1b
. - Bones
M
lc
- Other tissues or organs
SYMPTOMS
Currently, PC is most commonly found in asymptomatic phase or by elevated
PSA, or DRE. These investigations should be applied to all patients over 45 years, as
screening. Thanks to the aggressive screening policies in countries like USA, Austria,
England, France, the mortality due to this pathology decreased. At the same time, PC
may also be discovered incidentally on the pathological examination of the tissue
obtained by transurethral resection of the prostate adenoma, for example.
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The localized PC rarely generates symptoms. Sometimes, the occurrence of
bone metastases orients the clinical examination toward a suffering prostate, where
cancer, by then asymptomatic, is detected.
Sometimes, even from the early stages of disease, the development of the
tumoral process in the cervical - trigonal region leads to the occurrence of the
dysectasia syndrome, characterized by dysuria, pollakiuria and urination pain. In the
prostate cancer it is usual that dysuria worsens rapidly, the patient sometimes
suffering of acute urinary retention or chronic incomplete retention with bladder
distension, in a few months.
Initially, terminal hematuria, then total hematuria, but low-intensity and
persistent, is frequently added to the dysectasia syndrome in PC, unlike prostate
adenoma. Some patients may present hemospermia. Very rarely, PC occurs in a
hemorrhagic syndrome due to fibrinolysis.
In extended prostate cancer, the general condition is also influenced;patients
lose weight, paleness due to anemia also occurs, sometimes due to persistent
hematuria less abundant, but persistent, as well as by the inhibitory action of the
neoplastic process on the bone marrow.
CLINICAL EXAMINATION
Digital rectal examination has a major role in the diagnosis of PC, which
may detect the lesion even before clinical manifestation.
In the beginning, the tumor lesion is represented by an intra-prostate nodule,
difficult to differentiate from an inflammatory one. The prostate nodule inflammation
protrudes at the surface of the gland and has precise limits; the cancerous nodule is
inserted in the gland, tough, well-defined and painless. Sometimes the whole lobe or
entire gland is affected, which in case of tumor is hard, with irregular surface,
painless, well confined. Most of the times, the median ditch is maintained. In
advanced stages, the gland is fixed on tissues and bones surrounding sacral
excavation. In this phase, at the DRE, a hard, woody mass is found, occupying all the
pelvis, where the prostate cannot be detected; frozen pelvis.
Any hard, painless prostate nodule requires clarification by biopsy.


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Fig. 7.3. Transrectal prostate biopsy.
DIAGNOSIS
Transrectal ultrasound. Today there are special ultrasound probes with
appropriate frequency of 7,5 MHz or more for rectal or vaginal examination.
Typically, the PC node occurs as a hypoechogenic area. This sign is not specific,
since HBP, blood vessels, cysts, inflammatory processes appear as hypoechogenic
areas. If they are located in the peripheral area of the prostate, they should also be
investigated by biopsy. The main advantage of the transrectal prostate biopsy
compared to the supra-symphyseal or transurethral biopsy is that of sampling
ultrasound guided biopsies, by adjusting the needle guidance system for transrectal
ultrasound probe, which allows adequate sampling of biopsies from suspicious areas.
This will enable pathologist to determine the stage and grading, which are the most
important factors in determining prognosis. The limit of the transrectal ultrasound is
the lower accuracy of magnetic resonance imaging (MRI) in assessing extracapsular
extension, failure to appreciate the regional lymph node invasion and make
differential diagnosis with other hypoecogenic images due to adenoma or prostatitis
(specificity 78-99%).
Prostatic biopsy puncture needles have been much improved by adapting
them to biopsy guns.
Prostate biopsy. It may be transrectal, transperineal or transurethral biopsy.
Transrectal biopsy. It is carried out by means of transrectal ultrasound (fig.
7.3). Currently, it is the most
used technique in asymptomatic
patients with elevated PSA. 12
biopsies are performed under
ultrasound guidance. In addition,
the ultrasound guidance may
identify hypoechogenic areas
(pathognomonic for PC) that are
not detected in DRE and may
guide the biopsies to the
transition area located above the
prostate and that is not accessible to DRE. Rarely, it may be performed without
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ultrasound guidance. The palpating finger (index) feels the node and the biopsy
needle is inserted in the lesion. Tru-Cut biopsy needles (Travenol) are used.
Transperineal biopsy. It is performed with the same type of needle, but
only preceded by local anesthesia.
PSA values. Prostate specific antigen (PSA) is a glycoprotein secreted by
prostate, which prevents sperm clotting. PSA may be determined from serum by
radio- or immunoassay methods, with elevated values both in HBP and in PC. But
appearance of the PC tissue increases the serum value of PSA 10 times more than the
same quantity of BPH tissue. However, 20% of the PC found are accompanied by
normal levels of PSA. Generally, the maximum normal value of PSA is 3,2 ng / ml.
PSA is an extremely useful value for incipient and early prostate cancer diagnosis.
PSA has a special value in the control and monitoring therapy.
We may conclud that PSA is a useful marker for post-therapy screening and
tracking. Thus, the total acid phosphatase, prostatic acid phosphatase and alkaline
phosphatase are no longer used in the diagnosis and therapy monitoring of the
prostate cancer.
CT examination is not an appropriate examination to evidence PC
metastases in lymph nodes. CT may detect these lymphatic invasions only in the case
of massive node invasion, with lymph nodes having a diameter larger than 1.5 cm.
Even in assessing local tumor invasion (T staging) CT is an investigation with
modest results.
Bone scintigraphy. It is the most important investigation for highlighting
bone metastases. Sensitivity of the method in detecting these metastases is
approximately 100%. All processes of bone healing after fractures, inflammation,
etc., may cause similar changes in osteoblastic metastases.
Magnetig resonance imaging (MRI). An expensive and time-consuming
investigation. It is superior both to transrectal ultrasound in assessing extracapsular
invasion, and to the CT in assessing lymph nodes invasion, especially when MRI
with endo-rectal probe is performed. It is restricted to young patients, where the
preservation of the peri-prostate vascular-nervous packages is needed (their bilateral
intraoperatory cutting generates erectile dysfunction).
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Fig. 7.4. Digital rectal examination
IVU and renal ultrasound show urethral obstruction by the infiltration of
terminal ureters at the level of the bladder, in a PC with local invasion.
The most important diagnostic measure before radical prostatectomy is a
local lymphadenectomy for the nodes in the obturator fossa (6-9 lymph nodes on
each side). If these nodes are invaded, we may assume with a probability of 90% that
there are distance lymphatic metastases.
DIFFERENTIAL DIAGNOSIS
There are other prostate disorders that may mimic a PC such as prostate
adenoma, chronic prostatitis, prostatic tuberculosis, fibrosis caused by previous
biopsies, cysts and prostate stones. The occurrence of PSA decreased the number of
patients undergoing prostate biopsy.
1. Prostate adenoma is usually associated with a long history of obstructive
symptoms and the prostate volume is usually higher than in CP.
2. Prostatic tuberculosis is often associated with damages of epididymis,
history of pulmonary tuberculosis, fever and sterile pyuria.
3. Chronic prostatitis has a long history, and leukocytes are identified in
urine or prostatic secretion.
4. Prostate cysts or stones are easily identified at transrectal ultrasound.
5. The differential diagnosis of Paget's disease is taken into consideration in
asymptomatic patients with bone metastases who present increased values acid
phosphatase and alkaline phosphatase.
STAGING
The assessment of the clinical stage of cancer can be made by DRE,
transrectal ultrasound, computed tomography or magnetic resonance imaging. DRE
(fig. 7.4) may assess the extracapsular extension, seminal vesicle attachment,
extension to pelvic wall or
the rectum. The
examination depends on the
experience of the examiner;
it cannot identify the T
stage and it cannot clearly
differentiate the prostate
conditions described above.
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Transrectal ultrasound may diagnose 60% of the PC because of their
hypoechogenic aspect (40% are isoechogenic or hyperechogenic) and it also serves
to the eco-guiding of the biopsies (the guidance allows adequate sampling of biopsies
of suspicious areas, which allows the pathologist to assess the stage and grading, the
most important factors in determining the prognosis). The limit transrectal ultrasound
is accuracy, lower magnetic resonance imaging (MRI) in assessing the extracapsular
extension, failure to appreciate the regional lymph node invasion and the differential
diagnosis with other hypoechogenic images due to adenoma or prostatitis (specificity
78-99%).
TREATMENT
1. Treatment of localized PC (T
1
,T
2
, N
X
N
0
,M
0
)
1.a. Monitoring of the patient (Watchful waiting - WW).
Watchful waiting may be considered in patients with localized PC, but with
a reduced life expectancy or elderly patients with less aggressive tumors.
The current treatment for T
1
and T
2
stages is the radical prostatectomy or
radiotherapy, both with a long-term survival of 80-90% and mortality less than 1%.
1.b. Total prostatectomy may be transperitoneal and / or retropubic.
Laparoscopic lymph node dissection allows perineal approach in obese patients,
without the need for another suprapubic incision. In this intervention, besides the
removal of the prostate, the seminal vesicles will also be removed and the bilateral
lymphadenectomy will be performed.
The survival rate from 10 to 15 years, in T2 patients, is 68%, respectively
62% respectively.
Similar results (in terms of oncology) with open radical prostatectomy were
obtained by laparoscopic radical prostatectomy, or even robotics.
The immediate complications of total prostatectomy are intraoperative
bleeding, injury of the obturator nerve, the ureter or rectum. Immediate postoperative
complications include: venous thrombosis, pulmonary embolism, symptomatic pelvic
lymphocele, wound or urinary tract infections, etc.. The incidence of these
complications is less than 3%.
Long-term complications are urinary incontinence and erectile dysfunction.
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PSA level after radical prostatectomy should be 0 ng / ml at about 6 weeks.
Otherwise, it is considered tumor residue or metastasis (PSA remains high or
increases rapidly after prostatectomy) or tumor recurrence (PSA to 0 ng / ml and then
increases).
Other surgical techniques which may be applied to these patients, but that
have no intention of oncology treatment are represented by cryotherapy or ablation
with high frequency ultrasound (HIFU), perineal or transrectal techniques.
1.c. Radiotherapy. Brachytherapy and external conformational therapy
seem to have similar results with the surgery. Since in this case, the staging is only
clinical and imaging (not pathological), the comparative studies between the two
methods are difficult to perform.
Transperineal brachytherapy is the transperineal implantation in prostate of
radioactive seed under ultrasound control. It is reserved for the patients with small
prostate, low PSA and low Gleason score.
Conformational external therapy is a new technique that, due to three-
dimensional determination of the tumor and surrounding tissue, the radiation dose is
administered directly on the targeted tumor tissue, protecting the surrounding tissues.
Doses of 74-80 Gy are used in short sessions, 5 days per week for 6-7 weeks.
It is estimated that 10-year survival is 68% for T
1
and 52% for T
2
. In case of
effective radiation therapy, PSA levels should reach 0.5 ng / ml; level reached in a
long interval of up to 3 years. At the same time, the increase of PSA in these patients
is tumor recurrence. The increasing of PSA after the radiation therapy always shows
failure. PSA above 30 ng / ml before radiotherapy is usually associated with modest
results.
The complications of radiation therapy depend on total dose, tumor volume,
spatial distribution of the dose and schedule of the radiotherapy used.
The use of external conformational therapy or brachytherapy reduced these
complications. They consist of intestinal distress (rectorrhagy, tenesmus, diarrhea,
incontinence for feces, rectal stricture or bowel obstruction), urological distress
(dysuria, cystitis, hematuria, urethral stricture), erectile dysfunction and pelvic
lymphatic edema of the pelvic limbs. The major complications, as rectal or bladder
fistulae (2-4%) require surgical treatment.
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There is no cure in stage T
3
or T
4
. However, today, according to some authors,
total prostatectomy in stage T
3
N
0
M
0
is followed by relatively good survival results
at 5 years. If local lymph nodes are invaded, surgery is ineffective, the tumor cannot
be completely excised, and local or systemic recurrence rate is very high.
Relapse-free survival after radiotherapy is modest, 54% at 5 years and 36% at
10 years.
2. Treatment of locally advanced PC with or without metastases (T
3
, T
4
,
N
1
, M
1
)
Prostate carcinomas are heterogeneous tumors composed of hormone
sensitive and hormone resistant cells. The degree of hormone sensitivity will
determine the initial response to androgen deprivation. Although dihydrotestosterone
(DHT) is the active metabolite necessary for the normal prostate cell growth, PC may
use other hormone precursors for its growth (ex. those from the adrenal gland).
After androgen deprivation, approximately 40% of the patients experience the
cessation of the disease progression, while 20% of the cancers will continue to grow
and evolve. Treatment results are modest, over time they become ineffective due to
the proliferation of certain hormone resistant tumor cells. The average survival time
of patients with metastases is 2 years. Approximately 80% of them die within the
first 5 years.
Hormone therapy. Estrogens. Until recently, estrogens (diethylstilbestrol -
DES) and orchiectomy have been the most important alternatives to hormone
therapy. DES, at a dose of 3 mg/day, acts by suppressing LH and probably, also by a
minor effect (little known) in cancer cells. The efficacy of estrogen use is similar to
orhiectomy, but combining the two methods (orchiectomy + estrogen) is not superior
and life expectancy does not change. Estrogens tend now to be abandoned because
20-30% of the patients present lethal cardiac or pulmonary complications, as
thromboembolism, peripheral edema and fluid retention, in the first 3 months (at the
mentioned dose). Painful gynecomastia is another complication that is resolved by
radiotherapy.
Orchiectomy is the cheapest and safest method of blending testicular
androgens. At present, local anesthesia may be given, requiring 1-2 days of
hospitalization. It is difficult for patients to accept it, because it is psychologically
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traumatizing. Usually, surgery is accompanied by hot flashes, which decrease at the
administration of Cyproterone acetate, DES (diethylstilbestrol) 1 mg twice / week or
monthly injections of depot progesterone preparations.
LH-RH agonists. Also known as analogues (leuprorelin, goserelina,
buserelin, etc.) work by stimulating the production of pituitary gonadotropins, for 2-3
weeks, then inhibiting it. Their effecacy is similar to the estrogens and orhiectomy
(they reduce testosteronemia to the castrating level) and they are administered as
subcutaneous injections or as depot at 1, 2, 3 or 6 months. Side effects include hot
flashes 50%, nausea 5% and gynecomastia 3%. Currently, depot preparations of
gosereline (Zoladex) or difereline, with monthly administration (3,75 mg) and more
recently at 3 months (1 l, 25mg) are manufactured.
LH-RH antagonists
In contrast to LH-RH agonists, LH-RH antagonists bind rapidly to LH-RH
receptors in the pituitary gland, resulting in rapid decrease in LH, FSH and
testosterone. Studies on this type of hormone therapy are still at beginning. There are
no such forms as depot as for LH-RH agonists. As representatives, we may mention
abarelix, degarelix.
Antiandrogens include drugs that act either a) by the inhibition of androgen
synthesis, or b) by blocking their action in the target organ.
a) androgen synthesis inhibitors include spironolactone, aminoglutethimide
and ketoconazole and block the synthesis both at testicular and adrenal level.
Ketoconazole, imidazole derivative, initially conceived as antifungal, has significant
side effects including: hepatotoxicity, gastrointestinal intolerance, gynecomastia and
hypocalcaemia. It is indicated that fast-acting drug in patients with bone pain and
spinal cord compression.
b) androgen antagonists act through a competitive mechanism of blocking the
androgen receptor. They may be steroid anti-androgens (cyproterone acetate 200
300 mg/day Androcur) or non-steroid antiandrogens (flutamide - Eulexine 3x250 mg
/ day, nilutamida - 2x150mg/zi, bicalutamide - Casodex 50-100 mg / day). The
advantage of these drugs is to preserve libido in most patients.
Maximum androgen blockade (CAB = complete androgen blockade) is an
anti-androgen in association with orchiectomy or LH-RH analogue. This association
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is based on the idea that hormonal treatment failure is due to inadequate suppression
of adrenal androgens and not to the selection of the hormone resistant cancer cells.
Recent studies have not demonstrated the superiority of the method in terms of
increased survival or quality of life.
Minimal androgen blockade is the combination of a minimum non-steroid
anti-androgen 5 reductase inhibitor (finasteride). By this combination the
testosterone level is low, without significant effects on sexual function.
The anti-cancer drugs may be used in metastasis hormone-resistant PC.
Various types of anti-cancer drugs have been studied: taxanes, mitoxantrone in
combination with corticosteroids, estramustin phosphate, cisplatin or carboplatin, etc.
Suramin, an anti-parasitic agent, is currently the subject of several studies. It
works by blocking growth factors (b FGF and EGF), having anti-enzymatic effects,
cytotoxic effects on PC cells and suppression effect on the corticosuprarenal gland,
all resulting in a decrease of plasma androgens. It determines a reduction in the oral
tissue, which persists on average 4-11 months (at 33-50% of hormone resistant
patients). PSA decreases by 75% to 29% of men receiving such treatment.
Recent phase III trials have shown encouraging results on the effects of the
treatment with certain Sipuleucel-T (Provenge) vaccines in patients suffering of
hormone resistant PC with metastases.
The palliative treatment refers to the patients with bone metastases and to the
patients with subvesical obstruction. In the first case, we use radiotherapy or recently,
the administration of strontium 89.
The patients with subvesical obstruction are treated with orchiectomy, CAB
and / or transurethral resection, with the intention of removing the largest possible
amount of the tumor tissue, leaving a prostate lodge type cavity after the resection,
being mandatory to keep the striated sphincter.
CONCLUSIONS
Prostate cancer is a disease of older man. It is the most common urological
malignant tumor and it is the second as a cause of cancer death in men, after
bronchial carcinoma. Prostate cancer is an extremely slow growing adenocarcinoma
that grows very slowly and whose early forms noticed in the autopsy of the men over
70 years are found in half of the autopsies.
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The aggression of the tumor is closely correlated with its volume. From a
tumor volume (ex. 0,5 cm
3
), there is a clinically manifested tumor that may be
palpated at DRE. Up to a volume of 4 cm
3
, the tumor is almost always limited to the
prostate. At higher volumes, it penetrates the capsule and it metastasizes first to the
lymph nodes (lymphatic metastases), and then the bones (hematogenous metastases).
By the digital rectal examinations, we may discover prostate tumors clinically
relevant. Early detection of prostate cancer was much improved by determining the
level of the prostate specific antigen PSA. Transrectal ultrasound is the diagnostic
method that may be used to diagnose prostate cancer in early stage. The diagnosis of
PC is determined by histopathological examination of a tissue fragment taken by
prostate biopsy, ultrasound guided.
PC limited to the organ will be treated by radical prostatectomy. Radiation
therapy does not have a curative, but palliative role.
PC with metastases will be treated by one of the various forms of anti-
androgenic therapy.
PSA is an organ-specific marker. After total prostatectomy, it becomes a
tumor-specific marker, very useful in monitoring the evolution of surgery. Based on
serum PSA values, the effect of radiotherapy or hormone therapy is monitored.

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The most common kidney tumor is kidney cancer, an adenocarcinoma of the
proximal tubule. Other malignant or benign tumors appear at the level of the kidney,
as the starting point from other tissues.
A fairly accurate and comprehensive classification of kidney tumors is that of Glenn
(1980):
I. Benign tumors coming from:
- kidney capsule
- parenchyma
- fat
- kidney cysts, dysplasia of cystic epithelium
- mesenchymatous tumors
II. Malignant tumors
II.1. pelvis, caliceal and ureteral tumors:
- transitional carcinoma
- flat epithelial carcinoma (malpighian, squamous)
II.2. Pararenal tumors:
- Malignant
- Benign
II.3. Embryonal tumors - malignant renal tumors of child:
- Nephroblastoma (Wilms tumor)
- sarcoma
II.4. Nephrocarcinoma - malignant renal tumor of the adult
- adenocarcinoma
- oncocytoma benign tumors
II.5. Secondary renal tumors (various metastases).
MALIGNANT KIDNEY TUMORS OF THE ADULT
The tumor described by Grawitz in 1883 as hypernephroma, initially
considered as having adrenal gland inclusions in the renal parenchyma, turned out
8. Kidney tumors
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(Sudeck - 1893) to be a tumor developed in adult renal tubular epithelium, actually
being a nephron epithelium. Today it is known as renal cell carcinoma (RCC).
Renal cell carcinoma (RCC) develops more often in men and today, its
incidence on sexes is 1.5 / 1 of cases against women. It represents 2-3% of all
tumors. Besides oncocytoma (benign tumor) it represents 86% of all kidney tumors.
Its frequency increases with age, being exceptional in children and rarely in
adolescents; most cases are grouped between the 5
th
and the 7
th
decades. In patients
suffering of von Hippel Lindau disease, RCC occurs at a higher rate. In this
category of patients, unilateral or bilateral synchronous or metachronous carcinomas
may be met.
ETIOLOGY
RCC is a tumor of the proximal tubule. The immunological marking of the
tumor with monoclonal antibodies or cytological markers casts doubt on the origin of
RCC of the proximal convoluted tube. The etiological factors are not established
with certainty. However, an increased incidence of RCC occurs in smokers.
Because in some families kidney cancer is more common, in the recent years
progress has been made in tumor genesis. Thus, the gene responsible for the
occurrence of the tumor syndrome of von Hippel-Lindau disease has been identified.
The carriers of this gene are predisposed to develop nephron epithelium.
Von Hippel - Lindau syndrome
The kidney involvement in von Hippel Lindau syndrome is known since
1926, when Lindau, who described for the first time this syndrome, recognized the
existence of a link between von Hippel retinal angiomatosis and the other
manifestations of the syndrome, noting that renal manifestations are associated with
2 / 3 of cases.
The syndrome includes retinal and cerebellar hemangioblastoma, pancreatic
cysts and cysts or tumors in the kidney, epididymis, or in other viscera (Melman and
Rosen 1964). Gene identification through a blood test allows the identification of
individuals at risk. Researches bring evidence that this gene would be involved in the
genesis of renal cell carcinoma, which occurs in individuals who do not suffer from
von Hippel - Lindau disease.
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The examinations performed at the molecular level have shown that RCC
occurs sporadically and the one occurring in patients with von Hippel - Lindau
syndrome is accompanied by loss of chromosomal material in the short arm of
chromosome 3 (3p) with common genetic mechanisms.
PATHOLOGY
Macroscopic - RCC has a round characteristic appearance and it is
surrounded by a pseudocapsule. Because of central necrosis and hemorrhage, it
results a multilocular appearance on the surface of the section. The tumor has a
yellow or white gray area. A feature of RCC tumor is the tumoral thrombus
reaching the vena cava, or even to the right atrium. This is due to a feature of the
kidney cancer to invade early the renal venous sinuses. Rarely, besides the tumoral
pseudocapsule, small tumor nodules in the renal parenchyma are noticed. In 1-3% of
cases, the tumors occur bilaterally.
Microscopic the architecture of the tumor cells is frequently that of an
adenocarcinoma. According to WHO, at least 3 histological subtypes of RCC are
distinguished: with clear cell (80-90%), papillary (10-15%), chromophobe (4-5%)
As with all tumors, there are various degrees of malignancy. Currently, we
use the system proposed by Fuhrman, which refers to the characteristics (size,
number, shape) of the nuclei, nucleoli and chromatin. Four degrees of malignancy are
distinguished:
1
st
degree - well differentiated tumors, with tumor cell like the kidney tissue
2
nd
degree - tumors with increased nuclei, but less visible nucleoli
3
rd
degree tumors with increased nuclei and large nucleoli
4
th
degree tumors with anaplastic structure
Oncocytoma was described by von Zippel in 1942. About 5% of all kideny
tumors are the oncocytoma. The oncocytes are cells with eosinophilic cytoplasm,
very well differentiated. They may reach considerable size without giving
metastases, the cells being well differentiated in the tumor. They are always
encapsulated and on the surface they have the color of mahogany.
Based on imaging procedures, the nephron epithelium oncocytoma cannot be
distinguished, so their treatment is still nephrectomy, although they are considered to
be benign tumors.
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LOCAL-REGIONAL AND DISTANCE EVOLUTION
Local the tumor increases relatively slowly (doubling time, approximately
500 days); it pushes, deploys, disrupts and invades the pyelo-caliceal cavities, breaks
the capsule and infiltrates the perirenal fat, invading the adrenal gland, pancreas,
spleen and descending colon on the left, or the adrenal gland, colon, duodenum and
liver on the right. At the same time, the psoas muscles and lumbar square may be
invaded. In addition to local invasion, kidney cancer also invades the veins and
lymphatic vessels.
Venous invasion - it is independent of the tumor volume or histological type.
The neoplastic thrombus obstructs the whole venous lumen, adheres to the endovein,
and in advanced cases it infiltrates the wall, which it may penetrate. Generally, the
invasion of the main renal vein invasion has a poor prognosis and the cava vein has a
very serious prognosis, because it increases operative mortality. Venous obstruction
leads to development of supply collateral circulation. When the varicocele (spermatic
veins dilatation) appears to the right, it represents the clinical expression of
thrombosis or compression of spermatic vein (venous obstruction).
Lymphatic propagation - is relatively common (25-38%) and it manifests as
pedicular or periaortocaval adenopathy. Regional lymph nodes are lombo-aortic.
Through the thoracic duct, the lymph disseminations may occur in the mediastinum,
supraclavicular, or lungs. The neoplastic nature of adenopathy has to be proved
histologically.
Metastasis develop on the venous and lymphatic system; they occur
independently of the tumor size and its evolution stage and they affect the lung,
bones, brain, adrenal glands, skin, vagina, penis and orbit (Hutchinson syndrome:
exophthalmia + retro-orbital tumor).
CLINICAL SIGNS
In the early stages, the kidney cancer presents no symptom. At this stage, it is
discovered incidentally at ultrasound examination. The most common clinical
manifestations are urological and they are grouped in a triad represented by
hematuria, pain and kidney tumor.
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Hematuria is macroscopic, total, isolated or it accompanies other clinical
signs; it is difficult, unique or repeated, of low intensity, or massive intensity with
clots, which sometimes determines the acute, complete retention of urine.
Flank tumor. The absence of the tumor cannot invalidate the diagnosis of
kidney cancer. When the tumor develops in the upper pole of the kidney, the
neoformation cannot be palpated, unless it is larger. Like pain, the palpation of the
tumor is a sign of late diagnosis.
The palpation characters of the tumor are the lumbar contact and baling. The
tumor may be fix or mobile, which is very important, because it shows a great
tendency to local invasion and even the impossibility of excision.
Rarely, the tumor ruptures spontaneously, especially when it presents cystic
areas or spread necrosis, making a syndrome composed of brutal back pain,
retroperitoneal hematoma, signs of peritoneal irritation that associated with signs of
internal bleeding, leading to Wunderlich syndrome.
Pain - dull and constant pain predominate, caused by the distention of the
capsule and renal pedicle traction. The renal colic occurs in the case of hematuria
with clots; in this case, the secondary character of hematuria is essential.
Symptomatic right-sided varicocele the control of varicocele is necessary
in all cases where there is a suspected renal tumor. This exploration shall be made in
standing position. The varicocele may have an early onset, when renal tumor is not
yet palpable.
CLINICAL FORMS
1. Hematuria form is a typical form: hematuria is total, spontaneous,
difficult, painless, isolated and variably abundant.
2. Tumor form. The kidney is palpable, ballotable, with lumbar contact.
3. Febrile form with oscillatory and prolonged hyperpyrexia, it is not
influenced by antipyretics and antibiotics, it is due to some pyrogenic proteins
resulting from tumoral necrosis. The fever disappears after nephrectomy, if it still
persists, the presence of metastases or incomplete excision should be taken into
consideration.
4. The forms with polyglobulia may long precede the occurrence of the
characteristic manifestations of cancer. The syndrome may be present in the cases
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with liver metastases or bone marrow metastases and it is due to erythropoietin
secretion by the tumor tissue or its metastases.
5. The HTN form, due to the existence of an arterial - venous fistula in the
tumor or it may occur secondary to a tumor that develops in the renal hilum. The
vascular compression may lead to renal ischemia.
6. Hypercalcemia syndrome forms - neuromuscular, gastrointestinal and
cardiovascular disorders. These disorders are due to calcitonin secretion by the
tumor, which may be taken for a secondary hyperparathyroidism.
7. Silent forms, discovered by chance because of hematuria with
albuminuria, hypertension, etc.
8. Metastatic forms, about 10% of cases. The first sign of the disease is
caused by metastasis (hemoptysis, spontaneous pathological fracture). Primitive
renal tumors are not only asymptomatic but also hard to reveal.
9. Other forms: with hepatic dysfunction (Stauffer syndrome), Cushing
syndrome, or Sanarelli syndrome (calcium deposits in the myocardium, brain or
periarticular).
DIAGNOSIS
The various clinical characteristics the kidney cancer may manifest, its
paraneoplasic very common symptoms, insidious, slow, evolution, often
asymptomatic for a long time, lead to the establishment of the diagnosis in the late
phase.
The paraneoplastic syndrome requires strict control of the entire body through
a complete examination. In terms of urology, two symptoms dictate their
identification: hematuria and large kidney. For this goal the following paraclinical
investigations shall be made.
In positive diagnosis of kidney cancer, the X-ray examination represents the
basic element and any clinical presumption of kidney cancer requires detailed and
precise radiological exploration.
1. KUB X-ray identifies partial or global increase in the volume of the
kidney. The partial one is the most common; it may involve one of the poles or the
middle area of the kidney. The global increase of the volume is met in infiltrative
large tumors that invade almost completely the parenchyma.
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We may also identify a number of pointed calcifications. They are found in
the renal tumors with slow evolution, where the hemorrhagic or necrosis areas had
time to be impregnated with lime salts.
2. IVU allows the assessment of the functional value of both kidneys, which
is very important for total or partial nephrectomy of the tumor kidney. It is a
fundamental examination, which highlights the changes of the pyelic structure,
characteristic for an expansive process, which in its development, draws, diverts,
lengthens, compresses, deforms and amputates the calices, compresses and deforms
the basinet and moves the lumbar ureter.
When the tumoral kidney is nonfunctional at urography, the cause may be the
obstruction by a neoplastic thrombus of the main renal vein, or of the inferior vena
cava; another reason may be the total destruction of the renal parenchyma.
3. Retrograde ureteropyelography focuses on the silent kidney in
urography. It highlights the morphology of pathways with details missing on
urography.
It results that both urography and retrograde ureteropyelography lack in
"stopping at the edge of the tumor, without penetrating into it." Small tumors do not
increase significantly the kidney, they do not deform the contour, and do not disrupt
the pyelocaliceal structure, and thus they are not visible on urography. Also, the
tumors that develop eccentrically may remain somewhat difficult to identify in the
diaphragm.
4. Renal ultrasound
confirms and locates the tumor,
differentiates the tumors with fluid
(solitary kidney cysts), specifically
their trans-sonic structure, from the
parenchymal, solid tumors (echogenic
mixed structure, with parenchymal
aspect). Sometimes, in the tumor
mass we may view one or more trans-
sonic areas - tumor necrosis. Using the Doppler module, we may identify the renal
venous thrombus or vena cava thrombus or neoformation vessels of the tumor (fig.
Fig. 8.1. Doppler US shows neoformation vasels
at the level of renal tumors
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8.1). It differentiates with the same accuracy the fluid expansive processes from the
solid ones.
5. Computed tomography (CT). It is a method of great interest for the
investigation of renal tumors, differentiating more accurately fluid masses from the
solid ones (fig. 8.2.), as ultrasound.
CT diagnoses 100% of kidney cancers, differentiating them from the renal
cysts. It provides optimal possibilities for the staging of the tumors. It highlights with
an accuracy of 97% the infiltration of vena cava, with an accuracy of 80% the
infiltration of the perirenal tissues, with an accuracy of 90% the metastatic regional
node invasion and with an accuracy of 100% of the cases the invasion of the adjacent
organs.
6. Angiography has lost much and it has very specific indications: single
kidney to evaluate partial nephrectomy. It shows the size of the renal artery and the
anarchic distribution, arterial vessels with irregular paths. We may view blood,
vascular amputation, arterial-venous fistula, a peritumoral major vein network.
The pharmacodynamic test (Adams) with angiotensin (powerful
vasoconstrictor) highlights the absence of vasoconstriction in the neoformation
vessels (tumor).
7. Magnetic nuclear imaging (MRI) it is useful for sagittal sections where
it is intended only partial nephrectomy. MRI can determine the extent of venous
thrombus in the vena cava.
8. Cavography allows the detection of the renal vein invasion and inferior
vena cava; it is required where this is assumed.
9. Scintigraphy contributes in a very limited way to the diagnosis of kidney
cancer, compared to the explorations mentioned.
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Laboratory tests provide information only in the case of paraneoplastic
syndrom forms, when various changes may be highlighted: polyglobuly,
hypercalcemia, elevated erythropoietin, renin, etc.
The biological markers have non-specific relative value. Kidney cancer does
not have specific biological markers. In some cases, you may identify elevated
values of lactate dehydrogenase (LDH), carcinoembryonic antigen (CEA), alfa fetal
protein (AFP) or of immunoglobulins, etc.
DIFFERENTIAL DIAGNOSIS
It is done for all the diseases that increase kidney and / or produce hematuria,
especially hydronephrotic kidney, polycystic kidney, renal tuberculosis,
pyonephrosis, xantogranulomatous pyelonephritis, and especially for solitary renal
cyst, especially when it has a significant volume and it is under tension, a situation
that causes hematuria. Cysts are the most common kidney expansive processes.
Ultrasound provides a good differentiation between simple renal cyst and
renal cancer in 95% of cases. Cysts are substitute formations of space, well defined,
round, hypo- or non-ecogenic, with back amplified sound. In the case of CT,
morphological criteria are valid, but in addition, it may be found the lack of cyst
capsule opacity, after the administration of the contrast substance, due to the absence
of renal parenchyma at this level.
In angiography and Doppler ultrasound it is typical to note the lack of vessels
of the cyst wall, which is well defined and as in CT, the cyst wall does not
accumulate contrast substance.
STAGING
Most classifications refer to the surgery findings and examination of the
removed tissue. For the staging of the renal cell carcinoma in the TNM system, we
use the clinical examination, urography, ultrasound, angiography and CT.
T - tumor
T
x
- the necessary investigations to clarify the existence of the tumor and
invasion have not been made
T
0
- absence of primitive renal tumor
T
1
- tumor 7 cm limited to the kidney
T
la
- tumor 4 cm limited to the kidney
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T
lb
- tumor >4 cm dar 7 cm limited to the kidney
T
2
- tumor >7 cm limited to the kidney
T
2a
- tumor >7 cm dar 10 cm limited to the kidney
T
2b
- tumor > 10 cm limited to the kidney
T
3
the tumor extends at venous level, invades directly the adrenal or
perirenal tissue, but it does not exceed the Gerota fascia
T
3a
the tumor extends to the level of the renal vein or invades the
perinephric tissue, but it does not exceed the Gerota fascia
T
3b
the tumor spreads to the vena cava below the diaphragm
T
3c
the tumor spreads to the vena cava above the diaphragm
T
4
the tumor exceeds the Gerota fascia
N - nodes
N
x
the regional nodes cannot be evaluated
N
0
no local regional node metastases
N
1
one regional node infiltrated
N
2
multiple regional lymph nodes infiltrated
M - metastases
M
0
no distant metastases
M
0
presence of distant metastases
PROGNOSTIC FACTORS
The volume of the tumor, the degree of differentiation and the lymph node
invasion correlate well with the prognosis. Regarding the correlation with G (degree
of differentiation), the 10-year survival rate is 40% in case of G
1
and 10% in case of
G
2
/G
3
. Depending on the stage (T), the 5-year survival rate in stage 1 and 2 is 80-
90%, in case of T
3
it is 50% and in case of T
4
, the 5-year survival rate is less than
25%. In terms of N (node invasion), the survival rate is at the most 25% at 2 years.
All the aforementioned survival times require a radical nephrectomy.
TREATMENT
The treatment of localized renal adenocarcinoma is partial or radical
nephrectomy, which may be performed in a classic, laparoscopic or robotic way.
For a T
1a
tumor, the indication is partial nephrectomy.
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Radical nephrectomy is the therapy of choice in stages T
1
-T
3
M
0
. This means
transperitoneal kidney excision, with primary approach of the renal vessels (artery,
vein), together with the kidney fat, Gerota fascia and regional lymph nodes.
Adrenalectomy is indicated if the CT, MRI before surgery or intra-operator
aspect does not show signs of invasion or metastasis in the adrenal gland.
Radical nephrectomy with local lymphadenectomy is made by transperitoneal
approach. The transperitoneal approach allows by an early ligature of the renal artery
and vein to avoid the dissemination of the tumor cells during surgery, allowing the
removal of the adrenal gland and regional nodes.
The thrombus in the vena cava has a poor prognosis only when it is adherent
to the vein wall or when it extends over the diaphragm. The neoplastic thrombus
existing in the renal vein or vena cava must be removed.
Despite radical nephrectomy, the survival rate in T-T
3
stages is less than 5
years in 50-80% of the cases.
A therapeutic problem, currently controversial, is regional lymphadenectomy.
The regional lymph nodes infiltrated are found in 6-32% of the cases. The regional
lymph nodes of the left kidney tumor are at the paraaortic level; in the case of right
kidney tumor, they are at the paracave level and intercavo-aortic level. Extended
lymphadenectomy does not improve long-term survival.
Minimum invasive percutaneous surgery techniques such as percutaneous
excision by radiofrequency, cryotherapy, laser therapy or high intensity frequency
ultrasound (HIFU) are indicated in elderly patients with small tumors detected
incidentally, in patients with genetic predisposition to develop multiple tumors, or
bilateral tumors. Generally, it is not indicated for tumors > 3 cm, for those located in
the hilum or with multiple metastases.
Hormone therapy, chemotherapy or radiotherapy before and after the
surgery does not lead to improved survival rates and it is not used in kidney tumors.
For the patients with bone metastasis, radiotherapy may reduce the pain caused by
this metastasis.
The treatment of metastatic nephrocarcinoma - 25-33% of renal cancers
have metastases at the time of referral to the doctor. Despite radical nephrectomy, in
stages T
1
-T
3
(apparently treated by surgery), 20-50% of patients die within 5 years.
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Regarding the evolution of metastatic kidney cancer operated on, we have found that
over 80% of these patients die within one year after nephrectomy, but there are others
who survive with metastases for five years or more. Therefore, any kidney tumor
should be removed, depending on general condition of the patient. Metastases may
occur in 5-10 years from the date nephrectomy.
In patients with metastatic RCC, the association of radical nephrectomy with
immunotherapy with alpha interferon gave superior results in terms of survival. The
removal of metastases should always be performed whenever it is possible in terms
of surgery.
Interleukin 2 can activate immune cells with antitumor defense role.
Interferon therapy was introduced in 1983, the remission rate was 14%, of which 4%
of patients experience complete remission. Despite the very high cost, remissions are
however not equivalent to cure, because they persist only a short while.
Systemic therapy in metastatic RCC patients experienced major changes in
the recent years. This was achieved by the introduction of angiogenesis inhibitor
therapy. Bevacizumab in combination with alpha interferon, sorafenib or sunitinib
are superior to monotherapy with alpha interferon or interleukin 2. They are vascular
endothelial growth factor inhibitors of receptor-2 (VEGFR-2), platelet-derived
growth factor receptor (PDGFR), tyrosine kinase, etc..
The monitoring of the patient with renal tumor is adapted to each patient
individually. Generally, the monitoring must be performed at 6 months, for one year
and then annually and it should include abdominal ultrasound, CT and chest x-ray.
CONCLUSIONS
The most common malignant tumor of the kidney is renal cell carcinoma
(nephron epitelium, clear cell carcinoma, Grawitz tumor), an adenocarcinoma with
the starting point in the proximal convoluted epithelium. Unfortunately, the
urological symptoms occur only in tumoral late-stage (hematuria, palpable tumor,
pain). Today, thanks to ultrasound it is found in early stages only by chance. Kidney
cancer presents hematogenous metastases (lung, liver, bone, brain) and lymphatic
metastases and may cause tumor thrombus in the inferior vena cava.
By means of CT, we may obtain a certain diagnosis and a good staging of the
T element, but not a stagig of the nodes invasion. In the case of renal expansive
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process, the most important differential diagnosis is made between kidney cancer and
renal cyst.
The two entities may be differentiated by ultrasound in approximately 95% of
the cases and by CT in almost 100% of the cases.
In the absence of metastases, radical nephrectomy is the therapy of choice.
Kidney cancer is resistant to radio-, chemo-and hormone therapy.
Modest therapeutic results are obtained in metastatic renal cancer, with
modern forms of immunotherapy (interferon, interleukin 2).
Superior results are obtained in metastatic kidney cancer with angiogenesis
inhibitors.


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GENERALITIES


They represent 7% of the totality of urothelial tumors. Tumor incidence
distribution in the renal pelvis, calyx, ureter, bladder and urethra coresponds to the
percentage of urothelial surface of these organs. A very important detail in the
appearance of urothelial tumors (the urothelium is the mucosa of urinary tract at
calyxs level, including the level of prostatic urethra proximal extremity of the
urethra) is the increased incidence of urothelial carcinoma in the obstructed and
dilated urinary tract.
The incidence on gender reveals a predominant reach on the male gender, and
the M/F ratio is of 3/1.
The incidence of upper urothelial tumors is increasing, but it cannot be
certainly appreciates if it is a real increase of incidence, or if this is the result of an
earlier diagnostic thorugh some improved methods.
Over 1/3 of the patients usually have a second urothelial tumor, generally
situated at the level of the bladder. The maximum frequency of these tumors is
situated around the age of 65 years old. Recent experience compels to an age
reconsideration, due to the fact that these tumors can be diagnosed even in the 5th
decade, or even lower.
Another characteristic of this tumor is the evolution gravity. Thus,
aproximately 25% of the patients die aproximately whithin 1 year from the discovery
of the disease. They are much more serious than bladder tumors (also urothelial), not
due to histological characteristics, but due to a faster possibility of penetration.
ETHIOPATOLOGY
In 1895, Rehn initially emphasised the increased number of bladder tumors in
the workers from dye industry (professional character of the disease), but afterwards
an increased frequency of UUTUCC was noticed for this professional cathegory.
For a long time it was thought that pyelocaliceal tumors distally disseminate,
carried by urine flux, to the bladder, where by local graft give birth to some bladder
9. Upper urinary tract urothelial cell
carcinoma (UUTUCC)
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tumors that are similar to those developed from skin mucosa. Further this hypothesis
was infirmed based on clinical observations.
The theory accepted nowadays is the theory of multicenter urothelial
carcinogenesis. According to this theory, the entire urinary tract, from the calyx to
the supramontanal urethra (posterior) is covered by urothelium and it is subjected to
the same carcinogenesis agressions. The entire urothelium must be interpreted as an
anatomo-functional unit, having the same physiopathology and the same pathological
manifestations. On the other side, there is a random appearance of tumors, correlated
with the urothelium surface of each organ and with a higher incidence of urothelial
tumors to the urinary pathways with urinary statis.
Urothelial carcinomas can be exogenously induced. It has been proven that
many chemical substances can lead to the appearance of urothelial tumors.
Compromised professional groups are the workers in textile industry, leather and dye
industry, which are subjects to aromatic amines: benzidine, a- naphtylamine, p-
naphtylamine, auramine, 4-aminophenol. The latency period between the exposure to
a carcinogen and sickness is usually longer than 10 years.
Apart from stated carcinogens, it was observed that some chemotherapy, such
as cyclophosphamide, lead to the appearance of urothelial carcinomas.
Phenacetin, cyclamate abuse determines also an increased incidence of
urothelial tumors. Saccharin also has a proved carcinogene effect.
Nicotine abuse (over 20 cigarettes/day) in an interval of over 20 years has an
increased risk of appearance of urothelial cancer. In smokers, a and p-naphtylamine
are eliminated through urine.
Nitrates and nitrites have a urothelial carcinogene role (meat products
preservatives, well water).
PATHOLOGY
Macroscopically, upper urothelial tumors are presented as papillary tumors,
sessile (large implantation). They can be totally solide or can have more firm areas.
Oftenly they are unique, but in almost 50% of the cases they can be multicenter.
Microscopically, they can be show in a different way. The majority of high
urothelial tumors, (over 90% of them) are pappilar carcinomas with transitional cells
(Tabel 9.1). Rarely, but with increased aggresivity, there can be flat epithelial
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carcinomas. In a smaller number of cases, adenocarcinoma and sarcoma can be
encountered.
Upper urinary tract carcinoma %
Transitional cells carcinoma > 95%
Epidermoid carcinoma (squamous-cell) 4%
Adenocarcinoma 1%
Sarcoma < 0,5%
Table 9.1. Incidence of high urothelial tumors
Extension
Locoregional extension of high urothelial tumors is achieved by contiguity (in
oil stain) and by deep parietal penetration. The locoregional extension performs a
real very thick neoplastic locoregional fibrosis, that incorporates the renal pedic, the
renal pelvis and the ureter, le, joining the peritoneum and the large vessels.
Incomplete removal (partial nephroureterectomy) determines local relapse and
metastasis, that appear more often in the first 3 years.
Metastasis
The ganglionar invasion is early and frequent, and takes place in para-aortic
and paracaval (in the right) lymph nodes. The localization of primary tumor is of
great importance for this type of invasion. Distal ureter tumors produce a parabladder
invasion, while middle ureter tumors metastasis in iliac lymph nodes. Superior ureter
tumors invade paraaortic and paracaval lymph nodes.
Sangvin invasion, more oftenly encountered in epidermoid formes, produces
pulmonary, bone and hepatic metastases; rarely, spleen, pancreas or suprarenal
metastases can be encountered.
TNM STAGING
Tumoral differenciation, based on cytological and histological criteria is made
according to IJTCC (Internation Union Against Cancer) after the TNM system. Also,
the depth of epitelial tumors, the same staging being used for bladder tumors.
T primary tumor and infiltration depth
T
x
primary tumor cannot be appreciated
T
0
no renal tumor was revealed
T
is
- carcinoma in situ
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T
a
non-invasive transitional carcinoma ( it does not invade lamina propria of
urothelium mucosa)
T
1
the tumor exceeded lamina propria
T
2
the tumor infiltrates muscular tissue
T
3
the tumor invades adventicea and perirenal or ureteral fat
T
4
the tumor invades adjacent viscera
G differentiation level
G
0
- benign papiloma
G, - high differentiation level carcinoma
G
2
moderatly differentiated carcinoma
G
3
- weakly differentiated carcinoma
G
4
undifferentiated carcinoma
N regional lymph nodes
N
0
absence of regional adenopathy
N, - one infiltrated regional lymph node with a diameter up to 2 cm
N
2
multiple locoregional lymph node involvement
N
3
metastases in locoregional lymph nodes with diameters larger than 5 cm
M distant metastases
M
0
there are no distant metastases
M
1
- there are distant metastases
SYMPTOMS
Total hematuria is present in over 90% of the cases. It has the characteristics
of neoplastic hematuria: it is spontaneous, followed by pain due to ureter obstruction
with clots and it is capricious.
The pain has the aspect of a nephretic colica, it appears after hematuria,
being triggered by clots migration.
Flank tumor or lumbar region tumor is rarely consecutive to the tumor itself,
and more frequently it is caused by the hydronephrosis resulted from ureter
obstruction by the tumor volume or through wall invasion (neoplastic stenosis).
Another simptoms that are associated to urothelial tumors are: asthenia,
anemia, pallor, signs of intoxication neoplastic.
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Fever is a detrimental sign and it is very rarely encountered, in cases of stasis
and infection.
THE LABORATORY INVESTIGATIONS reveal microscopic hematuria,
anemia whithin neoplastic intoxication, impaired liver function in the presence of
hepatic metastasis. Pyuria and bacteriuria is observed in patients with associated
urinary infections, consecutive to urinary stasis by tumoral obstruction.
Cytological diagnosis is an important component in urothelial tumor
diagnosis. It is true that the cytological investigation does not allow a tumor
localization, but in the case of a trained cytologist, the diagnosis can be established in
90% of G3 and G4 undifferentiated carcinoma , based on this investigation. The
method cannot be used as a mean of exclusion of the diagnosis, especially in the case
of very well differentiated urothelial tumors, where the sensitivity of the method is of
only 50%.
IMAGISTIC INVESTIGATIONS
KUB x-ray. It may reveal potential bone metastases that are osteolithic.
IVU. It gives decisive indices over high urothelial tumours in 50 75% of the
cases. The presumtive diagnosis of urothelial tumour may be made on the basis of
the two radiological signs of this lesion.
- the gap of irregular form and interrupted contour corresponding to the
parietal insertion of the tumour (Bergman sign).
- stenosis translated in rigidity, assymetry, deformation or amputation at the
level of calices and renal pelvis;
- the gap in the form of a cup (Bergman sign) and stenosis (tumoral) which
angrenate the dilatation of the supradjacent urinary tract.
Retrogadred ureteropyelograpy has better accuracy in making diagnosis
than the IVU. 75 80% of the pyelocaliceal and ureteral tumours may be revealed
with the help of this method.
Ureteroscopy combined with the tumour biopsy, it is the diagnosis
investigation that has the greatest sensitivity and specificity.
Echography. It is not a specific diagnosis method in the case of UUTUCC; it
allows for the exclusion of the renal lithiasis, esepcially translucent lithiasis, as
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differential diagnosis. It also enhances highlight of retroperitoneal lymphatic nodes,
locations of possible metastasis.
CT and MRI are limited in making a diagnosis on this type of tumoural
pathology; neverthelss, they offer precious information in investigation of the
retroperitoneal region while highlighting on metastasis of regional and juxtaregional
lymphatic nodes.
Out of the imagistic investigations, IVU and retrogadred ureteropyelograpy
still have great importance. The best diagnosis value is rendered by the ureteroscopy
combined with cytology and tumour biopsy findings.
Cytoscopy is used for and is important for the exclusion or identification of a
simultaneous vesical tumour. The echography allows for identification of
ganglionary or visceral metastasis when there is no indication of or the CT and MRI
cannot be performed.
DIFFERENTIAL DIAGNOSIS
The most important medical conditions that are taken into account are:
Radiotranslucent lithiasis pain is prevalent, haematuria is proviked and the
gap image has the "mantel symptom" (is surrounded by contrast agent, teh sign of the
mantel), with no pareital insertion.
Renal (parenchyma) cancer it is different from the pyelocaliceal tumour,
which remains stuck at this level, through the modifications of the pyelocaliceal
system (traction, recurving etc.). echographically, differentiating is easier, simpler
and more specific in the case of renal cancer.
Congenital or secondary hydronephrosis is easy to recognize
echographically. It is more difficult to make the diagnosis of a urothelial tumour
accommodated by the renal pelvis or ureteral regions and which is joined by
hydronephrosis due to the obstruction- in these cases UPR is an imagistic
investigation of great accuracy.
The urographically nonfunctional kidney as a consequence of the
pionephrosis, xantogranulomatous pionephritis or tuberculosis, which all have
sufficiently obvious pyelographic images with retrogadred ureteropyelograpy in
order to render the diagnosis.
SURGICAL TREATMENT
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Tumours of renal pelvis and ureters with no metastasis
The standard therapy of urothelial carcinoma with no mestastasis located in
the pyelocaliceal and ureteral regions is nephroureterectomy with perimeatic
cystectomy.
The solitary superficial urothelial tumours that are well differentiated may be
treated through conservative interventions too, in cases well selected, single
functional kidney, old age and organic diseases that do not allow a far-reaching
intervention: endoscopic resection, laser coagulation followed by topic chemotherapy
- Mitomicine, Adriamicine and Epirubicine.
CHEMOTHERAPY
Tumours of renal pelvis and urothelial tumours with metastasis or
tumours advanced at local level
The treatment that is recommended in these forms of evolution of the disease
are systemic chemotherapy with Cisplatin and Methotrexat. The shortcoming of this
chemotherapy consists in the nephrotoxicity of these agents. Due to the reduced
numbers of cases and the lack of random research, it cannot be proved with no doubt
that this therapy extends or not the life of patients in advanced tumoral stages.
RADIOTHERAPY
High urothelial tumours are radioresistant; the better differentiated they are,
the more radioresistant they get.
CONCLUSIONS
The tumours of the renal pelvis and of ureter summon 7% of the total of
urothelial tumours. Approximately 95% of the tumours of the ureter or of the renal
cavitary system are urothelial carcinoma. These tumours may be induced through
exogenous way. The carcinogen factors that are known include aromatic amines,
abuse of nicotine and phenacetin.
Staging of these tumours is done after TNM system. In cases of lymphatic
metastasis the paraaortic, iliac and paravesical nodes are invaded.
Haematogenic metastasis localizes at the level of bones, lungs, liver, pancreas
etc.
The most important role in diagnosis: IVU, ureteropyelography and
ureteroscopy combined with cytological investigations. In case of high urothelial
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tumour, it is compulsory to perform cystoscopy in order to discover possible
simultaneous vesical tumor, because this possibility is of 30%. The prevalent clinical
symptom is macroscopic haematuria in over 60% of cases.
The standard therapy of urothelial tumours and of tumours of the renal pelvis
with no metastasis consists in nephroureterectomy with perimeatic cystectomy.
The well differentiated pyelocaliceal and ureteral tumours may be solved with the
help of conservative methods too, endoscopic resection of tumours, laser coagulation
with URSR or partial ureteral excision with terminal anastomosis.
Renal pelvis and ureteral carcinoma, with metastasis via lymphatics or
hematogenous can be treated by induction systemic chemotherapy. The
chemotherapy will consists of administration of different therapeutic plans that
contain Methotrexate and Cisplatin.
Radiotherapy is unimportant in the treatment of superior urothelial tumors. It is
not proven an obvious survival of patients after radiotherapy.
The tumoral stage in which the patient is caught at the moment of diagnosis is
decisive in the prognostic of patients with superior urothelial tumors, taking into
consideration the depth of tumoral infiltration, regional lymph nodes situation and
the existance of metastases.



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EPIDEMIOLOGY
The cancer of the bladder represents 2% of all malignant tumors. It is the 4
th

place in men cases after pulmonary, prostate and colon tumors, while at women it is
on the 10
th
place.
It is the most common tumor of the urinary tract. The age of choice of cancer
of the bladder occurrence is 65-70 years. Similarly to the pyelocaliceal and ureteral
tumors a noticeable downward trend in age of bladder tumor occurrence can be
observed, which can be found in recent years even in the second decade of life. Men
are affected at a 3-4 times higher rate than women. The difference increases with age.
About 75% of all patients with bladder tumors at the time of first diagnosis
present a superficial bladder tumor, 20% an invasive cancer, while 5% have a
metastatic bladder cancer.
The incidence of bladder cancer is higher in industrialized countries than in rural
areas.
ETIOPATHOGENESIS
Involvement of toxins in the bladder tumor carcinogenesis has been studied
and clarified the most complete, compared with other tumors.
In 1895, Rehn observed the more frequent occurrence of cancer of the bladder
in workers in aniline dye industry. In 1938 it has been experimentally proved at
animals that aromatic amines produce cancer of the bladder. The best known
carcinogenic substances acting in the bladder are: 2--naphthylamine, 1-
naphthylamine, benzidine, magenta, phenacetin, cyclophosphamide, diclorbenzidina
and aniline. Latency time between the exposure to pollutants and development of
cancer of the bladder is 10-40 years.
Aromatic amines: become cancerigenic after hepatic metabolism by
hydroxylation and glucuronation and it is then excreted by urine. They can be
activated with N-acetyl-transferase. Individuals who due to genetic have a
10. Urinary bladder tumors
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rapid acetylation, have a lower cancer risk, compared to so-called more slow
acetylated persons.
Smoking: smokers have a 2-6 times higher risk of developing cancer of the
bladder. After 40 years of smoking the risk is 2 times higher than after 20 years
of smoking. And in this case 2 - -naphthylamine has the decisive role in
occurrence of cancer of the bladder. Saccharin and cyclamate according to
studies have a carcinogen action in humans.
Drugs: 3 drugs may be involved, certainly, in the increased frequency of
cancer of the bladder:
Clornafazine, a therapeutic agent of polycythemia, which, from the point
of view of its chemical structure, is related to the of 2 - -naphthylamine,
but no longer used since 1963;
Phenacetin produces, in addition to an increased incidence of cancer of
the bladder an interstitial nephritis (nephropathy of analgesic);
Cyclophosphamide - alkylating anticancer agent.
Chronic urinary infections chronic carriers of bladder catheter by the
bladder mucosal epithelium metaplasia, especially develop epidermoid cancer
cell (pavement or squamous) or epidermoid cancer. Most at risk are patients
with neurogenic disorders of bladder evacuation, bearing for decades this
catheter. Urinary infection, blader catheter, bladder stones produce chronic
irritation of the lining of the vesical mucosa.
Bilharzia is an endemic parasitosis in various countries in Africa and Arab
countries, in the acute phase of infection with hematobium Schisostoma
granulomatous polyps form in the bladder. It is assumed that the increased
incidence of cancer of the bladder in patients with chronic urinary infections is
due to the growth of nitrosamines in the urine during urinary infections.
Balkan nephropathy. Etiologic factor seems to be a fungus. It grows as a
saprophyte on stored grain and produces nefrotoxine and mycotoxins with a
cancerigenic action.
PATHOLOGY
Macroscopic - about 75% of all bladder tumors are localized in the trigone -
during development they catch ureteral orifices, 10% are localized in the bladder
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dome and have other embryological origin and the remaining 15% are distributed in
the lateral and posterior bladder wall mucosa. On inspection they have the following
aspects:
Pediculated tumors - single or multiple, implanted in the bladder mucosa
by a thin pedicle.
Sessile tumor with large implantation basis, with short fringes, less
mobile, they seem to be fixed to the mucosa, less exophytic than the
previously described category.
Infiltrative tumors they are vegetative tumors, with large implantation
in the bladder wall, with an irregular surface.
Generally, the larger a tumor is, and has a larger implantation basis, the more
malignant it is.
Microscopic they are divided into epithelial tumors and non-epithelial ones
(Table IV).
PRIMITIVE TU.
I . EPI THELI AL TU. (95%)
A. Benign - papilloma
B. Malignant:
Transitional carcinoma
Epidermoid carcinoma
Adenocarcinoma
2. TU. MEZENCHI MALE (4%)
A. Benign (3,5%): fibroma, myoma, etc.
B. Malignant (0,5%)
Sarcoma
Reticulum cell sarcoma
Lymphosarcom
SECONDARY TU.
1. Gastric metastasis, ileal or colic, pheochromocytoma, from the lung, mammary
gland, pelvic organs.
2. Endometriosis, dermoid cysts.
Table IV - Histological appearance of bladder tumors

In the epithelial tumors, urothelial carcinomas are most common. In 7% of
cases, epidermoid carcinomas are found and in 1% of cases bladder adenocarcinomas
are found, in the anterior wall of the bladder, opening place of the urachus.
Normal bladder urothelium is composed of 6-7 cell layers. The number of cell
layers reduces upward to the pelvis of the kidney, where only 2-3 layers can be
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found. Typical for urothelium are the so-called umbrella cells located on the
lumen. These cells are covered with a layer of mucopolysaccharides containing sialic
acid, forming mucous layer, in the area from muscle, the epithelium is delimited by
the basal mucosa.
Papillomas are considered benign tumors. This rare form of tumor is
composed of microscopic view of a normal epithelium, which increases similarly to a
cauliflower to bladder lumen (exophytic) with a greater number of cell layers (T
0
G
0
).
G
1
carcinomas have multiple epithelial layers with partial loss of appearance of
stratification. The nucleus is uniform and resembles to the cells of the basal
membrane. Cellular polymorphism has not yet outlined. G
3
tumors - this group of
tumors is malignant aspects with anaplasia are evidenced, with increased nuclear
polymorphism. Epithelial stratification can no longer be recognized. G
2
tumors are
located between those with G
1
and G
3
. Currently, there are two types of grading for
bladder tumors:
WHO 1973
Urothelial papilloma
Grade 1: well differentiated
Grade 2: moderately differentiated
Grade 3: poorly differentiated
WHO 2004
Urothelial papilloma
Urothelial papillary neoplasm with low malignancy
Urothelial papillary carcinoma of lower malignancy grade
Urothelial papillary carcinoma with high degree of malignancy
Carcinoma in situ - is an intraepithelial neoplasm with a high degree of
malignancy. Pathological studies performed on total cystectomy pieces showed
urothelial bladder tumors are tumors with multicenter growth. Because they have a
high potential of malignancy, all epithelial bladder tumors should be considered
transitional carcinomas.
Extension at distance - bladder carcinoma invade locally penetrating the
bladder wall layers. Perivesical ganglions, pelvic, of obturator fossa, presacrum and
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iliac are infiltrated through lymphogene way. Hematogenous metastases occur in
lung, bone and liver.
T
1
G
3
tumors present, in over 10% of cases, invaded lymph nodes or hematogenous
metastases. In T
2
stage 29-30% of cases there are invaded lymph nodes, and in T
3a

and T
3b
stages in 40-60% of cases metastases can be observed.
STAGING
Bladder tumors are classified as other urogenital cancers by TNM system.
T
x
- Primary tumor cannot be explored
T
0
- no primary tumor highlights
T
a
- Noninvasive papillary carcinoma in the lamina propria
T
is
- carcinoma in situ
T
1
- carcinoma that invaded the lamina propria
T
2
- carcinoma which permeates the muscle layer of the bladder
T
2a
- tumor invades superficial of the muscle layer of the bladder
T
2b
- tumor invades deep of the muscle layer of the bladder
T
3
- Tumor invades perivesical tissue
T
3a
- microscopically
T
3b
macroscopic
T
4
- Tumor invades prostate, uterus, vagina, pelvic or abdominal wall
T
4a
- Tumor invades prostate, uterus, vagina
T
4b
- Tumor invades pelvic or abdominal wall
N- ganglions
N
x
- Regional ganglions cannot be evaluated
N
0
- no lymph metastasis reveals
N
1
- one lymph node invasion with more than a 2 cm in diameter
N
2
- invasion of one lymph node with a diameter between 2-5 cm, or more
than 5 cm diameter lymph
N
3
- lymph nodes over 5 cm diameter
M - Metastases
M
x
- possible metastases cannot be explored
M
0
- no metastasis
M
1
- distant present metastasis
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If P element is added, this means the correct staging of the tumor (T) by histological
exam-PT.
EVOLUTION
Non-infiltrative papillary tumors - can be radically cured by total exeresis,
but a proportion of up to 50% relapses in the next 5 years and 80% in the first 10
years. Relapses are of the same type T and G, or progress to invasion (T) and (G)
anaplasia.
Invasive tumors - evolve locally by direct extension, invade lymphatics and
lately it metastasizates hematogenous,
SYMPTOMATOLOGY
In about 20% of cases, in early stages, cancers of the bladder have no
symptoms, they are accidentally discovered during the occurrence of hematuria or
when conducting an endoscopic examination for other conditions (BPH, prostatic
cancer, urethral strictures after urethrotomy or when installing ureteral catheter for
PCNL).
The most common symptom in bladder cancer is macroscopic haematuria,
painless, but macro-and microscopic hematuria can be caused by other urinary tract
tumors. In general, papillary tumors are massive bleeding, blood clean that clots
either in the bladder. In contrast, infiltrated tumors hematuria may be of lesser
intensity, but may accompanied by signs of suppurations of pathological mucosa of
the bladder capacity reduction.
Pollakiuria - is especially observed in infiltrated forms, which reduces
bladder capacity and flexibility. It is generally a sign of late stage in the evolution of
bladder tumors.
Dysuria it appears as a consequence of infiltration after bladder neck, in
case of cervico-trigonal location of the tumor. Sometimes, dysuria may result from
the presence of clots in the bladder, or appearance of tumor (pediculated) in cervix.
Pyuria - is a rare sign, is present mainly in infiltrative tumors.
Pelvic pain - is due to perineurial neoplastic infiltration. It manifests as a
painful sensation with hypogastric, pelvic or perineal center.


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Fig. 10.1. Cystoscopic aspect of
bladder tumors
DIAGNOSIS
Cystoscopy. In patients with macro and
microscopic isolated hematuria, carrying out a
cystoscopy is mandatory. This method of
investigation will be preceded by non-invasive
methods such as ultrasonography which is useful
also for exclusion of renal origin of hematuria.
Cystoscopy is performed either with rigid
cytoscopes or lately, with flexible ones. The
bladder will be examined using an optical angulated - 70 . If no changes appear in
the bladder, ureteral orifice from which the bloody urine is coming should be
pursued, hematuria is sometimes bilateral. With a 0 optical the distal urethra can be
explored, bulbar or prostatic (Fig. 10.1).
Cytology - transitional epithelial cells (normal) and the carcinoma can be
identified in samples of urine, testing is performed by repeated instillations of 50 ml
physiological saline into the bladder. The first morning urine should not be collected
because cells that have stalled for some time in the bladder may be damaged. Urine
samples are kept for sedimentation or passed through micro-filters. The supernatant
is mounted and studied under a microscope as the native preparation, either using
different staining techniques: Papanicolau technique or Giemsa. It is studied the
microscopic appearance of cells, studying the following malignancy criteria:
the changing of nuclear plasma
protrusions and irregular of nuclear membrane
increasing the amount of chromatin, with decrease of the nucleus transparency;
multiplication and change of shape of nuclear particles;
various aspect of the form of nucleus.
After carrying out the Papanicolau test, there are five gradations of cytology
appearance: grade 1 and 2 shall be considered as benign, grade 3 is atypical, grades 4
and 5 shall be assessed as malignant. The sensitivity of urinary cytology is 30% in G
1

tumors, of 40-60% in G
2
tumors and 80-90% in G
3
tumors, including carcinomas in
situ. False positive results are frequently found in chronic inflammation, especially in
urinary stones.
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Fig.10.2. US aspect of the bladder tumors

Biological markers - have a decreased role in bladder tumors and therefore
they are no longer used for diagnosis.
IMAGING
Ultrasound in many cases it can
identify a bladder tumor, if the examination
is carried out in a state of bladder fullness
(Fig. 10.2). Tumor located on the anterior
wall is more difficult to identify in a
transabdominal ultrasonography, or small
ones with any location.
I VU is mandatory for a macro or
microscopic investigation of hematuria.
Bladder tumors are satisfactory noticeable on the cystography of the urography,
which allows the exclusion of a likely cause of bleeding with a pyelo-calyx, basin or
ureteral center. It also gives information about renal echo, when the bladder tumor
has produced the infiltration of the terminal ureters, with secondary
ureterohydronephrosis.
CT in most cases identifies the bladder tumor. Also can provide information
on local expansion, especially the neighboring organs. Lymph nodes cannot be
identified very well with CT, because only lymph nodes over 1 cm in diameter, can
be identified, ganglions with micrometastasis cannot be identified.
MRI gives less good results compared with CT. Although imaging methods
progress, neither ultrasound, nor CT or MRI cannot accurately fit a bladder tumor in
one of the stages of the known TNM staging, cannot allow a full diagnosis of
primary tumor.
CYTOSCOPY AND TUR B
The final confirmation of bladder tumor diagnosis is made by cystoscopy in
anesthesia. In TUR-B tumor is usually removed entirely. Samples are taken from the
basis of tumor which is sent to histopathology examination, separate from the rest of
tumor, allowing a sure classification of depth of tumor invasion secure employment.
Biopsy samples are taken from the apparently normal urothelium, to identify the
precancerous state such as dysplasia or carcinoma in situ. At the end of the operation
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the bladder examination is performed by bimanual examination. Relaxation of the
abdominal wall after anesthesia, allows appreciation of bladder tumor infiltration in
the bladder wall and into neighboring organs, or pelvic wall. Thus it is possible to
differentiate a tumor in T
3a
stage from one in a T
4
stage.
If bladder wall has an increased consistency, or even hard, but mobile, we can
talk about a tu. that penetrates muscles, excluding stages T
a
and T
1
.
After the diagnosis of bladder tumor is established, one will proceed to tumor
staging, especially to exclude the presence of metastasis. The following
investigations are used:
CT of the pelvis, which allows the identification of lymph nodes in the
iliac area, obturator fossa and lymph paraaortic ganglions;
The upper abdominal US allows to identify the status of the liver;
Lung x-ray in two planes permits to exclude any lung metastasis;
Bone scintigraphy, excludes bone metastasis. Bone metastasis are
characterized by increased accumulation of the isotope. This sign may
be due to different processes of bone regeneration, caused by chronic
inflammation, healing after fractures, etc..
New diagnostic methods
Cystoscopy in polarized light after the hematoporphyrin.
A DNA analysis of mucosal epithelial cells using flow cytometry can
be performed. You can use cell surface markers (ABO antigens) for
determining prognosis of the bladder tumor. The prognostic
significance is the loss of surface antigens, which are always present
on epithelial cells. Using monoclonal antibodies one may identify
tumor antigens on the surface of tumor cells, using immunohystologic
or immunocytologic processes.
DIFFERENTIAL DIAGNOSIS
Due to these complex investigative methods that allow not only to objectify
the tumor, but also to know its histological nature, the possibility of confusion with
another urology entity seems impossible. Before having these very complex
possibilities of diagnosis, the differential diagnosis is made with: bladder
tuberculosis - as proliferative form, bladder stones, prostate adenoma, hypertrophic
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cystitis, ureterocele, bladder clots, etc. The diagnosis of bladder tumor is determined
by several methods of investigation that converge.
PROGNOSIS
Assuming that all bladder tumors are malignant (except papilloma), we must
admit that there are very different degrees of malignancy, ranging from favorable
prognosis, to the perception of very short survival.
The most important prognostic factors are:
the stage of tumor invasion (the invasion is more advanced, the prognosis is
worse);
histological grade - lethality index of bladder tumor directly increases with
tumor gradation;
according to histological type, epidermoid tumors and adenocarcinomas have
a worse prognosis;
tumors that develop on the lesions of carcinoma in situ are infiltrative from
the beginning and aggressive.
TREATMENT
At this stage with multiple technical resources, the only way to improve the
prognosis of bladder tumors is early detection of tumor, correct treatment and
complex of this first urothelial neoplasic manifestation and permanent monitoring of
the patient. Urologist is faced with two major groups of tumors: superficial, localized
in the mucosa and infiltrative, penetrating the detrusor urinae, with the possibility of
invasion at distance.
3. Treatment of bladder tumors non-invasive muscle (Ta, T1, N0, M0)
1.1. Surgical methods
1.1.1 Transurethral resection of the bladder tumors (TUR B) - is open to all
superficial bladder tumors T
a
, T
1
. After resection of the exophyt portion and basis of
the tumor 5 biopsies will be taken (in the center of the basis of the tumor and 4 points
of the resection surface, at 3, 6, 9, 12 hours) to be sent separately from resected
fragments of tumor itself - biopsies Bressel. Histopathological outcome of these
biopsies is an objective information of the radical endoscopic tumor resection.
1.1.2. Total cystectomy - the man is made a total cystoprostateveziclectomy,
which means removal of the bladder and seminal vesicles with prostate block with all
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perivesical fat. At women, total cystectomy combines with total colpohysterectomy,
making so-called previous peivectomy. Muscle non-invasive bladder tumors
cystectomy indication is reduced and relates to tumor malignancy highly recurrence,
with T1 or CIS bladder tu with high degree of malignancy.
1.2. Adjuvant therapy
1.2.1. Intravesical chemotherapy. A single dose of mitomycin C, epirubicin
or doxorubicin. This instillation is carried out within 24 hours after TUR V and is
designed to kill circulating cells after resection. This therapy reduces the risk of
relapse by 12%.
1.2.2. Intravesical immunotherapy with BCG. Intravesical BCG therapy after
TUR has superior results comparetive with TUR alone or TUR and intravesical
chemotherapy. After an induction period of 6 weeks with weekly BCG instillation the
treatment is continued at 3, 6 months, then every 6 months for 3 years. This led to a
reduction in tumor recurrence and progression of bladder tumors by about 37%. BCG
treatment imply some risks on its advese effects: fever, arthralgia, cystitis, hematuria,
even deaths by sepsis. These were due to systemic absorption of BCG. To prevent
this administration will not be faster than 2 weeks after TUR B or if the patient has
hematuria.
FOLLOW-UP patients with nonivasive bladder muscle tumor will be based
on tumor grading:
for low-malignancy tumors cystoscopy should be performed at 3 months and
then every 9 months (if it is negative);
for highly malignant tumors with cystoscopy and urinary cytology will be
performed every 3 months.
2. Locally advanced bladder tumors (T
2
-T
4a
, N
0
-N
x
, M
0
)
2.1. Surgical methods
2.1.1.Radical cystectomy - is the main indication of surgery in
patients with locally advanced bladder tumors. The following
derivatives can be made vacant by ureters urinary total cystectomy:
implantation in sigma
in Bricker ileal bladder
at the skin level (ureterostomy)
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neobladder
urinary bypass pouch of ileum or colon: Mainz II, Koch,
Indiana, Padua, etc.
Indication for this operation were the following situations:
bladder tumors are not resectable endoscopically
papillary bladder tumors, even superficial, associated with multiple anaplastic
carcinoma in situ sites;
bladder tumors in stage T
2
-T
4a
without lymphnode invasion.
2.1.2. Partial cystectomy - is extremely limited indication that just about
tumors because of size, location or intraoperative complications occur in TUR B
(bleeding, peritoneal perforation). Resection must include 3 cm of healthy tissue to
limit apparent parietal insertion of parietal tumor. All the bladder wall thickness
resection.
2.1.3. Transurethral resection of the bladder tumors (TUR B) is not a curative
therapy in the majority of these patients. Is a viable alternative in patients who re-
TUR showed a pT
a
or pT
1
bladder tumor. For other patients TUR V is performed only
palliative purposes (haemostatic, for heavy bleeding, bladder capacity reduction, to
increase)
2.2. Radiation - the tumor is well differentiated, is more resistant to
irradiation. Undifferentiated tumors are radiosensitive. Today, using either external
radiotherapy with high energy radiation such as electron linear accelerator, or
interstitial radiation therapy consisting of intratumoral implantation, of radium,
radioactive gold or tantalum in bladder wall after excision of the tumor. Radiation
therapy is used only in patients who are not candidates for radical cystectomy or
hemostatic effect when this can be done by TUR B. Preoperative radiation therapy is
used to prevent the local relapses after radical cystectomy.
2.3. Chemotherapy as a unique therapeutic method, gave poor results. For
systemic combination therapy methotrexate, vinblastine, adriamycin plus cisplatin
appears to have encouraging results.
3. Metastatic bladder tumors treatment
In this population chemotherapy with methotrexate, vinblastine, cisplatin plus
adriamycin can bring survival up to 14 months. A second line chemotherapy consists
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of paclitaxel, docetaxel, etc. It seems that the last generation of chemotherapy -
vinflunina - has the best results and therefore the only chemotherapy approved for a
second line chemotherapy.
In patients with bone metastases bisphosphonates in combination with
calcium and vitamin D improves quality of life by decreasing pain and reducing the
number of pathological fractures.

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Testicular cancer is about 1% of all male cancers and 5% of the urogenital
tract cancers. It is the most common cancer between 15-35 years. In 97% of cases,
the tumor is growing unilateral and only in 3% of the cases, testicular tumors are
bilateral. About 5% of testicular cancers develop in abdominal ectopic testicle, but
most of them develop on testicles descended into the scrotum
HISTOGENESIS AND CLASSIFICATION OF TESTICULAR
TUMORS
Approximately 80% of testicular cancers from Germinal tissue (60%
seminoma and 20% diysembryoma). The other 20% are non-germinal cancers (either
endocrine or non-specific).
Germinal testicular tumors, except of spermatocyte seminoma which is rare, have a
starting point from a common stage - testicular intraepithelial neoplasia (TIN). TIN
has its origin in fertilized primordial germ cell that has multiple development
potential. Two lines of cells develop from it: embryonic and extra-embryonic
(trophoblast). Somatic cells develop from the embryonic cells that form the
ectoderm, mesoderm and endoderm, on the one hand, and on the other hand, germ
cells, which, depending on the maturation embryonic carcinomas occur, and
teratomas seminoma. Extra-embryonic cells (trophoblast) choriocarcinomas develop
as a yolk sac tumor (Yolk).
Of fetal germ cells where TIN occurs, more clones are decoupled from the
during fetal period of hormonal development, going under TIN form in the newborn
testicle, where it develops inside the seminiferous tubules and can reach other
compartments through rete testis. At this stage, by testicular biopsy, the imminent
tumor can be identified in the precancerous stage. From this time by stimulus that
escape for the moment, one can get to invasive, destructive increase.
CLASSIFICATION OF TESTICULAR TU. (after WHO classification 1977)
Table IV
PRIMARY TU. SECONDARY TU.

11. Testicular tumors (TT)
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Germinal Non-germinal Carcinoma methastatic
Reticul-endothelioma,
Malignant lymphomas,
etc.
Seminoame
Pure
Spermatocit
Embryonal carcinoma
Teratoma
Mature
Imature
Undifferenciated
Choryocarcinoma
Endoden sinus tu.
Sertoli cells
Leydig cells
Gonadoblastoma
other tumors
In terms of clinical and therapeutic we may distinguish between pure
seminoma tumors and non-seminoma.
EPIDEMIOLOGY
Compared with other cancers, germinal tumors of the testicle are rather rare.
Of the 44 types of malignant neoplasia, testicular tumors occupy only 23 place as a
hierarchy and frequency. Germinal tumors are more common in whites, African
blacks and Asians are more rarely affected. Approximately 1-2% of all testicular
tumors occur in childhood, it is almost exclusively of yolk sac tumors or teratoma.
ETIOLOGY
There is not a clearly proven cause to date of germinal testicular tumor. An
important risk factor is the existence of a testicular tumor in history.
Cryptorchism is considered to have a 4-8 times higher risk to cause a
testicular tumor. Surgical cure of testicular cryptorchism does not reduce the risk of
malignant degeneration.
Testicular trauma and mumps orchitis do not have etiological importance in
testicular cancer. After testicular intraepithelial neoplasia has been recognized as a
precancerous condition, today they are trying to find stimulus that produce TIN in
fetal germinal cells and what are the factors responsible for the production of TIN
transformation into manifest testicular cancer.


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PATHOGENESIS
When a precancerous state transformation in a manifest germinated tumor,
TIN cells take the proliferation property towards tubular lumen, thus the growth of
intratubular tumor occurs. Then, tumor cells get the invasion ability and penetrate the
basal membrane of the seminiferous epithelium of the tube. Seminiferous tubules in
the vicinity of tumor almost always contain TIN cells. Much of the remaining
testicular parenchyma becomes atrophic. Finally, the tumor invades blood vessels
and lymph vessels, giving rise to metastasis.
Lymphatic metastasis. Usually, germinal tumors give metastasis initially in
the lymph nodes located in the same part in the renal vessels (lumbar-aortic lymph
nodes). This first location of metastasis is explained on the basis of embryonic
development, because during descent, the testicle descends with its blood and
lymphatic vessels, from the lumbar region to the hemiscrotum the same side. Further,
a metastasis takes place in both parts of the retroperitoneal as well as upward in the
supra-phrenic lymph. Metastasis can be very large, with a diameter over 6 cm (bulky
disease), leading to pain and problems caused by replacement of space (eg
hydronephrosis by ureter compression).
Hematogenous metastasis usually occur only after damage of the lymph
nodes, but about 10% of all germinal tumors (especially choriocarcinoma) may
become metastasis also in primary hematogenous way. The most frequent seat of
hematogenous metastasis is the lung, then the brain and bones.
Tendency to metastasize via the blood is especially in non-seminoma tumors.
STAGING
TNM classification has gained, in practice, of little significance. Most
common is clinical staging, the widest practice finding staging in 3 steps, due to its
usefulness for therapy and prognosis.
TNM classification of testicular germinal tumors
T tumor
Tx = primary tu. cannot be described
Tis = carcinoma in situ
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T1 = the tu. is limited in testicular parenchyma and epididymis without
vascular or lymphatic invasion: tumor may invade tunica albugineea but not tunica
vaginalis.
T2 = the tu. is limited in testicular parenchyma and epididymis with vascular
or lymphatic invasion or the tumor can invade the tunica albugineea and tunica
vaginalis.
T3 = tu. invades the spermatic cord
T4 = tu. infiltrates the scrotal wall
N lymph
Nx = lymph metastasis cannot be explored
N0 = no ganglion metastasis could be found
N1 = solitary lymph node metastasis or multiple lymph nodes metastasis with
less than 2 cm in diameter
N2 = solitary lymphatic metastasis with a diameter greater than 2 cm but less
than 5 cm, or multiple lymph nodes metastasis, none exceeding 5 cm diameter
N3 = metastatic lymph node with more than 5 cm in diameter
M metastasis
Mx = the necessary investigations cannot be performed for evidence of
metastasis
M0 = could not reveal distant metastasis
M1 = presence of distant metastasis
S = serum tumor markers
Sx = tumor markers were not studied or done
S0 = normal tumor markers
LDH (U/l) -HCG (mIU/ml) AFP (ng/ml)
S1 < 1.5 x N and < 5,000 and < 1,000
S2 1.5-10 x N or 5,000-50,000 or 1,000-10,000
S3 > 10 x N or > 50,000 or > 10,000
CLINICAL EXAMINATION
The initial stage is characterized by the absence of local revealing signs and
in general the absence of any symptom. Discovery of the tumor is completely at
random, at a systematic examination or local trauma.
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The lesion is small, usually hard, with particular sensitivity lost organ, located
in an otherwise normal gland.
The tumor stageis in a more advanced stage in which a tumor intrascrotalum
located should be diagnosed. Identify the epididymis is the essential maneuver of the
exam. Usually, one big and heavy testicle is found. Tumor itself uniformly increases
the testicle, usually keeping its oval symmetry, has a smooth surface, is painless,
opaque to trans-illumination and causes local embarrassment. Any tumor that has on
its surface epididymis is necessarily a large testicle (Chevassu). Comparison with the
contralateral testicle is indispensable. So, diagnosis is based also at this stage on a
intratesticular center of a lesion that complies with the other testicular appendices.
Any isolated testicular abnormality in a young man to be considered, until
proven otherwise, as a testicular cancer.
Late stage. At this stage, testicular cancer is found by one of its
manifestations remote extension. The clinical presentation is polymorphous and
distract from intrascrotalum lesion. Can be found:
mediastinal compression syndromes;
Pleuropulmonary syndromes;
lumbar syndromes;
bilateral gynecomastia.
DIAGNOSIS
It is based on history, bimanual palpation of the testicles and laboratory
investigations.
Between laboratory investigations one may particularly distinguish testicular
sonography (fig 1). imaging exam that made it possible to avoid a bloody
exploration of the testicle. It can discover testicular tumor that are not palpable.
Seminoma is a testicular tumor with a hypoechoic appearance, clearly
demarcated from the rest of testicular parenchyma. Unlike seminoma, non-seminoma
tumors due to the different histological components have a non- homogeneous
appearance, hypoecogene areas alternating with hyperecogene areas. both are clearly
differentiated from uniform ecogen structure of the testicle.
Chest x-ray is used to diagnose lung metastasis.
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I VU identifies lateral movement of the ureters and / or kidneys,
ureterohydronephrosis, nonfunctinal kidney, which are indirect signs of presence of
regional lymph metastasis.
Retrograde ureteropyelography is indicated when urography signs are
unclear (nonfunctinal kidney)
Abdominal CT gives information on retroperitoneal lymph nodes and also on
other abdominal organs. Abdominal metastasis can be recognized as such by CT,
when they have 0.5-1 cm in size. For this reason at CT false-positive images may
appear in 20% of cases. Lymphogram rarely brings an improvement in diagnosis.
Chest CT examination is essential whether there is retroperitoneal lymphatic
metastasis, because in these cases there is an increased probability of mediastinal
metastasis. In case of bone metastasis, bone scan will be present in addition and brain
CT to reveal any metastasis.
Tumor markers - an important role in diagnosis, treatment and monitoring of
patients with testicular tumors oncofetal tumor markers have: alpha-fetoprotein
(AFP) and beta-human chorionic gonadotropin (-HCG) and secretory tumor marker,
LDH.
AFP has elevated serum values in yolk sac tumors and embryonic
carcinoma, the hormone level in serum is 7-10 U / l and is in direct correlation with
tumor mass. In seminoma AFP has normal values.
-HCG is secreted by cells similar to syncytiotrophoblast from
choriocarcinoma and it can reach very high values of more than 100,000 U / l.
Normal values are up to 5 U / l. And other germinal testicular tumors may secrete -
HCG, but serum values are not so high.
Kinetics of markers (-HCG, AFP.) gives particularly useful information on
treatment outcome. Persistent high levels of markers after radical orchiectomy
indicate viable tumor cells, ie persistence of metastasis. A slow decrease in the level
of markers during an inductive chemotherapy may reveal resistance. Post-
therapeutically, a level of tumor markers that increases the dynamics of exploration,
may signal a tumor recurrence. Before this can be evidenced by imaging
investigations.
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AFP and -HCG are not strictly specific for germinal tumors. Increases in the
level of AFP are found in hepatic carcinoma and other liver diseases. -hCG can be
produced in rare cases also by urothelial tumors and renal carcinomas.
Oncofetal markers are negative in 80% of all seminoma and 40% of non-
seminoma tumors.
DIFFERENTIAL DIAGNOSIS
The most frequently the common acute epididymitis should be excluded.
Fever, pollakiuria, altered urinary sediment, and strong pain located in the
respectively hemiscrotal, tumefaction and congestion of the scrotal argues more for
epididymitis. Similarly to testicular tumors, epididymitis is not rare in the 2nd and
4th decade.
It must however be considered also the other intrascrotal parties as space-
replacement such as inguinal-scrotal hernia, hydrocele, spermatocele, as well as
more rare benign tumors of the epididymis and testicle and chronic testicular
granulomatous inflammation.
On the other hand, exclude the presence of painful symptoms does never a
concomitant testicular tumor. Tumor markers have a secondary role in the positive
diagnosis of testicular tumors, because the absence of elevated tumor markers does
not exclude the presence of a tumor.
EVOLUTION
The evolution of testicular cancer, as any cancer, is done to death. Testicular
cancers metastasize faster than other urogenital cancers and quickly evolve to death.
Approximately 20% of seminoma tumors give lymphoid metastasis with non-
seminoma germinal cells that are resistant to radiotherapy. CT control and of tumor
markers can capture elevated values of AFP and -HCG, which is why, to this
category of patients retroperitoneal lymphadenectomy is indicated, although the
primary tumor is a seminoma. It is an example that demonstrates the need to monitor
the dynamics in the treatment of a patient with testicular cancer of serum values of
tumor markers in time (in evolution). In addition, a careful monitoring of these
patients is necessary, which in 10-15% of cases, after complete anatomic and clinical
remissions recurrence may occur that should be treated identically: retroperitoneal
lymphadenectomy and associated chemotherapy.
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PROGNOSIS
It should be considered seriously, including all current therapeutic advances
because these tumors occur in young age, lymphatic dissemination area is very large,
and the diagnosis is established exceptionally in the initial phase. Prognosis also
depends on the location or existing dissemination at diagnosis, histological nature of
tumors, their endocrine activity and efficacy of treatment.
TREATMENT
Surgical
The first therapeutic measure in all testicular tumors is radical inguinal
orchiectomy, with the initial approach of pedicle, ligation and its sectioning.
Preparation of testicle and exteriorization from the scrotum through the inguinal
wound is achieved only after clipping or sectioning of the spermatic cord.
Histological examination will determine whether it is a seminoma or a non-
seminoma tumor.
Retroperitoneal lymphadenectomy (LAR) (fig. 2) is indicated in all non-
seminoma germinal tumors and / or seminoma tumors when tumor markers are
raised and also indicates the presence of other types of tumors in lymph nodes
metastasis. The intervention is of a large-scale and consists of avoiding lymph nodes
and fat between renal artery and hypogastric artery, pre-, retro-lateral aortic, and vena
cava.
Radiotherapy - seminoma is radiosensitive and has telecobaltotherapy.
Chemotherapy in radio-resistant neon-seminoma tumors adjuvant
chemotherapy is applied, a combination of cytostatics: Cysplatin, etoposide and
bleomycin. Inductive chemotherapy consists of 3 cycles with three cytostatics.
Residual tumor (lymph node) must be excised, because in 20% of cases there are
vital tumor tissue. Then it continues with adjuvant chemotherapy 2 cycles of
combination with 3 above mentioned cytostatics. The greatest risk of recurrence is in
the first 2 years after complete remission.
CONCLUSIONS
About 90% of all testicular tumors are germinal tumors. Germinal tumors
start from the precancerous condition of testicular intraepithelial neoplasia (TIN),
which occurs years before the appearance of clinical signs of tumor. Germinal tumors
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in terms histomorphology mimics embryonic development. Clinical and therapeutic,
pure seminoma and non-seminoma tumors may be distinguished. The most affected
age is between 20-40 years. At this age, germinal tumors are the most common form
of cancer. Risk factors are disorders of testicular descending, and tumor history. on
the contra-lateral testicle. The first station of lymph node metastasis are the iombo-
aorta lymph nodes. Hematogenous metastasis occurs most frequently in the lung.
AFP and -HCG are the most important tumor markers whose serum
concentration can be correlated with tumor mass.
The main symptom of testicular tumefaction is painless, but the presence of
pain does not exclude the presence of a testicular tumor.
The first therapeutic measure inguinal radical orchiectomy. In case of
seminoma, a retroperitoneal irradiation will be performed, while for non-seminoma
tumors LAR will be applied. Voluminous nodal metastasis as well as hematogenous
metastasis require, in all germinal tumors, a chemotherapy with Cisplatin. Etoposide
and bleomycin. The prognosis is relatively good. In stages with low metastatic
masses a cure rate of 80% of cases is obtained.
After achieving complete remission, the evolution is characterized by the
occurrence of recurrence in 10-15% of cases, that should again be treated in a
curative way.







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Acute renal failure (ARF) is defined by a urinary syndrome, clinical and
humoral caused by potentially reversible alteration of renal function. The evocative
symptom is anuria. Basically, it comes to suppressing of micturition and the absence
of urine in the urination bladder (verified by probing or ultrasonography) in 24 hours.
This includes all oliguria less than 100 ml/24 hours.
The physiological renal function is conditioned by three main factors: 1) TA
filtration efficiency and hydroelectrolyte composition of blood, 2) the state of renal
parenchyma and 3) the permeability of the upper urinary tract. Thus, there are three
types of anuria: pre-renal, renal and post-renal.
Rapid differentiation of causes of the acute renal failure is very important in
order to establish a prompt and appropriate treatment.
ETIOLOGY
Pre-renal ARF is actually inadequate renal perfusion or insufficient
intravascular volume. The most common cause of this type of ARF is the dehydration
by fluid loss in the urine, or extra-renal: improper administration of diuretics,
diarrhea, vomiting. A relatively common cause is the toxic-septic shock with extra-
vascular fluid storage.
Renal anuria is an acute tubular defect by: hemolytic nephropathies
(postabortum sepsis), toxic-septic shock (Gram-negative germs), acute toxic tubular
defects (sublimed, carbon tetrachloride, etc.), incompatible transfusion. The anatomic
substrate of these forms is entirely characteristic being represented by lesions of
acute necrosis of epithelial cells urinifer tube, that entirely intersects the urinifer tube
and have the peculiar feature to heal completely, without sequelae, with recovery of a
normal urinifer tube; being provided the integrity of basal membrane, for
regeneration of tubular epithelium.
Post-renal anuria - obstructive acute renal failure (urology) which is
characterized by failure of leakage of urine in the bladder due to mechanical
obstruction of the upper urinary tract. There is no particular manifestation linked to
the nature of obstacle, the consequences are the same, whether intrinsic or extrinsic
obstruction is of neoplastic nature or calculus.
12. Acute renal failure (ARF) in urology
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The most representative type that will be taken as a model of openness is
calculus obstruction, known as calculus anuria.
Anuria is the result of a calculus migration in the main urine tract (calyx,
renal pelvis), its closure then in the UPJ or ureter, followed by mechanical
obstruction of UPJ lumen or ureter. In all cases, the functional element is associated -
muscle spasm and mucosa edem - which complements obstruction.
Another cause are tumors developed in the small pelvis renalis, that reached
the advanced stages: cervical neoplasia, metastatic adenopathy, retroperitoneal
fibrosis, prostatic cancer or of the bladder in the final stages.
Obstructive anuria of iatrogenic cause are rare, but possible: after
hysterectomy (bilateral ligation of the ureters) after transvesical adenomectomy
(hemostatic ligatures at the bladder neck intersects ureteric orifices in trigone).
PATHOGENESIS
Anuria pathogenesis is explained by the influence that blood pressure has on
urine formation. Effective filtration pressure in the glomerulus is 40 cm water, and
then decreases along the uriniferous tube to 10 cm water: in the renal papilla and then
increases again, reaching 50 cm water in the terminal ureter. Complete ureteral
obstruction leads to equalization of pressure throughout the urinary tract obstruction
superjacent. As long as the pyelo-ureteral pressure does not exceed the effective
glomerulus filtration pressure, the urine continues to form, accumulating over the
obstacle, and giving rise to hydronephrosis or acute uretero- hydronephrosis.
From a clinical point of view, this means nephric colic. In terms of humor,
there is a complex syndrome characterized by:
hyperazotaemia and retention of all compounds resulting from protein
catabolism (uree. uric acid, creatinine, etc.);
fluid disorders: extracellular dehydration with cell hyperhydration;
electrolyte disorders: global hypoconcentration of electrolytes in the plasma with a
decrease of plasma osmotic pressure. Ion concentration decreases characteristic the
extracellular space (hyponatremia, hypochloremia, HCO3-ion decreases and ion
concentration increases in plasma prevailing in the cell (hyperkalemia,
hypermagnesemia);
metabolic acidosis by invading plasma with acid radicals (S, P);
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hematology disorders: cytopenia, hypo-thrombocytemia, decreased plasma
coagulation factors.
Clinical syndrome is the term for hydro-electrolyte disorders and retention of
nitrogen catabolism products.

SYMPTOMATOLOGY
CLINICAL TOLERANCE PHASE
On clinical examination, that renal lomb is painful, sometimes filled, with
muscle contracture. There are not rare cases with insidious onset and moderate
lumbar pain.
Digestive signs are always present: nausea, vomiting, abdominal distension,
paralytic ileus may appear sometimes.
Usually the temperature is normal.
High fever, prolonged, rebellious to antibiotic treatment means a septic
complication in the obstructed kidney.
Urinary syndrome is characterized by sudden and complete suspension of
diuresis, urinary bladder is "dry" in explorer catheterization or empty in
ultrasonography examination.
CRITICAL OR UREMIA PHASE
Symptomatology is increasing and becomes dominant. Clinical signs of renal
failure are on the forefront, while local events go into the background.
Vomiting is incoercible, gastric intolerance installs, abdominal meteorism
increases, causing pain that masks the original nephretic colic. Respiratory
phenomena is added characteristic to metabolic acidosis (Cheyne-Stocks dyspnea)
and neuropsychiatric events culminating in coma uremia. In the uremia stage, the
clinical aspect of obstructive anuria is similar to ARF of medical cause.
DIAGNOSIS
Usually, it is not difficult, given the particular conditions of occurrence of
anuria: a characteristic history, nephretic colic, local signs, empty bladder at
ultrasonography examination or explorer catheterization of bladder.
Ultrasonography examination offers complex morphological and
extremely useful data. In case of a single kidney, the voluminous dilation of the
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whole system pyelo-calyx (rarely obstructive anuria is accompanied only by a
discrete dilatation of collectig system). Sonography captures possible echogenic
images with shadowed in the pyelo-calyx system (calculus images), sometimes
calculus with described ultrasound features can be identified in UPJ. When the
calculus is located in the ureter at any level, together with the collecting system
dilation appears the more or less important dilatation of the ureters.
When both kidneys are present, besides the previously described aspects, the
ultrasonography informs about the morphological situation of the kidney opposite
with dilation of renal cavitary system and ureter (bilateral obstruction by calculus or
possibly neoplastic). Kidney may be the site of some abnormalities: of location,
volume and structure, etc. or the parenchyma is greatly diminished (congenital
hydronephrosis, stoghorn lithiasis) and it is with no function.
In the event of bilateral obstructive lithiasis (colicative bilateral pain, of
variable intensity), the ultrasonography examination is a true test that gives
information on the state of parenchyma on either side and directs on the part where
urinary deviation has to be performed (kidney with a better parenchymal index, with
less important morphological alterations).
KUB x-ray - allows assessment of renal size and the presence of radiopaque
calculus. The absence of radiopaque calculus raises the suspicion of an acid uric
lithiasis, the most common cause of stone anuria.
I VU - when there is an ultrasonography, it has lost its importance. It
specifies whether or not there are two kidneys, their size and location of obstacle,
when renal function is not severely impaired (creatinine values up to 1.6 mg%).
Ureteral catheterisation Injection of contrast agent by ureteral catheter is
dangerous because of its infectious aspect but this investigation precisely specifies
the stone location in the ureter and its number, shape and dimensions. It is a
procedure that can be used before surgery (urinary derivation or extraction of
calculus).
Descending pyeloureterography - ultrasonography percutaneous puncture
of the kidney in question and injection by needle puncture of the contrast agent, it
allows the optimal visualization of SPC and of ureter downstream to the obstacle.
TREATMENT
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Aims at restoring patency of the main urinary track as soon as possible,
before general condition damage and installation of irreversible renal lesions. One
emergently proceeds to the urinary tract disobstruction, from the time of the
diagnosis establishment, as every moment is precious to limit suffering from renal
parenchyma. Treatment should be made mandatory in an urology department.
If the department has the necessary equipment, time should not be wasted by
ureteral catheterization, which in addition to possible benefits has its infectious
character and sometimes it fails. An urinary derivation is carried out from the start.
The simplest and most effective, when etiology obstacle is not known precisely, and
in case of lithiasis, the number and location of calculus, is the minimum
percutaneous nephrostomy. This derivation is recommended in patients with
impaired general condition, advanced bio-humoral imbalances, in an uraemic coma,
due to simple execution, rapidity and efficiency of derivation.
When location, the number and size of the calculus are known a high
diameter nephrostomy is performed (a maxima nephrostomy-22 Ch).
Whether it is a minimal PN derivation or a maxima PN , these will be
maintained until the established treatment normalizes the biological constants and the
overall condition is better. Only in case of a rebalancing of the patient condition, one
can remove the obstacle - lithiasis.
If the urology department, where the patient is brought, is not equipped in
order to perform a PN, ureteral catheterization is tried, which is not always
practicable (ureteral meatus too medialized or too lateral, voluminous prostatic
adenoma, genital ptosis in elder women, bladder tumors that are developing on the
ureteral meatus, masking it, etc.) a classical nephrostomy will be performed, or
cutaneous ureterostomy. If the patient's general condition allows it, he can be
urgently sent to a department equipped for percutaneous derivation, after prior notice
by telephone.
After the urinary derivation (PN, unilateral ureteral catheter, or bilateral) the
emergently set medical treatment will be addressed to the ARF humoral syndrome.
Diet - is low-calorie, 900 cal/24 hours, only of carbohydrate form, to
compensate for losses of patient, which is held in a slightly negative balance.

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HYDROELECTROLYTE REBALANCING
For hyperpotasemia hypertonic glucose is administered, Ca chloride,
metabolic acidosis is balanced with bicarbonate solution, Ringer lactate, Tham
solution, iv diuretics (Furosemide). The amount of fluid administered depends on the
hidric balance /24 hours (output), anemia is combated by blood transfusion. MFth
careness to stomatitis (glycerin borax), alpha and beta blockers for abdominal
distension, chlorpromazine. Metoclopramide, Torecan to combat nausea and
vomiting.
Ureteral obstruction may be associated with urinary infection, especially with
Gram-negative germs. In particular conditions created by the obstacle worst renal
parenchyma association occurs: stasis and infection. While stasis persists, antibiotics
have a very limited value. Major therapeutic gesture is restoring the main urinary
path patency.
HEMODIALYSIS
At patients hospitalized in advanced uremia stage, with severe humoral
disorders, hemodialysis is optimal. Postponement of urinary derivation, or ureteral
catheterization is an error. Haemodialysis has no effect on renal lesions nor the
obstacle and consecutive stasis. Deleting clinical signs and humoral of urea,
hemodialysis gives a false sense of security. Therefore, only hyperpotasemia that
threatens with ventricular fibrillation, imposes hemodialysis before urinary
derivation.
SOLVING THE OBSTACLE
After the rebalancing of the patient's bio-humoral and the return to a normal
general condition, one should begin to remove the obstacle (removal of calculus).
When the urinary derivation was PN a minima, it can be solved after a precise
location (IVU, uretrography) by ESWL. Extracorporeal lithotripsy can solve even in
full anuria episode of a smaller calculus located in the JPU, lumbar ureteral or pelvic
in a patient with a short period of anuria, without large bio-humoral imbalances.
At patients with larger calculus in the JPU, lumbar ureter, multiple
urolithiasis, etc., ablation of calculus is made percutaneous by percutaneous
nephrolithotomy (PCNL), anterograde ureteroscopy or retrograde ureteroscopy.
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Note that if bio-humoral imbalances are not serious, the patient's general
condition is good, endoscopic maneuvers (PCNL) to extract the calculus are not
laborious and do not require prolonged execution, percutaneous removal of calculus
may occur in an emergency. After extracting the calculus, the PN tube is kept for
urinary derivation, until the improvement of the biological constants. In these cases,
suppression of PN tube occurs 7-8 days after surgery.
If the department is not equipped for ESWL, PCNL, ureteroscopy, calculus
removal is done by conventional surgical methods: pyelolithotomy, nephrolithotomy,
or lumbar, iliac or pelvic uretherolithomy.
When the obstacle of the main urinary tract is not the lithiasis of urinary tract,
but a neoplasm in advanced stage from the small pelvis (genital tu. in female or male,
rectal cancer, retroperitoneal fibrosis, etc..) PN is an intervention that may prolong
the patients life. If after PN practice in emergency, the general condition of the
patient improves and the biological constants return to normal, and a longer survival
can be seen, PN a minima should be converted into circular PN by creating a second
trajectory of PN and inserting a circular polyethylene tube. This type of nephrostomy
offers very good possibilities, cheap, avoiding the usual tube dislocation of PN Foley
tube.
EVOLUTION AND PROGNOSIS
Lithiasis anuria, with an origin of metabolic cause, through repeated
recurrences and irreversible renal parenchymal lesions, lead to impaired of kidney
and renal death.
Neoplastic anuria usually have few months life and rarely 1-2 years to death
by metastasis, urinary derivation is a CPN (circular percutaneous nephrostomy), with
finality.
Iatrogenic anuria by ureteral ligation require immediate intervention,
sometimes uretero-vesical reimplantation is required, sometimes the ureters are just
side pinched, if occurs shortly after surgery, the patient can hope to solve the disease,
by disobstruction and stenting of both damaged terminal ureters.
Iatrogenic anuria after transvesical adenomectomy require reopening of the
bladder, the release of OU and bilateral ureteral catheterization. One way of solving
can be an endoscopically approach and cutting ligatures.
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In anuria by retroperitoneal fibrosis treated by ureteric stents,their removal
may be followed by recurrence of anuria. It is therefore more useful for the PN final
circular derivation in time, the intraperitoneal transposition of the ureters, or total
replacement of ureter with ileal loop (enteroureteroplasty).
Dialysis, correct resuscitation, background treatment of urolithiasis and renal
transplantation have improved the prognosis of these patients.
CONCLUSIONS
ARF is a complex syndrome, where the nephron is affected completely,
interesting the overall renal functions. Their alteration is potentially reversible, with
complete morpho-functional recovery, there is no previous suffering, without sequel.
In its development there are only two possibilities: cure or death.
In ARF bio-humoral regulation mechanisms suppression causes a disease of
the whole organism with general symptoms.
The anuria term, wrongfully used by some persons, instead of the ARF, is not
correct, because there are anuria of other causes than the ARF, such as all sub-renal
obstructive cases are.
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Male erectile dysfunction (ED), formerly known as the impotence, is defined
as the inability to achieve a sufficient erection for a satisfactory sexual intercourse.
The incidence and prevalence of erectile dysfunction have spectacular increased, the
causes are not only an aging population and the more marked action of risk factors
on the population, but especially the increasing addressability to a specialized
medical service and the appearance at the end of the last millennium of drug for this
pathology.
EPIDEMIOLOGY
The prevalence of erectile dysfunction worldwide exceeded 500 million men
and the prevalence of erectile dysfunction is forecasted to double by 2025.
Among Eastern European countries Romania ranks I in terms of erectile
dysfunction prevalence, according to a study in 1999 with an estimated 1.3 million
men with erectile dysfunction.
ERECTION PHYSIOLOGY
Sexual response of men can have four phases:
Excitation phase when the erection appears with the elongation and
narrowing of the urethra, cremaster contraction with partial ascending of testis,
tachycardia, increased blood pressure. In the plateau phase vascular congestion is
present of the glans crown, complete ascending of testis, tachycardia, further increase
in blood pressure, sexual congestion, increased muscle tone, voluntary anal sphincter
contraction. Orgasm phase: emission, ejaculation and the orgasm, hyperventilation,
tachycardia, increased blood pressure and involuntary rhythmic contractions of the
anal sphincter with the periurethral muscles. The resolution phase gradually
decrease of the organ, reduced length and diameter of the urethra, scrotal resolution,
decreased respiratory rate and heart rate, blood pressure decrease, loss of sexual
congestion and involuntary perspiration reaction.
Neurophysiology of erection
Parasympathetic innervation has the main role in initiating erection.
From the central nervous system under the action of erotic stimuli (sexual, tactile,
olfactory, imagined) proerectile pulses are generated. Parasympathetic nerves leaving
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the reflex centers of erection from S2-S4 form and after entering the cavernous
bodies, parasympathetic fibers divide into two types of terminal nerves:
Cholinergic nerve ending in the endothelium and having a role in
activating nitric oxide synthase (NOS). Types of NO synthetase use arginine and
oxygen molecule to produce nitric oxide and citrulline.
In the smooth muscle cell NO activates guanylate cyclase that will catalyze
the conversion of guanosine triphosphate (GTP) into 3.5 cyclic guanosine
monophosphate (cGMP), the active form. It activates protein kinase G that triggers a
cascade of intracellular events that include loss of contractile tone (smooth muscle
relaxation) by: hyper-polarization, closing voltage-activated calcium channels,
calcium sequestration by intracellular organelles, decreased intracellular calcium,
changes in affinity to calcium of the contractile system.
Penile smooth muscle contraction is achieved by adrenergic stimulation.
This causes vasoconstriction of penile arteries and trabecular muscle contraction, the
consequence is the decompression of emissary veins and venous drainage of the
lacunar spaces. This mechanism is largely mediated by 1-adrenergic receptors.
ETIOPATHOGENESIS OF ERECTILE DYSFUNCTION
Etiopathogenesis of erectile dysfunction knows more factors: psychological,
neurological, vascular, hormone, local. Altering any of these factors may be sufficient
to produce erectile dysfunction, but most times it is a plurifactorial etiopathogenic
complex.
Psychogenic erectile dysfunction. Depression, anxiety in
performance, relationship disturbance can be causes of psychogenic erectile
dysfunction.
One of the main factors associated with erectile dysfunction is the existence
of conflicts between partners. The persistence of unresolved conflicts between
partners significantly affects the couple relationship satisfaction and, therefore, and
satisfaction with sexual relationship.
Neurogenic erectile dysfunction. Etiological classification of
neurogenic erectile dysfunction: peripheral by destroying sensitive innervation, or
by destruction of autonomous innervation which mediates artery dilation and relaxes
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trabecular smooth muscle; spine- spinal cord trauma, multiple sclerosis, etc; central
brain tumors, cerebrovascular accidents, encephalitis, etc.
Vascular erectile dysfunction
It may be arterial, veno-occlusive or mixed. Endothelial cells are very
sensitive to ischemia and hypoxia, often affected in diseases such as diabetes,
uremia, atherosclerosis, hypertension, coronary heart disease.
Endocrine erectile dysfunction. Approximately 95% of serum testosterone
concentration derives by direct release from the testis, only 5% resulting in
production at CSR glands. Hypogonadism in men is a syndrome resulting from the
inability of the testicle to produce physiological levels of testosterone: primary
testicular damage - with low testosterone levels, impaired spermatogenesis and
elevated gonadotropin levels; secondary testicular damage - with low testosterone
levels and normal or low gonadotropin levels.
Penile disorders
Penile disorders, including history of priapism, penile trauma and Peyronie's
disease can cause erectile dysfunction due to fibrosis of sinusoidal spaces of
cavernous body, intracavernous artery occlusion or neurogenic mechanisms.
Drug erectile dysfunction: thiazide, spironolactone, 5 reductase inhibitor,
santidepressants, tricyclic antidepressants, ketoconazole (Nizoral), phenobarbital can
cause erectile dysfunction.
Toxins and erectile dysfunction. Erectile dysfunction is a common
problem in chronic alcoholism, responsible for hepatic insufficiency installation,
gonad dysfunction and polyneuropathy. Smoking causes profound morphological
alterations of vascular endothelium and increases platelet adhesion and leukocyte to
the vessel wall. Chronic use of narcotics - cocaine, heroin and methadone - increase
the incidence of erectile dysfunction.
DIAGNOSIS
Clinical. The accusations that most frequently appear in patients with erectile
dysfunction are: unable to obtain an erection, poor erections, decreased rigidity,
decreased sexual performance, repeated sexual failures, etc.


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Diagnostic protocol includes:
Clinical examination: history, questionnaires for the intensity and impact of
erectile dysfunction, physical exam
Penile ultrasonography
Inter-clinical counseling: cardiology, internal, endocrinology, neurology,
psychiatry, etc.
Pelvic arteriography (for selected cases)
Cavernousgraphy / cavernousmetry (for selected cases)
Clinical examination. At base of clinical evaluation of men with erectile
dysfunction is there is an initial assessment.
Medical and sexual history are the most important elements in evaluating
erectile dysfunction. Such a history based on the doctor-patient dialogue, should be
applied to all men who come to the doctor because of this problem.
Questionnaires - scale - for the intensity and impact of erectile dysfunction
are used.
The first rigorously validated questionnaire to assess male sexual function is
IIEF (International Index of Erectile Function - International index of erectile
function). It is a questionnaire consisting of 15 questions, serves as a standard in
evaluating the efficacy of erectile function and erectile dysfunction.
Objective exam will be focused and will include: evaluation of physical
constitution (the existence of secondary sexual characteristics, pilosity, obesity or
external cachexia, the existence of gynecomastia), assessment of the cardiovascular
system (intermittent claudication, fatigue in the legs walk, angina pectoris, skin cold,
etc.), the nerve system (paresthesia, pain, sensitivity disorders) and genito-urinary,
with a focus on examining the penis, testicles and anus
Andrology exam includes: penis examination, examination of scrotal
contents, digital examination, of the inguinal region, hypogastric, perineal
Recommended diagnostic tests include the following laboratory
examinations targeted: fasting plasma glucose lipid profile, assessment of
hypothalamic-pituitaro-gonadal axis by determining the level of testosterone.


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Specialized testing and diagnostic evaluation
Most patients with erectile dysfunction can be diagnosed and treated at the
clinic by family doctors, trained in the male sexual dysfunction. Particular
circumstances may dictate the need for specialized tests and / or treatment.
They can be represented by a psychosexual evaluation and relational,
sometimes even a psychiatric evaluation. Sometimes it is useful to assess vascular
organ by conducting with pharmacological trials by intracavernous injection of
papaverine or caverject, penile Doppler ultrasound, penile arteriography. Evaluation
of nocturnal penile tumescent and stiffness (TRPN), endocrinologist tests,
neurophysiological tests may complete full ED diagnose investigations.
Treatment of erectile dysfunction
Treatment of erectile dysfunction is multimodal and placed on several levels.
Firs line treatment
Methods of psychological intervention in erectile dysfunction
Selection and initiation of ED treatment largely depends on the etiology of sexual
disorder. Often, treatment has the same components (medication and psychotherapy),
which are initiated and conducted according to ED cause.
Inhibitors of phosphodiesterase 5 (PDE5)
Isoform selective inhibitors of phosphodiesterase 5 is the latest non-surgical
therapeutic line with clinically proven effectiveness. It includes: sildenafile,
tadalafile and vardenafile. They act as selective inhibitors of cyclic guanosine
monophosphate phosphodiesterase type 5.
Androgen replacement therapy
In accordance with WHO recommendations androgen replacement therapy is to
ensure serum testosterone as close to the physiological ones: undecanoate
testosterone, testosterone gel.
Second-line treatment
Vacuum erection devices is achieved by increasing the blood inflow to the
cavernous body due to a negative pressure around the penis. Erection is maintained
after removal of the vacuum device by blocking venous return with an elastic ring
mounted at the base of the penis.
Intracavernous injections
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Injecting substance is on the front side of the penis, as close to its base,
applying local compression after needle removal: alprostadil (prostaglandin E1 -
Caverject TM EndexTM), papaverine, Moxisylyte They are used either alone or in
various combinations.
Third line treatment. Surgical approach for erectile dysfunction is indicated
after failure of local and general medical alternatives:
malleable penile prostheses are mechanical structures with moderate
cylindrical stiffness but steady and unchanged,
inflatable penile prostheses. Inflatable prostheses consist of a pump, a tank
and two artificial corpus.






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DEFINITION. Couple infertility is defined as the inability of a couple to
obtain pregnancy after one year of unprotected intercourse.
EPIDEMIOLOGY. Most couples fail to conceive after about a year and
infertility affects at least 15% of couples. Maximum fertility both in women and men
is the age of 24 years, after which the fertility rate decreases in both sexes. It is
estimated that approximately of cases involve women men and both partners
simultaneously (infertility of the couple), the male factor is involved as more than
50% of cases of infertility.
PHYSIOLOGY. The formation of quality sperm that can ensure fertilization
depends primarily on the quantity and quality of sperm and sperm circulating organic
material, material produced by the vas deferens, seminal vesicles, prostate and
bulbourethral glands.
The main functions of the testicle are linked to the two cell groups that are at
this level: Sertoli cells stimulated by FSH are responsible for exocrine function,
spermatogenesis, and Leydig cell leads to the action of LH on testosterone
production - endocrine function.
Exocrine function. Spermatogenesis begins on average at age 13 due to
stimulation by hormones secreted by the pituitary gonadotropins before.
Seminiferous tubules contain numerous sperms and B (epithelial germ cells), located
in the basal membrane layers 2-3. Spermatogenesis type A divide to 16 days forming
the sperm B through mitotic divisions forming the spermatocytes. Spermatocytes will
rise, through meiosis, to 4 haploid spermatids with sexual chromosome (X or Y), that
mature and become sperms.
During the maturing changes occur at both cytoplasmic and nuclear level, but
these are not involved in cell division: the loss of cytoplasm, appearance of acrosome
and tail of the sperm. Spermatogenetic process in humans takes approximately 64
days and is responsible for producing millions of sperm per a day.
Sperms become mobile only after a period of 18-24 hours in the epididymis,
where they undergo maturation because of fluid secreted by it rich in hormones,
enzymes and nutritional products. Histological integrity of the epididymis depends
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on the concentration of androgen. Sperms are stored in small quantities in the
epididymis, vas deferens and the remainder in duct ampule, maintaining fertility at
least one month, but for normal sexual activity the depositing is much shorter.
Sperms are able to move in a straight line and not in circles. Flogging
movement is greatly increased in neutral or slightly alkaline medium, but is
depressed slightly in acidic environments. Strongly acidic media produce sperm
death. Life of sperm in the female genital tract is only of 1-2 days. Frozen at
temperatures below -100 C it can be preserved for many years.
The sperm results from a mixture of secretions from the vas deferens, seminal
vesicles, prostate bulbourethral glands. Fluid from the seminal vesicles and washed
sperm is ejaculated from the ejaculatory duct and urethra. The average pH is 7.5. The
average amount of semen ejaculated is 3-5 ml, with 120 million sperm per ml (35-
200 million). When the number falls below 20 million per ml there is a risk of
infertility. Although sperm fertilizes one egg, ejaculation should contain an enormous
number of sperm for fertilization to be possible.
For sperm to fertilize the egg, it must pass through the granulose cell layer of
the egg, to penetrate the pellucid area, a thick coating of egg. This is possible by the
release of acrosome hyaluronidase. Anterior sperm membrane binds specifically to a
protein receptor in the pellucid area. Here are issued all acrosome enzymes, which
opened a corridor for sperm head penetration and the genetic material enters the egg
to produce fertilization.
Endocrine function of the testicles is regulated by the hypothalamus by LH-
RH (Gn-RH), which stimulates the pituitary gland. In turn, the pituitary releases
FSH, which stimulates spermatogenesis and LH, which stimulates testosterone
production in Leydig cells. Testosterone acts by negative feedback on secretion of
Gn-RH and LH. Leydig cells secrete, in addition to testosterone and
dihydrotestosterone (DHT), 17-OH progesterone and estradiol. Normal serum
testosterone level is 300-1200 ng / dl and 30-60 ng / dl for DHT. From the age of 50
years, the endocrine function of testicles is altered. In the first stage it decreases the
free testosterone levels, being important in the fertile potential of men.


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ETIOPATHOGENESIS
The presence of previous surgery may explain the occurrence of male
sterility: testicular trauma or testicular torsions, retroperitoneal lymph dissection,
lesions of vas deferens or epididymis duct injury, interventions of the prostate (TUR-
P, adenomectomy) or surgery to the bladder neck, sometimes are followed by
retrograde ejaculation.
Infections, especially viral orchitis occurred after the age of 12-13 can cause
sterility, but its appearance in pre-teenage period is rarely followed by sterility,
bilateral epididymitis may be followed by azoospermia.
The effects of chemotherapy and radiotherapy on spermatogenesis are
known and proven. Restoration of spermatogenesis after chemotherapy or radiation
therapy after 3-4 years is the degree of destruction of stem cells. If their destruction
is complete will result in permanent azoospermia.
Testicular cancer is associated in more than 60% of cases with oligospermia
and an impaired morphology.
The effect of smoking. The association of smoking and varicocele greatly
increases the risk of male infertility
Bilateral cryptorchidism in turn produces a marked impairment of male
fertility.
DIAGNOSIS
Clinical evaluation of the infertile couple
Addressing male infertility should not be different from other medical
conditions. In the treatment of infertility, the doctor has to do generally with young
people, so the best approach is direct, practical, but delicate psychological
implications because of possible infertility. For this treatment to be effective, it is
necessary for the urologist to work with the gynecologist and occasionally the
endocrinologist.
Laboratory tests.
Analysis of sperm
Spermocytogram is one of the methods of choice in the investigation of
urology and andrology and recommendations are made after a period of "sexual rest"
of 3-5 days.
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Determination of antysperm antibodies. Infertility due to decreased sperm
mobility may be conditioned by the existence of antibodies specific antisperm (in
cryptorchidism, 50%, evidenced by massive agglutination,,head to head 'or' tail to
tail ".
Testicular biopsy has as main purpose the differential diagnosis between
obstructive azoospermia and the non-obstructive one. This invasive examination is
indicated only in patients with azoospermia. Another objective of testicular biopsy is
(in addition to the diagnosis) the collection of material required in vitro fertilization.
Imaging examinations are used to highlight the causes of obstructive
sterility.
Vasography is indicated in patients with suspected ductal obstruction
(azoospermia with normal spermatogenesis on testicular biopsy puncture).
Transrectal ultrasound (TRUS) has the advantage of minimum invasiveness
almost absent and optimal highlighting of the prostate and seminal vesicles.
Scrotal ultrasound, especially the Doppler is used for the diagnosis of
varicocele as a cause of male infertility.
TREATMENT OF MASCULINE INFERTILITY CAN BE:
Surgical-prophilactic treatment is indicated in cryptorchidism, torsion of
the spermatic funicular, varicocele.
Surgical-curative treatment is practiced in duct obstructions and consists of
excision of stenosed area of the vas deferens duct and different types of latero-lateral
anastomosis, terminal or latero-terminal.
Medical treatment. Endocrine treatment depends mainly on regulation or
substitution of gonadotropins FSH and LH. In patients with no neurological disease
secondary ejaculation there can be used external massage vibrator or electro
ejaculation.
Assisted reproduction techniques
Fertilization can be done "in vivo" or "in vitro". Controlled ovarian
hyperstimulation, hormonal stimulation and superovulation using gonadotropins,
play an important role in most forms of ART Because of the increasing number of
centers able to perform in vitro fertilization (IVF) with intracytoplasmic sperm
injection (ICSI), has formed a trend the use IVF as first-line treatment.
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This approach is not correct because on the one hand does not treat the
underlying disease, which often can be resolved, and on the other hand is more
expensive.
For many couples, infertility is caused by the male factors of mild severity
intrauterine insemination (IUI) or IVF is the appropriate therapy. Because of the low
cost of IUI, it is labor that is used as first-line treatment, after which, in case of
failure to carry out different types of IVF. If there is a well established indication
why sperm can not fertilize the egg, then ICSI may be adopted as a first method of
treatment.

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GENERALITIES
Autotransplantation: is the collecting and transplantation of organs from the
same individual.
I sotransplantation: the receiver and donator are identical from the gentic
point of view.
Allotransplantation: transplantation between individuals of the same
species, that are not identical from the genetic point of view.(for example from man
to man).
Xenotransplantation (heterotransplantation): transplantation between
individuals from different species (example: from pig to man).
Organs can be implented either orthotopically (to the same place), or
heterotopically (to another location in the body renal transplantation).
Allo- and xenotransplantation can produce a rejection reaction from the
receiver, being necessary immunosuppression.
SELECTION OF RECEIVERS
In fact the renal transplantation is applied at patient with renal insufficiency
in the end stage, at those patient who are dpendent of dialysis.
DONORS
The living donor: transplantations can be performed both from related
donors and from the not related ones. The premise is a comatibility in the blood
group system (ABO) and in the human leukocytes antigene system (HLA).
The ideal combination of donor and recipient is met at twins, according to
which there is a perfect concordance of the HLA system. In case of other degrees of
relationship there is also acceptable a haploid concordance of the HLA system.
Another important prerequisite is the so-called "cross match" negative. The
advantages of living donor transplantation are:
a higher rate of functioning of the trnsplanted organ
immediate continuation of diuresis due to the short time of ischemia
more reduced immunosurppressing medication
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short waiting period, a very important detail especially with children and
patients with diabetes
Transplantation from cadavers brain-dead donors with clearly proven and
circulatory function intact, from the age of 5 years to around 60-70 years. There are
not accepted that living donors who suffer from kidney disease, general illness
(diabetes, hypertension), diseases (TB, hepatitis, AIDS), or tumor (except for
individuals who have had brain tumors).
The diagnosis of brain death. Essential clinical signs such as spontaneous
respiration stop, no ocular-cerebral reflexes, no corneal reflex and no pharyngeal and
tracheal reflex. You can also use diagnostic methods using equipment: EEG, cerebral
angiography, Doppler sonography and the absence of potentials of brainstem
produced by acoustic stimuli.
Brain death has to be diagnosed by two doctors, not belonging to the
transplantation team, based on exact clinical signs established by the legislation.
APPROVAL. It is necessary to obtain approval for the removal of the
organ, in case there is no donor cetificate there is necessary an approval from the
donor during his lifetime or after his death from his relatives. In case of a violent
death there is necessary the approval of prosecution, being also necessary the
collaboration with legal medicine.
REMOVAL OF ORGANS
The vena cava and aorta is prepared and cut off above and below the
emergence of renal vessels, together with the entire ureter. Separation of right and
left kidney occurs after removal in the ice bath. Removal is carried out in sterile
conditions. Assisted respiration is suspended only after removing the organs.
CONSERVATION
The first gesture is hypothermic gravity kidney perfusion, infused solution
(Collins solution) with 4 C. The infusion takes place before any preparation of the
kidney by inserting the infusion catheter in the inferior aorta and pinching cranial
vena cava above the renal artery above the emergence of the renal vein. Vena cava is
also ligatured proximally and distally at the place of shedding of renal veins. With
the gravity infusion there are obtained the following goals:
blood is eliminated from the vascular system of the kidney;
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the organ is refrigerated at +4 C, because at this temperature the survival
time of cells is a few times longer than in case of warm ischemia;
washing solutions contain electrolites in a concentration similar to the
intracellular environment as well osmotic coloidal substances that diminish the
lesions on the level of cell membranes for not more than 24 hours;
TRANSPORTATION
The removed organs are packeged according to a standard procedure into a
sterile cellophane bag, containing cold conservation solutions, than into a second
bag, containing melted ice and in to a third bag, that is sterile isolates the content of
the first two. This package is wrapped as a whole into unsterile fields in a
transportation box filled with crushed ice.
IMMUNOLOGICAL CONSIDERATIONS
In case of allotransplantation there can be started an immunological response
consisting of the following components:
Histoincompatibility by the antigenes of the donor;
Recognition of these antigenes by the receiver;
Destruction and elimination of tissues containing foreign antigenes;
Two main antigenic systems are responsible for the barrier of
histocompatibility between donor and receiver:
1. The system of blood group antigens (ABO system)
2. Antigens from the major complex of histocompatibility (MHC)
An incompatibility of ABO type usually leads to an immediate rejection of
the transplanted organ, thus the ABO compatibility is the most important in
transplantation.
HLA antigens can be classified according to their structure, function and
repartition in the tissues.
Ist class antigens - are glicoproteins situated on the surface of cell
membrane of different organs that contain nucleated cells as well as on blood cells.
Ist class HLA antigens aare subclassified at man into HLA A, B, and C and
are coded on the 6.the cromosome. Antigens of Ist class represent the immunological
identity of the cell and are the aim antigens in the rejection reaction.
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The IInd class antigens are glycoproteins that unlike Ist class antigens are
represented on the membranes of all cells on the surfaces of the so-called dendritic
cells, such as: macrophages or activated T lymphocites, respectively B
lymphocites.Iind class antigens correspond for humans with HLA-D antigens and are
coded on the 6th cromosome. They of of uttermost importance for the regulation and
the intensity of immunological response and the rejection reaction.
Of great importance for transplant surgery are preformed cytotoxic antibodies
in serum receptor. This is when immunoglobulins are present in the moment of
transplantation. They are directed specifically against HLA antigens of the donor and
can lead to complement activation via a reaction and thus immediate destruction of
the organ. The most frequent cause of preformed cytotoxic antibodies are
presensibilization by blood transfusions, pregnancy or previous transplants.
Evidencing the crytotoxic antibodies at the receiver can be made with the
help of standardized serums, for example at pregnant women, by displaying in
percentage the "positive reaction" by soem serums. In the case of "cross match" there
are combined lymphocites of the donor with the srum of receiver.
Transplantations can be performed only in case of ABO compatibility and
negative Cross match.
Each receiver has registered blood group and HLA type in the central
Eurotransplant Leiden (Netherlands). In case of organ donation there can be
identified the most appropriate receiver in terms of the HLA system and having the
longest waiting time. In case of negative cross match kidney is shipped by plane,
train or car.
OPERATION
The kidneys are transplanted heterotopically, or retroperitoneally in the left or
right iliac fossa, where they are protected by the iliac crest.
At first renal vessels were anastomosed terminally with the internal iliac
artery and external iliac vein. reter is implanted in the bladder domme in an
antireflux method.
IMMUNOSUPPRESSION
Corticosteroids. Initial dosis is of 2-4 mg/kg, which in 2-4 weeks is reduced
to 0,1-0,2 mg/kg/day.
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Effect: antiinflammatory, inhibation of lymphocites and thus antibody
production (humoral defense), lymphocyte toxicity, inhibition of macrophages and
polymorphonuclear leukocytes.
Side effects: gastric and duodenal ulcers with bleeding and perforation,
diabetes, osteoporosis, aseptic bone necrosis especially in the femoral head,
cataracts, muscular atrophy and psychosis.
Azatioprine: 2-3 mg/kg/day
Effects: inhibation of T lymphocites (cell immunity, after metabolization on
the liver level in 6-mercaptopurine).
Sidev effects: hepatotoxicity, depression of bone marrow.
Ciclosporine A: is an antifungal derivative, which was introduced as standard
specific immunosuppressive. The dose is dependent on the appearance of blood
picture, analyzed 12 hours after drug introduction.
Effects: inhibition of proliferation of T lymphocytes specific phase by
blocking interleukin-2, inhibition of cell-mediated immunity and humoral antigens
from emerging. Mediated immunity does not inhibit the already established
immunity by T cells, no toxicity on lymphocytes.
Side effects: nephro-and hepatotoxicity, hypertension, hirsutism, gingival
hyperplasia, tremor in case of overdose.
Antylymphocite globuline T (A.T.G.)
By immunization of horses, rabbits and rats against human T lymphocytes,
there may be produced immunoglobulin. Antylymphocite globulins are shown in
phase induction or acute rejection reactions.
Effect: suppression of T lymphocites
Side effects: antiphilacteic reactions, high risk of infections and tumors.
Monoclonal antibodies - OKT3 is a monoclonal antibody from the mouse,
like ATG it determines the suppression of lymphocites T. Similar to ATG it can be
used in the phase of induction, but also for the treatment of rejection reaction.
In the early 1980s by then classical immunosuppressive therapy
(corticosteroids and azathioprine) was replaced by a combination with cyclosporine
and corticosteroids. The current trend is to use a low-dose triple combination:
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corticosteroids, cyclosporine A and azathioprine. The last two are used at a dose of
30-50% lower than the combination of two substances.
REJECTION REACTIONS
Hyperacute rejection. Destruction of the transplanted kidney consists of
humoral response within 48 hours after transplantation, associated with a toxic
clinical picture. ABO incompatibility is a cause, preformed cytotoxic antibodies in
the serum of receptor already exist purely by chance and are intercepted by the HLA
antigens of the transplanted organ. In terms of histological lesions there are mainly
endothelial lesions. A hyperacute rejection reaction has to be solved by providing a
negative cross match
Accelerated rejection. Transplanted organ rejection consists of between 2
and 5 days after surgery, the cause is a secondary immune response to HLA antigens
of the transplanted kidney (cellular rejection). In terms of accelerated rejection
histologically resembles to hyperacute rejection.
Acute rejection. Consists of a cellular immune response that may occur
during the first 3 months postoperatively. It is a specific reaction on
alotransplantation of the host organism, which can be modified by
immunosuppressive therapy. There is a transplanted kidney destruction reaction by
effector lymphocytes, sensitized by HLA antigens of the transplanted kidney.
Chronic rejection. It is a rejection probably induced by antibodies that
slowly progresses over several years and is refractory to therapy. In the foreground
are endothelial lesions and vascular proliferation associated with vascular
obstruction.
RESULTS
With modern immunosuppression and acute rejection therapy rates are
obtained on renal functionality for 1 year in 80-90% of cases.
COMPLICATIONS
In the early phase after transplantation may occur following surgical
complications: urinary fistula, obstruction and ureter necrosis in 2-5% of cases, renal
artery stenosis in the anastomosis or anastomosis above the intimal lesions, wound
infections in 2% of cases limphocele in 5% of cases.

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CONCLUSIONS
Renal transplantation is performed with kidneys coming from living donors
or cadavers, after brain death. Once consent is obtained from their relatives, the
bodies are taken in conditions of perfect circulation and artificial respiration, infused
with a preservative solution at 4 C. After temperature 24 hours, maximum 36 hours,
the kidneys are transplanted by anastomosis to the retroperitoneal large pelvic
vessels.
Receiver and donor must be compatible in terms of blood group and in terms
of HLA histocompatibility antigens. A cross match test must be preformed cytotoxic
antibodies to exclude HLA antigens of the transplanted kidney. Rejection reactions
can be prevented by administration of immunosuppressive agents: azathioprine,
cortisone and cyclosporin A. Acute rejection reactions can be treated with high doses
of methyl-prednisolone, ATG or monoclonal antibodies.
The rate of functional kidney transplants is 95% a year. Patient survival rate
in one year is over 95%. Surgical complications: limphocele, ureter necrosis,
thrombosis of venous, arterial stenosis, occurring in less than 5% of patients
operated.
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1. UROGENITAL TRAUMAS
Traumatic lesions of the urogenital apparatus recorded under the conditions of
modern life an increase in their incidence. Anatomical situation and the various
connections of its constituent parts, spaced from the diaphragm to the perineum, give
a different character of symptoms
The urogenital injuries may be closed (contusions, sprains) or open (wounds).
Sometimes they are serious, both in their immediate development and in the many
sequels that are generated. Often encountered often in multiple accidental trauma,
their clinical expression may be masked by that of other injuries. Wide exposure of
the subject was made in the chapter "urogenital trauma".
2. HEMATURIA
Elimination of blood mixed with urine - hematuria - is one of the most
common symptoms in urology. It varies in appearance, location and significance.
Blood in the urine impresses the patients and make them go to counseling. It is a
grave mistake to prescribe a haemostatic treatment before finding the reason and
location of bleeding, most often such a patient is a carrier of urinary tract tumors,
which will be implicitly a delayed diagnosis.
Excepting complete retention of urine by clots hematuria does not require
emergency treatment, but requires urgent exploration.
The causes of hematuria are:
general: hemophilia, leukemia, poisons, infections, liver cirrhosis,
conventional syndromes, C and K vitamin deficiencies, treatment with anticoagulant
substances that currently benefit many patients with cardiovascular disease
local (urological) with location in:
upper urinary apparatus (renal parenchyma tumors, tumors pielo-
pelvis, ureteral renovascular stones, renal tuberculosis, trauma, renal
papillary necrosis, renal infarction, renal artery aneurysm, etc.)
bladder (tumors, stones, endocrine cistophaty)
subvesical (enlarged prostate, prostate cancer, etc.).
16. Urological emergencies
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There is a group of hematuria where chemical, laboratory and imaging
examinations can not specify the cause, because they are so-called essential
hematuria, which highlight the cause later, when the determined condition is often
cured from therapeutical point of view .
Clinical examination. Hematuria has many features, depending on the
disease that determines it. The character of hematuria suggests a lithiasis disease,
while the isolated character of hematuria suggests cancer localized at various levels
of the urogenital apparatus. Hematuria may be associated in time, being preceded by
a series of symptoms that betray a suffering of the lower urinary tract: urinary
frequency, dysuria, urinary flow changes, etc.. In case of neoplastic affections
hematuria is macroscopic or microscopic (pathological when exceeds the number of
1000 red cells / minute) may be total, isolated or accompanied by other clinical signs,
whimsical, unique or repeated, of low intensity or massive, with clots, leading to
complete retention the urine.
Laboratory examination. CBC shows the degree of anemia, a series of
changes in leucocytes or platelets which explains hematuria. Hematic cylinders
present in urine sediment show haematuria located in the nephron. Crystal orients
towards litiasis, neoplastic cells to tumor, pyuria and bacteriuria to infection.
Endoscopic examination is very important, when possible (patient-related
causes, urinary condition, the abundance of bleeding). It can find the high or down
location of the bleeding, if there is high-sidedness (right or left) or bilateral.
Emergency endoscopic examination performed when possible to specify leading to
the location and cause of hematuria.
I maging examination. Since ultrasound, old and forever young urography,
especially as CT and MRI imaging provide essential details concerning the location
and cause of hematuria.
Treatment of hematuria is the treatment of the cause that determined it.
Microscopic hematuria does not require emergency treatment, but its diagnosis is
necessary. General hematuria generally has to be explored by the urologist and
treated according to etiology.
In "essential" hematuria bed rest is important, hemostatic treatment, and
further investigations sometimes repeated to establish diagnosis. Treatment generally
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has the following objectives: restoring urgent blood supply (through the use of
transfusions), anti-hypoxia (oxygen), hemostasis - surgical treatment which requires
adjustment of based therapeutic means to the location and causes of bleeding.
Clot evacuation through metal probe, after which there is ensured the efficient
bladder drainage on urethral-bladder double probe current for continuous washing
shall rest the bladder, thus stopping the heavy bleeding in the bladder.
Adenomectomy transvesical emergency purposes is the only effective method of
hemostasis in heavy bleeding with usually bulky prostate adenoma. Internal iliac
artery ligation is sometimes welcome in the massive hematuria bladder tumors or
from the lodge of prostate adenoma enucleated.
Nephrectomy is the last surgical method to use if hematuria is "essential"
serious, provided that the contralateral kidney exists and be functional.
All urological maneuvers necessary to achieve hemostasis should be
performed under the protection of antibiotics to prevent infection.
3. ACUTE SCROTUM
Represents the acute, painful swelling of the organs contained in the scrotum.
Onset is always brutal, but often pain radiation in the abdomen or lumbar region
sometimes makes diagnosis difficult, bringing up the possibility of appendicitis or
urinary stones.
3.1 ACUTE EPIDIDYMITIS is the most common cause of acute scrotum.
Highest incidence occurs at young people in full sexual activity and patients with
obstructive subvezical affections. At the young men most commonly we find bacteria
like Chlamydia trachomatis or Neisseria gonorrheae. At men over 40 most frequently
there are encountered pathogens from the family of Enterobacteriaceae and
Pseudomonas aeruginosa.
Diagnosis.
Clinical exam. Brutal onset, characteristic symptoms sometimes associated
with a urethral discharge, at a young man in full sexual activity, at a man carrier of a
urethral stricture or having suffered a surgery for prostate adenoma, orients the
diagnosis toward a diagnosis of acute epididymitis.
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Laboratory investigations evidence hyperleukocytosis in blood count. The
henoculture can be positive in frison, highlighting the mentioned germs, and the
urinary exam eviences the presence of a urinary infection, with the same germs.
I maging investigations - ecography evidences the characteristic signs of
epididimare infection, sometimes evidencing dispersed transonic areas
(microabcess), or large transonic areas (constituted abscess). Other times the whole
epididymis and testis are embedded in a large transonic cavity (reactive hydrocele).
Radiological investigations retrograde and mictional uretrocistography
retrograde and mictional, uroflowmetria or uretrocistoscopy can reveal a cause of
subvesical obstruction.
Treatment of acute epididymis consists of bed rest, pain relief by infiltration
with lidocaine 1% of the spermatic cord, nonspecific anti-inflammatory (Diclofenac,
Phenylbutazone, Indomethacin), antibiotics (Cefriaxon, Sulperazon IM or IV, then
may be given tetracycline or Doxyciline). It also may also be administered
quinolones with good chances of recovery due to the diffusion in the optimal acute
inflammatory process. Very important are local cold applications (ice pack) on the
scrotum priorly suspended and fixed in position.
The surgical treatment is indicated in the fistilized or constituted abscess
phase and consists of orchiectomy.
Prognosis. It is generally better if the diagnosis and the therapeutical
measures are instituted promptly, the healing can be without any sequlea. n the
abscessed forms there are cutaneous fistulas on the back of the scrotum.
3.2. SCROTUM ABSCESS
Is a bacterial inflammation, with a usual starting point from an epididymitis,
rarely can the inflammatory point coexist at a distance, where the epididymis or
testicle are seeded hematogen.
From the clinical point of view, the testicle and the epididymis are enlarged,
conglomerate, very painful to the slightest touch. The scrotal skin is red, relaxed, thin
and shiny. If it is not treated, it leads finally abscess on the back of the scrotum.
The treatment usually consists of orchitectomy, with excissing the skinon the
level of the absceessed area.

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3.3. TORSION OF TESTICLE
Is a great emergency, since in 2-6 hours from its start, necroses the germinal
tissue. More resistant to ischemia are the Leydig cells, responsible for the production
of the androgine hormone testosterone.
In the majority of cases, the testicle torsion is produced in the presence of
some congenital anomaly: cryptorchidims, or rete testis laxity.
Diagnosis. The torsion appears during the night waking up the child or
teenager by atrocious pain occuring spontaneously, at the level of a hemiscrotum.
Approximatively 10% of the patients can complain because of reduced intensity
pains, that can delay the positive diagnosis. The pain iradiates to the inguinal region
(on the spermatic cord track). At small children there are signalled even epigastric
pains, that can be associated with nausea and vomiting. But there are no signs of
peritoneal irritation.
On palapation of the scrotum there can be felt the torsioned area of the
spermatic cord as well as the epididymis is to be found on the side of the testicle,
normally it should be located on its posterior side. At the attempt to raise the organ,
there appears pain (Prehn sign). At the same manouvre in the epididymis there is an
acute tendency of diminishing the pain. The testicle is sensible even to a gentle,
superficial touch.
A Doppler ecography evidences the absence of spermatic artery pulsation
(fig. 16.2).
Treatment of testicle torsion. It is tried the detorsioning of the testicle
manually after local anesthesia with xilin 1%. The direction of detorsioning is from
right to left.
If the manouvre is not successful, there will be a surgical intervention. After
detorsioning both testicle will be fixed (bilateral orhidopexy).
If the detorsioning measures were not taken in time, there will be made an
orchectomy. In 24 hours the whole testicle will be necrosed. If the detorsioning starts
after this perio, there is no hope for saving the testicle.
4. DIFFUSE PERIURETHRAL PHLEGMON
The Fournier disease or genital organ gangrene described by Jean Alfred
Fournier in 1883 is characterized by a brutal start, the extremely quick progress of
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injuries in the absence of an evident cause. The necrosis starts at the level of genital
organs and is progressing along the fascia, has a reserved prognosis, being followed
by mortality up to 50%.
Diagnosis. The start is brutal, through pain at the level of the scrotum,
followed by swelling and increasing in volume. The scrotum very rapidly increases
its volume and it becomes red, tough, painful and with cianotic areas. In the same
time there is installed the general toxic sindrome, with alteration of general
condition, fever, chills, tachychardia, tachypnea, hipo-TA, hypogastric subcutaneous
crepitations at the level of thigh.
The infection is caused by aerobic and anerobic germs.
The quick apperance of vascular thrombosis due to these germs determines
eventually the gangrene and necrosis of the subcutaneous cellular tissue.
The initial injury is situated around the urethra, from where it difusses then to
the space between the superficial and the middle perineal aponeurosis. It propagates
towards the scrotum, penis, hipogastric region and the abdominal wall.
Treatment. In the case of periurethral diffuse phlegmon the treatment is a
surgical one of extreme emergency, under the protection of therapy with antibiotics,
serotherapy and hydroelectrolytical rebalancing. There will be made multiple
incisions into the infiltrated tissues, with large openings and efficient drainage of
these areas: abdominal wall, scrotum and perineum. The tissues are debrid and are
drained with draining tubes, there are introduced inhibited tampons with oxigene
water or cloramine.
Often, being about patient with a long past of uretral pathology urethral
stricture there is necessary a urinary derivation by minimal or classical cistostomy.

With all the correct and active reanimation for fluid, cardiovascular and
methabolical support and oxygentherapy, the mortality is very high. Castration is
generally not necessary, but cutaneous correction, after ther removal of all necrosated
tissue needs repeated plastical surgical interventions.
Good to know: any patient with an urogenital trauma, urethral strictures, or
who suffered surgical interventions in the area of the outer genital organs
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(apendectomy, herniorafii, etc.) is suspectable of developing a Fournier gangrene,
especially when he is diabetic.
To avoid: Temporization of such patients that have to be resuscitated and put
on the surgery table as soon as possible.
5. UROSEPSIS
The incidence of toxic-septiv shock is of 0,5-3% in the urology services. The
most frequently met germs are the negative Gram germs, germs of urinary infections:
Pseudomonas aeruginosa, Klebsiella, Enterobacter, b.Coli, b.Proteus, Seratia. More
rarely there are met the positive and anaerobic Gram germs. It is known that 50% of
the septical processes come from urological infections.
Among the favorizing factors there can be mentioned: inefficient urinary
drainage, alcoholism, diabetes, immunosuppression, liver failure, pulmonary disease,
etc.
Diagnosis.
Clinical examination. The start is usually brutal, with agitation, fever, chills.
At debilitated patients the noisy phenomena can be absent. The main sign is the net
and prolonged decrease in blood pressure. It is associated with tachychardia and
hyperventilation. Without going into details of pathophisiology, the endotoxines of
negative Gram germs activate a series of mechanical mediators of plachetary and
trombocitary origin that are responsible for the hemodynamic disorder occuring in
two phases. From the clinical point of view these are:
- heat shock: warm, normally coloured, dry teguments, normal AT, agitation,
tachypnea, tachycardia;
- cold shock: pallor, cyanosis, cold perspiration, marbled teguments, hipo-
AT,filiform pulse, disapnee, dizziness.
The diagnosis is based on the onset signs, low values of AT, pulse character,
respiratory disorders and decreased urine output (oliguria or oligo-anuria).
Laboratory examination. There can be evidenced a series of m odifications,
like a deviation to the left of the leucocitary formula, thrombocytophenia, metobolic
acidosis, hyperkalaemia, hypophosphatemia, positive uroculture.
Treatment. Schematically in the therapy of septic shock, it is important:
1. stabilizing vital functions;
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2. treatment with antibiotics;
3. local treatment, addressing the source of germs (septic point).
1. Under control of central venous pressure there will be administered
perfusions and transfusions.
Cardiotonical and vaso-active substance treatments (Dopamina) will be
administered only after the correction of hypovolemia and only under control of
central venous pressure. Dopamine in dosis of 1-3 cg/Kgc can be useful to maintain a
higher urinary debit and the prevention of IRA at patients with oliguria.
For coagulation disorders (disemined intravascular coagulation), under
control of bleeding and coagulation time there will be administered Heparin 10-
20000 u/day.
Orotracheal intubation will be necessary when there is installed the
pulmonary insuffiency, with the decreasing og blood oxigenation.
There will be administered hepatoprotectives, roborants, diuretics and
oxygentherapy.
2. the treatment with antibiotics will be energical and sustained. Usually there
will be administered 2 bactericidal antibiotics, with large spectrum, one of them has
to have spectrum for the negative Gram germs. Then, the treatment will be
administered according to the result of antibiogram or hemoculture. The dosage will
be adapted to the grade of hepato-renal failure. The most efficient antibiotics are:
cephalosporines, aminoglucozidele, beta-lactamines, etc.
3. The local treatment has as its aim the solving of the high stasis
(percutaneous nephrostomy) or low (minimal cistostomy). Evacuation and large
drainage of some purulent collections, abscesses, phlegmons, etc. These measures
have to be as prompt as possible, being among the first measures that have to be
taken in the treatment of septic shock. Later, after the amelioration of the general
condition there will be treated the favorizing factors, that determined the stasis and
the infection: prostate tumour, lithiasis or urethral strictures.
Prognosis
Approximatively 50% of the septic processes come from some urological
affections. The risk grows 2-3 times in the presence of some factors that diminish the
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resistance of the organism: diabetes, TBC, age, alcoholism, a seriees of medicines
(corticoids, immunosuppressors, citostatics).
Despite the modern therapy and the treatyment with antibiotics, the incidence
of mortality reaches 50% even nowadays.
Good to know the entrance gate of germs is most commonly the urinary
track. Uroculture and hemoculture usually show the presence of the same germ.
To avoid temporization of surgical solution for the source of the germs.
6. PARAPHIMOSIS
The impossibility of degloving of the gland because of a narrowed prepuce
slit makes it possible after a forced degloving the impossibility of collect of gland,
because of a tight preputial ring that goes beyond it, in the balanopreputial
separation. Compresion that is exercited in the balanopreputila bed determines
disorders in the returning circulation and the gland swells. Regloving is practically
impossible. Prolonged strangulation leads to the apperance of necrotic lesions of the
gland (fig. 16.3).
Not treated, paraphimosis may have severe evolutions, necrosis and general
infections with septic complications (phlegmons, cangrenes).
Diagnosis. Local symptoms are: pain, rarely fever, impossibility of glan
recoltare a glandului.
Treatment consists of bringing back to normal position of the prepuce. In an
initial phase this desideratum can be realized without surgical intervention. The gland
is compressed digitally all around and after its volume decreased, the prepuce is
pulled to normal position.
In case of older lesions (a few days), the reduction of paraphimosis is possible
only after the dorsal sectioning of the scleral preputial ring, followed by the
reduction of phimosis (re-gloving). The appearance of necrosis makes necessary the
excision of devitalized tissues and antibiotherapy. Great losses of substance will be
eventually treated thorugh different plastic interventions.
7. PRIAPISM
Is a painful erection, long-lasting, without sexual excitation, ejaculation and
orgasm. At the reerection there only participate the cavernous body not also the
spongy body. Phisiopathologically there are 2 mechanisms: a neuro-vegetative
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disorder and the mechanical obstruction of the venous system. The pain in priapism
can be explained by the tissue ischemia and growth of CO
2
pressure in the
cavernous body, which in short time (hours) leads to irreversible lesions, with the
installations of impotence.
Diagnosis
Clinical examination. In anamnesis there can be noticed the presence of
painful and long-lasting erection, that appears suddenly without libido and it is not
accompanied by ejaculation. Characteristic is the fact that in the erection the spongy
body and the gland do not participate. It is important to find the existence of other
diseases: leukemia, sickle cell disease, thrombocytopenia, polycuthemia, a series of
medicines the patient uses: antihypertensive, antideppresive, antipsychotic can also
be induced be alcohol or marijuana consumption.
A series of affections cand be mentioned from the anamnesis: injuries of the
spine, local inflamations, diabetes, multiple schlerosis, brain affections. Rarely there
can be also implied infectious diseases: mumps, limphogranulomatosis.
At inspections and palpation the cavernous body is tough, rigid, while the
spongy body and the gland are soft.
Laboratory examination. Hemoleucogram evidences the leukocytosis,
anemia, thrombocytopenia. Glicemy can be high in cases of diabetes, other times
there can be shown the high values of global renal functionality tests (urea and
creatinine).
I maging examination. Urography may evidence tumours of the urinary
apparatus. CT and RMN will identify tumours or thrombosis of the venes in the
small basin.
Treatment. Without treatment the erection disappears spontaneously in 2-3
weeks. The result is a bold, rigid cavernous body with no possibility of erection.
Major complications besides impotence are: fibrosis of cavernous body and penile
cangrene.
Treatment has to be isntituted on mergency and consists of painkillers
(morphine), sedatives, local cold applications (ice bags), local anesthesia of the penis
base. If these measures are not successful there will be injected intravenously 10
micrograms of adrenaline, under permanent control of AT.
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If after these measures no results are obtained, there will be used the method
of shunts. The first and easiest method, that can even be repeated, is the Ebbehoy
Winter shunt. It is a cavernous-spongy shunt, that is made with the prostate biopsy
needle Tru-cut. If this method is not efficient there will be used the surgical shunt
method: anastomosis between the saphenous vein and the cavernous body. If the
dorsal vene of the penis has an optimal caliber, it can also be used in order to make
the shunt.
Prognosis. It is distressing, because of the fibrosis, loss of erectile function
and appearance of erectile disfunction.
Good to know. Priapis has a great number of causes, from the idiopathic,
where one cannot find the onset cause, to extremely numerous other causes. Because
of this the diagnosis depends on the perspicacity and medical culture of the doctor.
To avoid delay of prompt treatment institution, in order to prevent impotence.
8. RENAL INFARCTION
Depending on the obstructed vessel renal artery we may talk about total
infarction, if a segmentary renal artery is obstructed we may talk about partial
infarction, the irrigated area by the segmentary artery suffering an aseptic necrosis.
The cause of renal infarction may be a thrombosis of the renal artery or an embolism.
There are also therapeutical renal infarctions, especially in case of renal tumors, as a
first step in trying to make a nephrectomy for a renal cancer that cannot be operated,
or in case of voluminous renal tumors in order to diminish the volume of the tumor.
Renal thrombosis can appear in case of generalized atherosclerosis,
periarthrytis, endarhrytis, scleroderm or anevrism of renal artery.
Diagnosis
Clinical examination. Small infarction can develop without any symptoms.
n case of great infractions the onset is brutal, with atrocious pains in the superior
abdomen or in the flank. There can be associated nausea and vomiting.
The urinary signs are absent in most of the cases and are not recognized only
in the presence of a bilateral lesion or in case the obstruction appears on a uniquely
functioning kidney, when anuria appears. The temperature is normal in the first 24
hours, afterwards the temperature grows reaching the values of 38,5 C 39 C. The
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artery tension is inconstant, high values can be related to painful syndromes.
Sometimes it can be associated with an ileus reflex.
Laboratory examination. Leukocytosis is a constant sign. There can be
noticed a growth of urinary lactico-dehydrogenase, characteristic and very constant
sign of renal infarction, especially when it associated with the growth of urinaru
alkaline phosphatase.
I maging examination. IVU mute urographic kidney, that has a normal
aspect at UPR. The renal contour is not regulated with numerous incisions that are
indirect signs of renal infarction. Computerized tomography evidences suggestive
images, but the diagnosis can be certainly stabilized at arteriography.
Treatment. In the septic renal infraction there is used the emergency
nephrectomy. When there are no septic necroses, in the first phase shock is treated,
antibiotherapy, anticoagulants and forcing of diuresis, major painkillers. If pain
persists and TA has high values there can be used the surgical methods.
Conservating operations thrombectomy, embolectomy are rarely successful,
after the deobstruction of the segmentary artery partial nephrectomy is done on the
necrosed area. In case of total renal infarction the nephrectomy is compulsory.
9. THROMBOSIS OF RENAL VEIN
Is a rare affection that propagates from the inferior vein and arcuate veins
towards the renal vein. It is unilateral but it can affect the veins on both sides when it
is very severe, with major vital risks. In the situation when the thrombosis develops
rapidly, there appears the hemorrhagic renal infraction and the arterial hypertension.
When the vein thrombosis is produced slowly, there appears a nephrotic syndrom.
The thrombosis of the renal vein can be favorized by a tumorous compression, can
appear during pregnancy or a venous stasis caused by cardiac insufficiency. Other
causes that can determine a thrombosis of renal vein are amyloidosis, generalized
melanoma, hyperparatiroidism or nephritic syndrome, due to massive treatment with
diuretics and steroids Diagnosis.
Clinical examination is a brutal onset. There appear acute signs n the
abdomen, kidneys have an increased volume, very sensitive, shock associated with
anuria. Other times the syndrome of arterial hypertension is associated with lumbar
pains sometimes very intense, kidneys with increased volume, hematuria and left
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varicoceles. These two forms are very rare and evokes and acutely installed
thrombosis.
Other times the clinical symptomatology is dominated by the nephrotic
syndrome, without suggesting a thrombosis occurring over a pre-existing
glomerulonephritis.
Laboratory examination: Hyperleukocytosis, cytolytic hepatitis syndrome
with increased SGOT and SGPT values. ESR values are increased. Urinalysis reveals
nephropathy.
Imaging examination. Ultrasound shows enlarged kidney with thickened
cortex and transonic without signs of pielo-pelvis stasis. The presence of thrombus in
the inferior vena cava and renal vein can be viewed by Doppler ultrasound.
Urography reveals a mute kidney. Arteriography has an extended nephrographic
time, eliminates the possibility of an arterial thrombus and highlights the existence of
a venous collateral circulation. Phlebography is very precise but also very risky, with
possible thrombus mobilization.
Treatment. When vein thrombosis is bilateral thrombolytic therapy is
random as well as surgical removal of thrombus, the patient is above any therapeutic
resources. The partial or progressive bilateral thrombosis anticoagulant therapy does
not provide certainty of resolution for the lesion and can destroy the substitute
circulation formed for this purpose.
Nephrectomy is imposed only when the renal suffering is total.
Anticoagulant treatment aims to prevent thrombus migration and facilitates
spontaneous recanalization. Heparin therapy by which anticoagulant treatment is
started is replaced by the therapy with K antivitamines.
10. URINARY RETENTION
According to its occurence and development, urinary retention can be acute
or cronical. According to its etiology urinary retention can be classified in 4 groups:
a. Obstructive retention.
Its cause is the obstruction of bladder neck and of the urethra. It is more
common in men, but can also occur in children and less often in women. Causes may
be benign prostatic hyperplasia, prostate cancer, acute prostatitis, bladder diseases
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(tumors, stones, bladder neck sclerosis, etc.) Urethral meatus stenosis, urethral
stricture, urethral valves, urethral foreign bodies, lithiasis, urethral tumors, etc.
b. Neurogenic cause retention.
Upper lesions of the spinal segments S2-4 cause reflex or spastic bladder, the
organ is no longer controlled by the central nervous system, urinary flow rate
decreases, increases the volume of bladder tailings. It appears in: spinal trauma,
tumors, multiple sclerosis.
Lower motor lesion interruption of reflex in ponytail. Bladder fullness
disappears; the muscles relax in the perineal region. The main cause is spinal trauma,
spinal tumors, multiple sclerosis, tabes, myelomeningocels, etc.
Leziunea direct a rdcinilor aferente sau eferente ale nervilor pelvieni. Alte
cauze pot fi: diabetul zaharat, herpes-zooster, intervenii chirurgicale care lezeaz
inervaia vezicii. Senzaia de miciune este abia perceptibil.
Direct injury or efferent roots for pelvic nerve. Other causes are diabetes, herpes-
zooster, surgeries violating innervations of bladder. The feeling of micturition is
barely perceptible.
c. Urine retention of pharmaceutical cause.
There are a number of drugs that can cause urinary retention:
sympathomimetics, antidepressives, antiarrhythmics, anticholinergics,
antipsychotics, antihypertensives, antihistamines, muscle relaxants, amphetamines,
dopamine, vincristine, morphine.
d. Psychogenic retention.
It is more common in young women and depressive reactions after trauma. It
is the rarest form, but sometimes difficult to diagnose.
Acute urinary retention is brutal, in patients without micturition disorders, or
disorders of small importance. Chronic retention of urine is the end of complete
bladder decompensation. It occurs slowly and is preceded by micturition disorders.
Retention of urine can occur at any age: the onset is sudden and dominated
the clinical picture of pain in hypogastrium of high intensity, in time the pain
becomes violent and the patient becomes very agitated and laments.
The diagnosis is easily established from a patient who has not urinated for
several hours, is in pain and feeling of micturition urgency that at the objective
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examination it is easily defined the bladder (hypogastric sensitivity, hypogastric
tumor, ovoid, remitting, well defined, very painful to palpation and dull to
percussion). After bladder catheterization or suprapubic puncture in case of
contraindication to catheterization (acute urethritis, periurthretis, acute basin trauma,
prostatic abscess, acute prostatitis) the patients is immediately relieved and
sometimes he can resume urinating.
There are examined the urethral meatus, penis, scrotum, perineum, vulva,
urethral discharge potential is observed. After emptying the bladder it allows
exploration DRE prostate, seminal vesicles, posterior bladder wall and membranous
urethra
Laboratory examination - urea and creatinine provide details about whether or
not echo subvesical high obstruction that led to retention of urine, urine culture is
important to know whether or not causally related urinary infection exists which led
to the installation of retention of urine.
Imaging examination are fundamental. Firstly ultrasound is the investigation
that allows the idetification of bladder and of the cause (adenoma, prostate cancer,
bladder tumor, etc.) and high echo of the subvezical obstacle. Urography specifies
renal function and can bring othe important elements for establishing the diagnosis.
Treatment. Urethral catheterization with a Tiemann catheter 14-16 Ch for
men, or metal catheter or a Nelaton probe for the women. After the toilet of male
glans or after vaginal lavage with a solution of potassium permanganate 1-2000,
insert the lubricated probe with gomenol oil 4% using sterile rubber gloves or
sterile forceps to maneuver the probe. Acute retention of urine in the bladder can be
emptied quickly, however, chronic retention of urine in the bladder emptying is slow,
in order to prevent bleeding ex vacuo.
The catheter is left in place if the introduction was difficult, urine is cloudy,
there is hematuria or nitrogen retention. Certainly to the pavilion of the probe there
will be attached a collector bag.
After the evacuation of the bladder there will be repeted the clinical
examination of the urinary and genital organs.
Bladder puncture is performed in order to empty the bladder at a patient by
who can not be performed catheterization for various reasons. The patient is in
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supine position, hypogastric region is disinfected. Local anesthesia is made on the
midline above the symphysis pubis, after which the needle is inserted pubic
symphysis, bladder area which is not covered by peritoneum at a patient who was not
previously operated.
Good to know: In acute urine retention the bladder can be rapidly emtied. In
cronical retention the emtying is made slowly to prevent bleeding ex vacuo.
To avoid: unexpected catheterization. At any obstacle there will be checked if
it is made correctly, otherwise it should be performed by a specialist, or by the use of
suprapubic puncture of the bladder to empty it for the moment.
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LIST OF ABBREVIATION
AFP - alpha-fetoprotein
ARF - acute kidney failure
AUA - American Association of Urology
BPH - benign prostatic hyperplasia
bK - Koch bacilus
CAB - comined androgen blockade
CEA - carcinoembrionar antigen
CRF - chronic renal failure
CT - computerized tomography
DES - dietilstilbestrol

DHT - dihidrotestosteron
ESWL - extracorporeal shock wavw lithotripsy
GH - growth hormone
-HGC - -human chorion gonadotrpine
HTN - arterial hypertensione
IVU - intravenous urogram
KUB x ray - kidney, ureter, bladder x-ray
MRI - magnetic resonance imaging







Abbreviation
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