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

=== Urology course – Daniel Porav-Hodade, Mihail Radu Boja =========== 1

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

– Daniel Porav-Hodade, Mihail Radu Boja =========== bbimage.ro - print.design.media.reclame.stampile -

bbimage.ro - print.design.media.reclame.stampile - 0265-268.023

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

UNIVERSITATEA DE MEDICINĂ ŞI FARMACIE TÂRGU-MUREŞ

CLINICA DE UROLOGIE

AUTORI

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

UROLOGY COURSE

Editura University Press - Tîrgu Mureş – 2012

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

Descrierea CIP a Bibliotecii Naţionale a României:

Urology Course/ Porav-Hodade Daniel, Boja Radu - Târgu Mureş :

University Press Tg Mures, 2012 270, 21x30cm, 250 exemplare ISBN 978-973-169-187-9 Porav-Hodade Daniel

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: University Press – Tg Mures, 2012 270, 21x30cm, 250 exemplare ISBN 978-973-169-187-9 Porav-Hodade Daniel 4

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

CONTENTS
CONTENTS

1. Congenital anomalies of urogenital tract

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2. Urogenital apparatus trauma

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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

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1. Congenital anomalies of urogenital tract \\\\\
1. Congenital anomalies of urogenital tract
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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

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

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

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).

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

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

Fig. 1.3. Left double kidney with complete ureteral duplication.

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.

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2. Renal hypoplasia represents a renal

Fig. 1.4. Left renal hypoplasia

Fig. 1.4. Left renal hypoplasia

dysplasia characterized by the incomplete development but with normal development of the ureter (fig 1.4). Kidney’s 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 cyst’s 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 90º, 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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=== Urology course Daniel Porav-Hodade, Mihail Radu Boja ===========

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 patient’s 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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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 patient’s 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;

Fig. 1.5. Horseshoe kidney

Fig. 1.5. Horseshoe kidney

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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4. Location anomalies. The kidneys

Fig 1.6. Various forms of direct renal ectopia. High (mediastinum) and lower: inferior lumb, iliac,

Fig 1.6. Various forms of direct renal ectopia. High (mediastinum) and lower:

inferior lumb, iliac, pelvic

don’t 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 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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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.

Fig. 1.7. Retrocava ureter.

Fig. 1.7. Retrocava ureter.

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

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 anomaly’s 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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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.

Fig. 1.8. Migration anomalies of the testis. 1 - lumbar cryptorchidism, 2 – iliac cryptorchidism,

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

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2. Urogenital apparatus trauma
2. Urogenital apparatus trauma

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

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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

Fig. 2.1. Different types of renal contusion. A - partial sissure; B - kidney explosion,

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.

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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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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

hematoma), or perirenal

Fig. 2.2. IVU – renal trauma

Fig. 2.2. IVU renal trauma

(interstitial

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(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

Fig. 2.3. CT – right renal trauma

Fig. 2.3. CT right renal trauma

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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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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.

Fig. 2.4. Median antero-posterior section, bladder and urethra male. 1 - abdominal muscles, 2 -

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.

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

diagnostic or therapeutic endoscopic maneuvers. PATHOLOGY Closed bladder trauma can cause tears, contusions and perforations.

Perforations occur after

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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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.

Fig. 2.5. Subperitoneal rupture of the bladder. a – Filling cystography extraperitoneal extravasated contrast agent;

Fig. 2.5. Subperitoneal rupture of the bladder. a Filling cystography extraperitoneal extravasated contrast agent; b - scheme.

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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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;

Fig. 2.6. Intraporitoneală rupture of the bladder. A - IVU with intraperitoneal extravasated contrast agent;

Fig. 2.6. Intraporitoneală rupture of the bladder. A - IVU with intraperitoneal extravasated contrast agent; b - scheme.

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 cliché 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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IV. URETHRA TRAUMA Their incidence is higher in men. After their location they classify in:

posterior urethral injuries,

anterior urethral injuries.

2. POSTERIOR URETHRAL INJURIES

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.

Fig. 2.7. Urethra rupture above urogenital diaphragm. a - scheme urinoma and hematoma subperitoneal extent

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.

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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 isn’t 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. ANTERIOR URETHRAL INJURIES 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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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

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

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

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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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3. Non-specific infections of the genitourinary system
3. Non-specific infections of the
genitourinary system

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

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UTIs is incomparably lower due to the length of the urethra and to the antibacterial properties of the prostate’s 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 creatinine’s 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 bacteria’s 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 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 β-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 β-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 patient’s 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 treatment’s 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 infection’s 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 latter’s 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 Gerota’s 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 patient’s 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 phlegmon’s 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 kidney’s 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 latter’s 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 kidney’s 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 patient’s 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 bladder’s 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 urination’s 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. INTERPRETATION OF FINDINGS 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 patient’s 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 fireskin’s 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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4. Specific urogenital infections (urogenital tuberculosis- GUTB)
4. Specific urogenital infections (urogenital
tuberculosis- GUTB)

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.

The frequency of tuberculosis (TB) is quite high

with the starting point of a lung or extra pulmonary outbreak. The frequency of tuberculosis (TB)

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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 Pott’s disease.

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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

isolated or combined

lesions:

dilation, ulceration

Fig. 4.1. Renal tuberculosis - different aspects to urography . a – tbs stenosis at

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

three

types

of

stenosis,

and

caverns

(fig.

4.1.).

Stenosis

 

consists

in

the

narrowing

of

the

to

healing

by

tubes

or

calyx or renal pelvis,

due

sclerosis. The

appear thinned,

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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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.

Fig 4.2. Ureter TB

Fig 4.2. Ureter TB

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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

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):

treatment.

Tuberculostatics

I

Tuberculostatics II

Tuberculostatics III

(major)

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)

acid (PAS)

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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4. Lithiasis of the urinary tract
4. Lithiasis of the urinary tract

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

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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 body’s 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 (Randall’s 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.

Carr’s 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

HARDNESS

NAME

I. CALCIUM Monohydrate Ca oxalate Dihydrate Ca oxalate Ca phosphate Apatite carbonate Dihydrate Ca carbonate II. Non-calcium Uric acid

Whewellit Wheddellit Hydroxiapatite Apatite carbonate Brushite

+++++

+/++

++

+++

+++

Uric acid

++++

Phosphate-ammonia-

Struvite

+

magnezium

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 patient’s 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

In 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.

In 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; Infectious 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.

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

Cronic kidney faliure

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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; alternativel y, 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 faliureit 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 patient’s 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