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Urology course The Lithiasis of the Urinary System

1.The Lithiasis of the Urinary SystemThe 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:

1. Crystallization theory: a solution is over-saturated when it contains a biggerquantity 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

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conjunction with the decrease of the urinary volume (the 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.

2. The matix theory. The crystals lay on an organic matrix made up of serumand 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.

3. The theory of the precipitation nucleus. According to this theory, theformation 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.

4. 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.

I. 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

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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.

Overdose of D vitamin brings about an increased intestinal absorption and anenhanced resorption of the calcium in the bones. Hypercalcemia leads to

hypercalciuria in the end.

Prolonged immobilization (after trauma, fractures, stroke etc) leads todemineralization of bones, consecutive hypercalcemia and hypercalciuria.

Absorbative and renal idyopathic hypercalciuriaAbsorbative 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.

II. 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 theileitis 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 theexcessive 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.

III. DISORDERS OF THE URIC ACID METABOLISMNormal 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,

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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 anexcessive amount of purines (over-eating), or the consequence of an increased

consumption of alcohol. Sometimes hyperuricazuria is brought about by a

massive distruction of the bodys proteines (consumptive diseases tumors, after

treatments 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).

IV. 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 contributeto 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 bottommembrane of the collecting tubes and on the surface of the renal papilla

(Randalls theory). Thus, the Randal plates are formed; they come loose and

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fall in the pelvis cavity where, by contact with urinary constituents, the

calculus grows bigger.

Carrs theory. The settling of the lithogenic material takes place in the renallymphatics 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 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 pylo-pelvis dilatation (hydro-nephrosis), which compresses the parenchyma and it makes it thinner leading to

attrofiation and to the loss of fuctionality of the kidney; Infection of the urinary channel in the long run it can be responsible for pylo-

nephritis (accute or chronic), pylo-nephrites or pylo-nephroses (final stage of

renal suppurations).

LITHIASIS CRYSTALOGRAPHIC

NAME

HARDNESS

I. CALCIUM

Monohydrate Ca oxalate Whewellit +++++

Dihydrate Ca oxalate Wheddellit +/++

Ca phosphate Hydroxiapatite ++

Apatite carbonate Apatite carbonate +++

Dihydrate Ca carbonate Brushite +++

II. Non-calcium

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Uric acid Uric acid ++++

Phosphate-ammonia-

magnezium

Struvite +

Cystine Cystine +++

Tabel II. Crystalographic classification of the urinary system calculi.

SYMPTOMATOLOGY

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 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 abdominalprojection 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, usuallycaused 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

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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.

Kidney faliure:

Accute. It is active in the form of anuria, and it usually appears on a sole functingkidney (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 oldlithiasis history, with bilateral manifestations, where the combination obstruction-

infection has caused extended parenchymal distructions.DIAGNOSIS

History

The patients living and working conditions have to be known. Also it is

important that the eating habits of the patient be known: meat characterized diet,

hypercalcium diet etc.

The family history is also important for the diagnosis: congenital anomalies,

cystine, uric lithiasis etc.

Thus, information about a series of personal diseases can be obtained:

tuberculosis, bladder-ureteral reflux or urination disorders caused by obstructions at the

level of the inferior urinary system.

Objective examination is an important moment with a view to establishing the

diagnosis of urinary lithiasis: the abdomen will be carefully examined in order to

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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 urinarylithiasis. 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.

The urea and the creatinineblood level provide information on the global renalfunction of a patient with bilateral lithiasis or with lithiasis at the sole kidney.

Imagistic investigations

Ultrasound. It is an important investigation with patients having renalinsufficiency, 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. Thecalculi 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 orconfirms 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.

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Retrograde ureteropylography. It is seldom used, namely when IVU is notconclusive, 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 24hrs-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 itscomposition the chemical analysis and, even more accurately,

radiocrystallography and X-rayed radiomicrography of the calculus, or the

spectral analysis of the calculus.

ANATOMICAL-CLINICAL FORMS

Ureteric lithiasis. It manifests usually through reno-ureteric colics, very oftenassociated 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-

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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 obstructiveunder 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.

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 Primitiveurethral calculi appear on an obstructive malformation of the inferior

urinary system which brings about stasis and urinary infection and are usuallyvery rare.

Secondary urethral calculi are more frequent, they form inside the kidneys or inthe 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.

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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 thepainful 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.

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 byvarious 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

1. 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 renalcolic, the patient does not have urinary infection history and does not have fever;

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- calculus anuria accompanied by infection is very severe, the patient hasfever, a general bad condition, the major complication being the installation of the toxic-

septic shock;

2. Infectious complications. The infection can be located in the channels or itcan 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.

3. Cronic kidney faliure.. It is the result of the parenchymal participation inthe 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 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.

A. EMERGENCY TREATMENT it refers to the complications of thelithiasis.

Mechanical complications require various measures, depending on thenature 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%.

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In case of heavy vomiting, 0,25-0,50 mg of Atropin shall be given i.v., which

apart from the antispasmodic effects, it also diminishes the digestive secretions.

Calculus anuria requires an emergency treatment. Irrespetive whether it is

infectious or not, the best solution is high urinary derivation nephrostomia. Whwn this

intervention cannot be made, a ureteral stent will be set up above the obstacle. If the

obstacle is surpassed, the surgical intervention (PCLN, ureteroscopy, ureterolithotomy or

pyelolithotomy) will be made in several days; alternatively, it will have to made

immediately.

Infectious complicationsAccute 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.

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 CKF it is treated by dialysis and possibly transplant.B. MEDICAL TREATMENTGeneral measures

Diuresis treatment. It is supposed to produce a diluted urine with lowsaline 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 uselessrestrictions, but also without abuses.

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Sedentary lifestyle is to be avoided Removal of the obstacle in the urinary channelSpecial 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, ifthere 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.

Uric lithiasis benefits of diuresis treatment with alkaline waters. The diet will be alow 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 carbohydratediet. 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 withgrowing 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.

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Xanthine lithiasis in principle, it requires the same measures as the cystinelithiasis. The administration of alkalizing substances and of Allopurinol leads to the

elimination of the hypoxanthine, which is more soluble than the xanthine.

C. SURGICAL TREATMENT

In general, with urinary lithiasis, surgical treatment is indicated for all stones

which cannot be eliminated spontaneously, be it open or endoscopic surgery. Today, the

majority of urinary calculi is solved by ESWL. These methods are supposed to be used

with calculi on the superior urinary channels associated with urinary infections that

cannot be treated otherwise, which cause progressive renal parencymal pain, the

obstruction of the main urinary channel and a persistent pain. In most cases, the surgical

treatment has to be applied only after the patients entire metabolic assessment. In

emergency cases, such as a complete obstruction of the main urinary channel, urosepsis,

it is first manadatory to make a urinary deviation by setting up a urethral stent or by

making a percutaneous nephrostomia. The lithiasis is solved afterwards, after the

treatment of the septic state.

2. OPEN SURGICAL INTERVENTIONS

The nephrectomy and the partial nephrectomy. The nephrectomy is a radicalintervention 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.

Fig. 5.1. Pylolithotomy

Pylolithotomy is an intervention meantto remove the calculus from the renal pelvis

(fig. 5.1), 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).

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Pylonephrolithotomy is a technique used to extract a pelvian calculus which hassome prolongations usually in the inferior pelvis (fig. 5.2. 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)

Fig. 5.2. A and B. Pylonephrolithotomy

Anatrophic nephrolithotomy (Smith and Boyce 1967) is recommended in cases ofcoral-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. 5.3.) It isused as a sole procedure or in combination with one of the

above-mentioned procedures. It is a technique usually

used to extract pelvian calculi associated with volumunous

calculi in the renal pelvis. Radial incisions are made on the

posterior side of the convex margin of the kidney. After the

calculus has been removed multiple nephrographies are

being done.Fig. 5.3. Radial polinephrotomy

Bench surgery and self-transplantation is a treatment method with patientshaving recurrent lithiasis, with many prior interventions and with renal pelvis and

urethral stenosis after the surgical interventions.

Ureterolithotomy is the extraction of a calculus from the ureter (lumbar, illiac orpelvic) through a classical surgery. After the discovery and the preparation of the ureter,

the longitudinal ureterotomy is being made (A), followed by the ureterolithotomy as such

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Fig. 5.4. Ureterolithotomy

Fig. 5.5. PCNL

(B), the operation by which the calculus is extracted from the ureter through the palgue

made by means of the ureterotomy. The intervention is finished by the ureteroraphy of

the ureteral plague (C) (fig. 5.4.)

In the age of the ESWL and of PCLN these interventions have only a historical

interest. However, ureterolithotomy remains an intervention only when ESWL, PCLN,

URSA or URSR fail from one reason or other, or they are couter-indicated.

2. PERCUTANEOUS NEPHROLITHOTOMY (PCNL)

It has opened the era of

the endourology of the superior

urinary system. Practically, any

stones, irrespective of its

location, size, hardness, volume

or number, can be solved

endoscopically. The

nephroscope can be introduced

through the nephrostomy path,

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allowing the extraction of the calculi from te renal plevis, pelvis or JPU (fig. 5.5.). The

ultrasound allows the fragmentation of the voluminous or coral-shaped renal pelvic

calculi and their extraction.

The advantages of this method consist in the fact that it is possible to remove a

renal calculus through a 1 cm plague, the convalescence is short and the full recovery of

the patient is made in a short while.

The complications and the PCLN morbidity are much reduced as compared to

open surgery. However, severe complications with serious consequences leading to

hemostatic nephrectomy or even death in rare cases are not excluded.

4. URETEROSCOPYIt is an endoscopic diagnosis and treatment procedure for

various affections of the ureter, among which lithiasis is the

most frequent. Pelvic ureter calculus is treated by means of

ureteroscopy with ultrasonic, electrohydraulic, pneumatic or

laser fragmentation, followed by the extraction of the fragments

(fig. 5.6). Other ureter diseases which can be solved through

retrograde ureteroscopy are the benign ureteral stenoses,

congenital hydronephroses through a UPJ syndrome. In well

selected cases, with a correct operational indication, ureteral or

peilo-pelvic tumours can be removed.

Antegrade ureteroscopy is an endocopic method to

solve calculi in the proximal (lumbar) ureter through the transrenal introduction (through

the percutaneous nephrostomy channel) of the ureteroscope in the ureter; contrary to the

retrograde ureteroscopy where the ureteroscope is being introduced in the opposite

direction of the urine flow, transurethrally in the bladder and from there in the ureter

through the ureteral orifice.

Besides lithiasis, the antegrade ureteroscopy is also used to solve benign stenoses

of the proximal ureter, external fragments (broken stents in the ureter) can be extracted,

and also to solve tumours of the proximal ureter in well selected cases, with an

operational clear indication.

4. LAPAROSCOPY

Fig. 5.6. Ureteroscopy

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The laparoscopic transperitoneum approach, but especially the retroperitoneum

one, can be utilized for pylo-, ureteral and even renal calculi. It is an alternative to open

surgery, for cases when the endoscopic intervention does not solve the lithiasis.

5. BLADDER LITHOTRIPSYThe treatment oft he bladder calculus is endoscopic (lithotripsy) in the first place.

The primary fragmentation of the calculus can be made mechanically (fig. 5.7),

ultrasonically, pneumatically, electrohydraulically or by laser, followed by the extraction

of the fragments through the pod of the Punch lithotripsy (mechanical lithotripsy), after

their processing.

In the case of ultrasonic, electrohydraulic, pneumatic lithotripsy, these forms of

energy produce the primary desintegration of the calculus which afterwards is being

processed mechanically by the Punch lithotripsy into fragments that evacuate through the

pod of the lithotripsy along with the stream of the irrigation liquid, or, in the case of

bigger fragments, they are extracted with the working element of the lithotripsy.

The surgical treatment (cystolithotomy) is used only in the case of voluminous,

multiple calculi, which cannot be solved endoscopically, or in the case of associations

with big prostate adenoma. The intervention consists of cystolithotomy (the extraction of

the calculus from the bladder) and simultaneous suprapubic adenomectomy. When the

prostate adenoma is small, and the open intervention (adenomatomy) is not indicated, the

transurethral resection of the adenoma will be made (TUR P).

Fig. 5.7. Mecanic bladder lithotripsy (Punch).

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6. EXTRACORPORAL SHOCK WAVE LITHOTRIPSY (ESWL)It solves the urinary lithiasis without incision. The shock waves produced by the

electrod are focused and directed towards the calculus through a digitalized system.

The principle of the extracorporal lithotripsy consists of the desintegration of the

urinary calculi under the effect of the shock waves generated outside the body and

focused towards the calculus. The penetration of the tissues by the shock waves cause

minimum cellular damage. The calculi are desintegrated in small fragments which can be

eliminated spontaneously. The location of the calculus can be set by ecography or

radiology (fluoroscopy). The localization allows the treatment of the calculi in the

superior urinary system, irrespective of their location, if they have dimensions up to 1,5

cm in diameter.

7. THE TREATMENT OF THE URETHRAL LITHIASISIt is a surgical intervention and it consists of the extraction of the calculus or of

the calculi, through external urethrotomy and the surgical correction of the urethral

anomaly (urethral stricture). In some cases (small calculi), the calculus can move into the

bladder, where it can be treated by mechanical lithotripsy (Punch).

Except for ESWL, all above-mentioned interventions are made on a general

anaesthesia with orotracheal intubation or anaesthesia: rachidian or epidural.

CONCLUSIONS

In 80% of the cases, the lithiasis of the superior urinary system has metabolic

causes. The ablation of a renal or ureter calculus represents just an episode of the

treatment. After this, the treatment needs to be continued, more exactly prophilaxis has to

be done.

This episode in the treatment of the urinary lithiasis is done in special centers in

other countries, where, along with the chemical analysis of the calculus, which leads to

better information about its composition, all metabolical blood and urine explorations are

being made to see the metabolic status of the patient.

Based on these investigations, and after a correct analysis of the results, plus the

removal of the risk factors, the prevention of the urinary lithiasis starts to be undertaken.

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The treatment of the urinary system lithiasis consists of several therapeutic

measures (diuresis, eating habits etc) and a metaprophilaxis directly linked to the nature

of the calculus, of the metabolic disorders and of the risk factors.

The introduction of the endoscopic surgery (PCLN, ureteroscopy), laparoscopy

and ESWL in the treatment of the urinary system lithiasis meant a real revolution. The

ablation of the lithiasis of the superior urinary system can be solved without a classical

surgical intervention in more than 90% of the cases. The treatment of the lithiasis cannot

and must not be confined to this side of the complex treatment of this disease.

In the future, it is possible that in our country too the patient should be studied

also from a metabolic point of view (after the removal of the calculus, be it

endoscopically, or through ESWL, as a sole therapy, or through an associated therapy

endoscopic surgery + ESWL), in order to pevent recurrent situations by association of

some special targeted measures, depending on the characteristics of the lithiasis.

05. lithiasis

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