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• UROLITHIASIS

Definition: Urinary lithiasis


- presence in the renal parenchyma or urinary
tract of concretion (calculi) formed from
crystalline components, (embedded in a protein
matrix).
Incidence:
Urinary lithiasis ranks third in urological diseases structure,
which makes up from 10% to 40 %, being inferior only to urinary
disease and prostate pathology, making up 59,6 % of total renal
pathologies. Nephrolithiasis is an estimated frequency between 1,0
% and 4,0 % of the general population, and it is very rare among
young people, and mainly affects people of productive age, with a
frequency of 70 % in patients between 4 and 6 decades of life, of
which up to 11% of patients treated become disabled. The
incidence of urinary lithiasis is three times higher in men than in
women, and the probability that a man is likely to develop a
lithiasis disease by age 70 is from 1 to 8.
Etiopathogenesis
Of the many etiopathogenetic theoriesEtiopathogenesis
(some even
contradictory) that try to explain the lithogenesis are the
following:
1. Crystallization theory (oversaturated urine) – according to
this theory, the concretion arises in an oversaturated urine,
passing through 4 successive phases.
2. Matrix theory – according to this theory, the crystals are
deposited on an organic matrix composed of serum and urine
protein (eg. albumin, α1 – and α2 – globulin, gamma globulins,
microprotein, glycosaminoglycans etc.)
3. Theory of precipitation nucleus – calculi formation is
initiated by the presence of a foreign body or a crystal in the
oversaturated urine.
Etiopathogenesis
4. Urinary crystallization inhibitors theory – absence or low concentration of
these substances (citrate, magnesium, zinc, pyrophosphate, phosphorus citrate,
some mucoprotein, ribonucleic acid, glycosaminoglycan etc.) allow
crystallization and contribute to formation of calculi.
5. Randall’s theory – according to this theory, the lythogen is deposited on the
basal membrane of tubular collectors and on the surface of renal papilla,
forming “Randall plates”, which through further appositions contribute to the
appearance of urinary calculi.
6. Carr’s theory – lithiasis precipitate deposit occurs within the renal lymphatics,
followed by breaking of the membrane that separates them from the collecting
tubules and their subsequent penetration in urinary tract.
Etiopathogenesis
Urinary lithiasis can be associated with a wide etiological
range:
•Renal tubular syndromes
Renal tubular acidosis
Cystinuria
•Hypercalcemia
Primary hyperparathyroidism
Sarcoidosis
Prolonged immobilization
Hypervitaminosis D
Neoplastic diseases
Cushing syndrome
Hyperthyroidism
Etiopathogenesis
• Uric acid lithiasis
Idiopathic
Gout
Myeloproliferative syndromes
Chemotherapy
Causes reducing urinary flow
• Enzymatic diseases
Primary hyperoxaluria
Xanthinuria
2,8 dihidroxiadeninuria
Etiopathogenesis
• Secondary urinary lithiasis
Enteric hyperoxaluria
Urinary infections
Urinary tract obstruction
Sponge kidney
Drugs
Urinary derivation
– Idiopathic calcium lithiasis
Hypercalciuria
Normacalciuria
Urinary lithiasis classification
Depending on cause:
Body lithiasis – the metabolic disturbances that
favors the lithogenesis have the essential role.
Organ lithiasis – due to local factors causing
obstruction-stasis-infection.
Mixed lithiasis – in its genesis occurs both
dysmetabolic and obstructive factors.
Urinary lithiasis classification
Depending on chemical composition:
Inorganic lithiasis – contains calcium, oxalate,
phosphate carbonate etc.
Organic lithiasis – uric, cystine, xanthine
Mixed lithiasis
According to radiological criteria:
Radiopaque calculi
Radiolucent calculi
Urinary lithiasis classification

Depending on urinary pH contributing to lythogenesis:


 “Acid” lithiasis – represented by uric lithiasis, cystine and
xanthine
 “Alkaline” lithiasis– pH is increased due to infections
with urease-positive bacteria (eg. Proteus, Klebsiella,
Pseudomonas etc.), which favor development of phosphate-
ammonia-magnesium calculi (struvite) and carbonate.
 Lithiasis with “indifferent” pH– does not present a
typical urinary pH, such as oxalic lithiasis.
Urinary lithiasis classification
According to macroscopic form:

Granular
Oval
Acicular
Radial
Muriform
Coraliform
Urinary lithiasis classification
Coraliform lithiasis classification (Proca E, 1984):
C = morphological type of calculus
C1 = coraliform calculus without calyceal parts
C2 = coraliform calculus with calyceal parts
R = renal parenchyma state
R1 = thin parenchyma
R2 = normal parenchyma
R3 = “juicy”, edematous, turgescent kidney
B = pelvis appearance
B1 = large pelvis „complesant”
B2 = small pelvis (intrasinus)
B3 = „scar” pelvis (iterative surgery)
Urinary lithiasis classification
Topographical:
Parenchymal lithiasis
Calyceal lithiasis
Pyelocaliceal lithiasis
Ureteral lithiasis
Bladder lithiasis
Prostate lithiasis
Urethral lithiasis
Urinary lithiasis classification
Depending on the number and distribution of calculi:
Single
Multiple, which, in their turn, can be located
•Unilateral
•Bilateral
Depending on the presence or absence of relapses:
Non-relapsing
Relapsing
Multiple relapsing (malignant)
According to the criterion of complications:
Uncomplicated lithiasis
Complicated lithiasis (association lithiasis-urinary infection-
hypertension-renal failure)
Urinary lithiasis classification
Depending on evolution, it can be divided in 4 groups:

Surgically active lithiasis – characterized by violent spasms, refractories to


treatment, severe obstruction, urinary infections. These complications require
surgery.
Metabolically active lithiasis – includes cases where, there was formed a new
calculus in the last year, a known calculus increased in size or eliminated calculus in
the last year.
Metabolically and surgically inactive lithiasis – includes patients who, after
the initial treatment of lithiasis, will remain stable, without relapses or clinical
symptoms at least 3 years.
Undetermined lithiasis – includes cases with clinical manifestations of
uncertain lithiasis or which period of assessment is less than 1 year.
Clinical diagnosis of urinary lithiasis:
1. Pain – can have variable intensity, from dull,
intermittent, bearable pain, up to paroxysmal,
lancinante pain, due to complete and sudden
obstruction, with distension and hyperpression in
urinary tract. Nephralgia is often caused by movement
and stops at rest. It is located in lumbar region and
radiates to iliac fossa, groin and genital region.
Clinical diagnosis of urinary lithiasis
In the painful syndrome, a special aspect is the renal colic (nephritic).
It appears as unilateral lumbar pain, very intense, with paroxysmal
emphasis and characteristic radiation (groin and to external genitalia),
the duration ranging from several hours to several days. The signs
accompanying it are very suggestive: pain intensity results in extreme
agitation, the patient is anxious, sweaty, seeks for an antalgic position
he cannot find. Nephritic colic is sometimes atypical, the pain being
located in iliac fossa, hypochondrium or throughout the abdomen,
with digestive signs that can dominate the clinical picture.
The differential diagnosis is performed according to pains in: shingles;
intercostal neuralgia; lumbago; cholecystitis, appendicitis (right side);
duodenal diseases; ileocolic diseases; salpingeal diseases (in women).
Clinical diagnosis of urinary lithiasis
2. Hematuria – is determined by urothelial
damage by contact with calculus and is caused
by motion, appearing after pain. Reverse
sequence (hematuria followed by pain) guides
the diagnosis to another source of bleeding,
probably tumor one!!!
Clinical diagnosis of urinary lithiasis
3. Infection – occurs, clinically, in several ways
 Urinary infection of attendance – cloudy, pyuric
urine, with positive urine culture, but no other signs
or symptoms associated.
 Urinary infection of “parenchymal” type –
acute pyelonephritis or lithiasic pyonephrosis with
perinephric suppurative reaction.
Urinary infection can evolve through general
manifestations of bacteremia type or even
endotoxic shock.
Clinical diagnosis of urinary lithiasis

4. Nephromegaly – consecutive to
hydronephrosis or lithiasic
ureterohydronephrosis, can be unilateral or
bilateral. Usually, it also associates other signs or
symptoms such as pain, pyuria, signs of cute
pyelonephritis or even signs of renal failure.
Clinical diagnosis of urinary lithiasis
5. Renal failure:
 Acute – is manifested as anuria, when lithiasis obstruction
occurs on one kidney congenital, surgical or functional. Less
often because of bilateral obstruction, by calculi.
 Chronic – occurs slowly, usually in patients with old history
of lithiasis, with bilateral manifestations, which the combination
obstruction+urinary infection caused extensive nephron
destructions, the functional deficit being compensated primarily
by polyuria, and then to establish the complex clinical picture
of uremia.
Clinical forms of urinary lithiasis:
Subclinical form – characterizes small calculi, fixed or the coraliform ones
and develop asymptomatically, the diagnosis being established, during a
radiological or ultrasound exploration for another disease.
Painful form – the dominant symptom is the pain that varies from
nephralgia to renal colic.
Hematuria form – hematuria can be solitary, raising problems of differential
diagnosis with tumor pathology.
Nephromegaly form – caused by stasis and hypertension superjacent to
calculus.
Febrile form – is determined by overlap of infection and requires
differential diagnosis between inobstructive acute pyelonephritis and lithiasis
one.
Hypertensive form – is characterized by presence of renal hypertension.
Digestive form – is characterized through digestive phenomena prevalent
reflexes and consist of abdominal and lumbar pains, nausea, vomiting,
flatulence.
Form with chronic renal failure
Laboratory diagnosis of renal lithiasis
Laboratory examinations – in order to specify the bioumoral status of the patient,
require, in addition to usual tests (complete blood count, urea and serum
creatinine, glycemia, liver and coagulation tests) and monitoring of diuresis, to
determine the urinary density and pH, urinalysis, leukocytes and erythrocytes
count in ruine (Addis, Neciporenko, Hamburger and Stansfeld Webb tests).
Specific laboratory examinations consist in:
 Serum dosing of: calcemia; phosphatemia; uric acid; bicarbonates.
 Urinary dosing of: calciuria; phosphaturia; uricosuria; cystinuria;
creatinuria; urea; oxaluria; magnesiuria; citraturia.
 Urinalysis: pH; urinary density; presence of erythrocytes, leukocytes,
crystals in urine.
 Urine culture with antibiogram.
Diagnosis of renal lithiasis
Imaging is represented by:
 Ultrasound
 Simple reno-bladder X-ray and intravenous urography
 Computed tomography and magnetic resonance imaging
 Retrograde or anterograde ureteropyelography
 Angiography
 Renal scintigram with isotopic nephrogram
Imaging
Ultrasound – is a noninvasive method, that can
allow revealing the calculus, and its echo on the
pyelocaliceal system and kidney (by assessing the
degree of hydronephrosis and renal parenchymal
index). Doppler ultrasound may reveal increased
resistivity index in obstructed kidney, as well as
asymmetry or absence of uretero-bladder jets.
Imaging
Simple reno-bladder X-ray (SRBR) and intravenous
urography (IVU) – SRBR is the first radiological exploration
within the initial investigation protocol. It can reveal the
presence of radiopaque images of various shapes and sizes,
located on the projection area of the kidney and ureter track.
IVU can reveal both the radiopaque calculi and the radiolucent
ones (as defective image surrounded all around by contrast
agent).
It specifies the location of lithiasis, its size, effect on urinary
superjacent tracts, the state of renal parenchyma and renal
function.
Imaging
Computed tomography (CT) and magnetic resonance imaging
(MRI) – CT allows a good retroperitoneal exploration, provides data on
“blind”, retroperitoneal areas. CT highlights the non-functional kidney at
IVU. Even if performed without contrast agents, CT manages to
decipher renal problems of uremics or the allergic ones to contrast
agents. Spiral CT examination with three-dimensional reconstruction is a
relatively new method, with demonstrated utility especially in coraliform
lithiasis.
MRI proved to be useful in detecting urinary tract obstruction and allows
assessing of hydronephrosis. This method can be used in patients with
impaired renal function or allergy to contrast agent, for whom the
ultrasound is contraindicated. Unlike CT, MRI does not allow
visualization of the majority of ureteral calculi, making rare use of this
method in assessing the lithiasis patients.
Imaging
Retrograde or anterograde
ureteropyelography– is used increasingly rare,
being useful for radiolucent calculi, which location
is difficult to determine by other means, in case of
non-function kidney, in patients with renal failure
or allergy to contrast agent.
Imaging
Angiography – It is rarely used for lithiasis patients. This
investigation can be useful when a vascular malformation is
suspected as a causal factor of stasis or in diagnosis of lithiasis
associated with reno-vascular hypertension.

Renal scintigram with isotopic nephrogram – provides


guidance on the functionality of renal parenchyma and the
urinary drainage at urinary tract level. The investigation is
useful especially in patients with renal failure, lithiasis on single
kidney, congenital, functional, surgical, or with allergy to iodine
contrast agents. It can contribute to establishing surgical
indication.
Treatment of urolithiasis
• Conservative treatment
• Extracorporeal lithotripsy
• Percutaneous nephrolithotomy
• Ureteroscopy
• Conventional surgical methods
• Palliative methods
Conservative treatment
Treatment of renal colic:

Calculi less than 3 mm can be eliminated spontaneously


in 90% of cases, between 3-5 mm in 60% and more
than 7 mm in 20% cases.
Conservative treatment
Treatment of renal colic
1. Analgesic treatment:
– AINS; Diclofenac (up till 100-150 mg/day, i.m./i.r)
– Metamizol derivatives: Pitofenon+Metamizol
– Opioid analgesics: sol. Tramadol obligatory with sol. Atropine
2. Antispasmodic treatment:
– Sol.Drotaverine, sol.Platifilin
3. Antibacterial treatment, initially empirical, then according to
urine culture:
– Ciprofloxacin 0.5g, 2 times per day or Amoxacilin 0.5g 2 times per day
Treatment of uric lithiasis
• Fluid intake at least 1.5-2 liters/day
• Allopurinol, by 1-3 pills / day
• Potassium citrate by 2-3 g/day in 2-3 doses (Urals U, Blemaren)
• Sodium bicarbonate (baking soda), up to 5 g/day
• Lacto-vegetarian diet with alkaline urine:
– Dairy
– Vegetables: all, except for corn and lentil
– Fruits: all, except for plums and blueberries
– Fats: nuts, almonds, coconut
• Limitation/exclusion of alcoholic beverages (especially wine and
beer)
Treatment of oxalic lithiasis
• Diet limiting products rich in oxalates (beetroot, chocolate,
coffee, cola, nuts, spinach, strawberries, tea, cocoa)
• Hypoglycemic diet, 3-3.5g/kg glucide
• Oxalic acid can be produced by microbial decomposition in the
intestine of: potatoes, vegetables, concentrated sweets, pasta
• In advanced hyperoxaluria it is administered Ca carbonate /Ca
citrate (0.5-1g x 2-3 times/day) or Cholestyramine (10-12g/day)
• Avoidance of prolonged administration of ascorbic acid in high
doses (>1g/day)
Treatment of cystine lithiasis
• Increased fluid intake, up to 4-5 liters/day
• Urine alkalinization:
– Dairy
– Vegetables: all, except for corn and lentil
– Fruits: all, except for plums and blueberries
– Fats: nuts, almonds, coconut
• Hypo-sodium diet
• Normo-protein diet to avoid high intake of methionine
Treatment of phosphatic lithiasis
• Phosphate-based lithiasis:
– Hypo-protein diet 0.7-0.8 g/day
– Limited dairy and fish
• Acidification of urine:
– Meat, cold meats, fish, eggs
– Cheese, dairy
– Vegetables: corn, lentil
– Fruits: plums, blueberries
Herbal treatment
• Anti-inflammatory, emollient, antispasmodic, diuretic,
antibacterial effect
• It is administered in long treatment, the minimum duration 3-6
months
• Change of herbal preparation every 10-14 days
• Medicinal herbs: corn silk, juniper, cranberry, birch leaves, horse
tail, pine buds, poplar buds
• Combined herbal remedies: Cyston, Shi Lin Tong, Kanfron,
Fitolizin, Cystenal, Urolesan
ESWL =Extracorporeal Shock Wave
Lithotripsy
• The method is based on
destruction f calculi with
ultrasound generated outside
the body and especially
focused on calculus
• Represents the first line
method and is applicable to
>90% of patients
Lithotriptor structure
1. Shock wave generating system
2. Shock wave focus system
3. Calculi location system
Piezoelectric principle
• Modified
ultrasonic waves
• Focusing using
spherical
arrangement of
piezo-ceramic
elements
Electrohydraulic principle
• Generating
shock waves in
liquid
environment
with their focus
through semi-
ellipsoid
Calculi location system
Requirements:
• To allow rapid tracking of calculi
• To allow control during surgery
• To allow assessing of the treatment results
• To expose the doctor and the patient to radiation as
little as possible
Location can be ultrasound or fluoroscopy, the most
common is the joint adjustment
Indications
• Caliceal calculi up to 2-3 cm
• Renal calculi with a diameter of 2-3 cm
maximum
• Lumbar and pelvic ureteral calculi
• Residual calculi after open surgery or
endoscopic procedures
Contraindications
Absolute:
• Coagulopathy + anticoagulated treatment
• Pregnancy
• Renal failure
Relative:
• Abnormalities of the urinary tract
• ITU including tuberculosis
• Arrhythmias
Technical:
• Obesity
• Children under 1 year
Complications:
Minor clinical complications:
• Hematuria
• Pain
• Urinary infection
Severe complications:
• Steinstrasse
• Subcapsular hematoma
• Renal colic
• Septicemia
Very rare complications:
• Liver hematoma
• Pancreatitis
• Ureterocolic fistula
• Sigmoid perforation
Distance complications:
• Nephrosclerosis
• HTA
• Decreased renal function
Effectiveness of the procedure
depends on:
• Characteristics of lithotriptor "gold standard“ -
Dornier HM
• Calculus size, optimal efficiency < 2cm
• Calculus density determined by chemical structure of
calculus (cystine and oxalate calculi decay harder)
• Number and location of calculus
• Anatomical peculiarities of calyces containing calculi
• Doctor’s experience
High endourology
• Ureteroscopy
• Ureterolithotripsy
• Percutaneous
nephrolithotomy
(PNL)
Ureteroscopy
SURGERY ROOM FACILITIES

Radiolucent endoscopy table


C-arm
Indications:
• Ureteral calculi therapy:
fragmentation
removal
dislocation
• Installation of catheters guides and autostatic probes
• Steinstrasse therapy after ESWL
• Residual calculi after ESWL
• Residual calculi in superior caliceal groups after PNL
• Ureteral trauma or suspecting
Contraindications:
Absolute:
• Untreated coagulopathy

Relative:
• Untreated urinary tract infections
• Tuberculosis
• Pregnancy
Ureteroscopy complications
• Ureter perforation
• Ureteral avulsion
• Intraoperative defects of endoscopic instrumentation
• Ureteric mucosal injury
• SCB perforation
• Late complications: ureteric stenosis <1%
ureteral-bladder reflux <1%
Percutaneous nephrolithotomy
PNL is endoscopic surgical procedure in which
the calculus from kidney is extracted after
percutaneous puncture of the renal hollow
system and dilation of the access channel thus
created. When the calculus size or its shape does
not allow direct extraction through the created
channel, various procedures of calculus
destruction are applied.
PNL stages
• SCB opacity
• SCB puncture
• Dilation and creation of percutaneous access
channel in the intrarenal urine tract
• Nephroscopy
• Extraction of calculi or lithotripsy "in situ" of
calculi
• Kidney drainage (nephrostomy)
PNL complications
Early complications Late complications
Fever 32% Arteriovenous fistulas <1%
SCB perforation 5-7% HTA <1%
Nephrostomy dislocation 4-16% Lithiasis relapse 3%

Hemorrhaging
Septicemia 3%
Hydrothorax 2%
Colon perforation 1%
Deterioration of renal function 3%
Open surgery
Being invasive they are being applied less Specific indications:
– Lack of technical possibilities of applying mini-invasive methods
– Failure of mini-invasive methods
– Require open surgery in order to correct associated pathologies (plastic
JPU, ureter)
– Afunctional kidney (nephrectomy)
– Large or complex shaped calculi
– Obesity II-III degree
– Skeleton deformations
– Coraliform urolithiasis with associated infundibular stenosis or calculus
with caliceal ramifications
Open surgery
• Pyelolithotomy
• Pyelonephrolithotomy
• Nephrolithotomy
• Ureterolithotomy
• Nephrectomy
Laparoscopic surgery
• Laparoscopic pyelolithotomy
• Laparoscopic ureterolithotomy
• Robotic assisted laparoscopy ”Da Vinci”

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