2. "View a negative experience in your life
like you'd look at a photo negative. A
single negative can create an unlimited
number of positive prints."
Gerhard Gschwandtner
Founder of "Selling Power" magazine
5. Renal Calculi
Called nephrolithiasis or urolithiasis
Most commonly develop in the renal pelvis
but can be anywhere in the urinary tract
Vary in size –from very large to tiny
Can be one stone or many stones
May stay in kidney or travel into the
ureter
Can damage the urinary tract
May cause hydronephrosis
More common in white males 30-50 years
of age
6.
7. CHANGING MODALITIES
WITH WESTERNIZATION, THE SITE OF STONE
FORMATION HAS MIGRATED FROM LOWER TO
UPPER URINARY TRACT
DISEASE ONCE LIMITED TO MEN IS
INCREASINGLY GENDER BLIND,
SURGICAL TREATMENT ALTHOUGH THEY
REMOVE THE OFFENDING STONE,DO LITTLE
TO ALTER THE COURSE OF THE DISEASE
THOROUGH UNDERSTANDING OF
ETILOGY,EPIDEMIOLOGY AND PATHOGENESIS
OF URINARY TRACT STONE DISEASE IS
NECESSARY
9. Kidney anatomy
Right kidney lower than left
Retroperitoneal
Reddish brown, bean shaped
Hilum – medial surface; vessels, ureter; renal nerves
Adrenal glands on superior poles of kidney
Located on either side of vertebral column
Renal fascia – connective tissue
Adipose capsule – fat pad
Hold kidney in place and protects kidney
Renal capsule - fibrous sac that encloses
kidney
10. 26-10
Internal Anatomy of Kidneys
Cortex: Outer area
Renal columns
Medulla: Inner area
Renal pyramids
Calyces
Major: Converge to form
pelvis
Minor: Papillae extend
Nephron: Functional unit
of kidney
Juxtamedullary
Cortical
13. At least 500 mL (17 oz) of
urine must be eliminated
every day because this
amount of fluid is needed
to remove potential toxic
materials from the body
to maintain homeostasis.
A normal adult eliminates
from 1.5 L (1.6 qt) to 2.3 L
(2.4 qt) of Urine a DAY,
depending on the amount
of water taken in and the
amount of water lost
through Respiration and
Perspiration.
Urine flows from the nephron
to the collecting ducts, which
extend to the tips of the
pyramids, and empty into the
calyces. All the urine will leave
the kidney via the ureters.
URINE FORMATION
14. INCIDENCE
12% have stone in their lifetime.
12% of men will suffer from kidney stone by
age of 70
5% of women will suffer from kidney stone by
age of 70
50% have recurrence with in 5-10 yrs
Highest incidence of kidney stone is in 30-45
years of age group, and incidence declines
after age of 50
7-10 of every 1000 hospital admission is of
renal stone
15. COMPARATIVE INCIDENCES OF FORMS OF URINARY
LITHIASIS
Stone analysis in Percentage
Form of Lithiasis India USA Japan UK
Pure Calcium Oxalate 86.1 33 17.4 39.4
Mixed Calcium Oxalate and 4.9 34 50.8 20.2
Phosphate
Magnesium Ammonium 2.7 15 17.4 15.4
Phosphate (Struvite )
Uric Acid 1.2 8.0 4.4 8.0
Cystine 0.4 3.0 1.0 2.8
16. In INDIA---STONE BELTS
“Stones belt" occupies parts of Maharashtra,
Gujarat
Punjab
Haryana
Delhi and
Rajasthan.
In these regions, the disease is so prevalent
that most of the members of a family will suffer
from kidney stones in some part of their lives.
19. Stages of stone formation
SUPERSATURATION
NUCLEUS FORMATION
CRYSTALLIZTION
AGGREGATION
MATRIX FORMATION
20. In normal human urine—concentration of
calcium oxalate--- four times higher than its
solubility in water
Precipitation occurs when supersaturation
exceeds the solubility by 7 to 11 times.
Homogenous nucleation is the process by
which nuclei form in pure solution.
Nuclei are the earliest structure that will not
dissolve.
If enough nuclei form and grow ,aggregation of
crystals will form larger particles—that can
occlude tubular lumen.
21. MATRIX– Renal calculi contain both crystalline
and non crystalline component . Non crystalline
component is termed Matrix.
Randalls plaque theory—
erosion and deposition of urinary
salts as Randalls plaque at the apex of renal
papillae.
Carrs postulate—
minute concretions are carried away by renal
lymphatics.If these lymphatics are blocked they
enlarge and act as nidus of stone formatin.
22. Inhibitors & Promoters of Stone Formation in
Urine
INHIBITORS
Inhibits crystal Growth -
Citrate – complexes with Ca
Magnesium – complexes
with oxalates
Pyrophosphate - complexes
with Ca
Zinc
Inhibits crystal Aggregation
Glycosaminoglycans
Nephrocalcin
Tamm- Horsfall Protein
Osteopontin
PROMOTERS
Bacterial Infection
Matrix
Anatomic Abnormalities –
PUJ obst., MSK
Altered Ca and oxalate
transport in renal epithelia
Prolonged immoblisation
Increased uric acid levels I.e
taking increased purine subs–
promotes crystallisation of Ca
and oxalate
?? Nanobacteria – seen in
97% of renal stones
23. URINARY GLYCOPROTEINS
TAMM-HORSFALL GLYCOPROTEIN
POTENT INHIBITORS OF CALCIUM OXALATE CRYSTAL
AGGREGATION
IT IS EXPRESSED BY RENAL EPITHELIAL CELLS IN THE THICK
ASCENDING LIMB AND THE DISTAL CONVOLUTED TUBULE
↓
AS A MEMBRANE ANCHORED PROTEIN
RELEASED IN TO THE URINE AFTER CLEAVAGE OF THE
ACHORING SITE BY PHOSPHOLIPASES OR PROTEASES
PROTECTIVE ROLE AGAINST CRYSTALLIZATION OF
CALCIUM SALTS
24. TYPES OF KIDNEY STONES
CALCIUM CONTAINIG STONES
Calcium oxalate
Hydroxyapatite
Brushite
NON CALCIUM CONTAINIG STONE
Uric acid Silica
Struvite 2,8Dihydroxyadenine
Triamterene
26. Uncommon Stones
XANTHINE STONES
– (Autosomal Recessive . Def of Xanthine Oxidase leading to Xanthinuria)
DIHYDROXYADENINE STONE
– ( Def. of enzyme adenine phospo ribosyl transferase )
SlLICATE STONES
– Rare in humans ( excess intake of Antacid with Mg Trisilicate. Mostly in cattle due to
ingestion of Sand )
MATRIX
- Infection by Proteus - Radiolucent (all calculi have some amt ( 3%) of matrix but matrix
calculus has 65% Matrix content in calculi)
34. CALCIUM OXALATE
ALSO CALLED MULBERRY STONE (75%)
BROWN IN COLOR, COVERED WITH
SHARP PROJECTIONS
SHARP MAKES KIDNEY BLEED
(HAEMATURIA)
VERY HARD
RADIO - OPAQUE
Under microscope looks like Hourglass or Dumbbell shape if monohydrate and Like an
Envelope if Dihydrate
35. Calcium Stones
Hereditary Hypercalciuria condition
Mean value of calcium in urine in excess of:
300 mg/day (7.5 mmol/day) for males
250 mg/day (6.25 mmol/day) for females
4 mg/day (0.1 mmol/kg/day) for either in random urine
collections
30-40% patients with calcium stones have
hypercalciuria
36. Calcium Oxalate Calculi
Multiple calcium
oxalate stones
(0.5 x 0.5 cm) in
the collecting
system of a
kidney
44. Medical Nutrition Therapy
Calcium DRI for “healthy bones
and less risk of stones”
1000 mg/day for men and women
aged 50 yrs and younger
1200 mg/day for those older than
50 years
Increase fluid intake > 2 L/day
May need to supplement
potassium
45. Calcium Study Findings
Low calcium diet
23 of the 60 men had stone recurrences
Oxalate excretion was increased
Normal calcium, decreased sodium and
reduced animal protein diet
12 of the 60 men had stone recurrences
Oxalate excretion was decreased
Contrary to previous therapy, calcium restriction
does not prevent prevent stone formation, but
may do the opposite.
46. Calcium Stones and Oxalate
Hyperoxaluria
Urinary excretion of oxalate in excess of 45 mg/day
Results from endogenous synthesis and from
absorption of dietary oxalate
Observed in 20% of recurrent calculi formers
Normal diet contains oxalate range of 80-100
mg/day (absorption does not exceed 10-20%
amount in food consumed)
Oxalate cannot be metabolized in body– renal route
is the only excretion method
Normal healthy adult excretion is 15-40 mg/day
47. Calcium Stones and Oxalate
Oxalate to calcium ratio 1:5
Low calcium diets increase passive absorption of
free oxalate and enhance urinary oxalate excretion,
promoting the risk of calcium oxalate stones
Disease states resulting in hyperoxaluria
Inflammatory bowel disease, ileal disease, short
bowel syndrome, gastrointestinal decolonization of
Oxalobacterformigens
Hyperoxaluria also due to:
Autosomal recessive genetic defect of a hepatic
enzyme, resulting in 3 to 8 times normal level
48. Medical Nutrition Therapy
Be aware of foods responsible for increased
urinary oxalate excretion:
Spinach
Rhubarb
Beets
Strawberries
Patients may benefit from pyridoxine (B6), which increases
transaminase activity responsible for the conversion of
glyoxylate, the immediate oxalate precursor to glycine (The
Merck Manual 2004).
Tea
Nuts
Wheat bran
Chocolate
49. Calcium Stones and Animal Protein
Increased protein intake facilitates
nephrolithiasis risk by contributing to:
Hypercalciuria
Hyperuricosuria (urinary uric acid > 750 mg/day for
women or > 800 mg/day for men)
Hyperoxaluria
Low urine pH
Hypocitraturia (urinary citrate < 350 mg/day)
1/3 of calcium calculi formers are sensitive to meat
protein and so excrete oxalate
50. Calcium Stones and Animal Protein
Male Health Professions
Observational Study found:
33% increased risk of
renal nephrolithiasis
with a 77 g/day versus a
50 g/day animal protein
diet
Medical Nutrition
Therapy: 0.8 g/kg body
weight (kg=2.2 lbs)
.
51. Calcium Stones and Citrate
Citrate: Acts as a urinary stone inhibitor
Prevents formation of calcium oxalate or calcium phosphate
stones
Disease states that decrease citrate levels in body: distal
renal tubular acidosis, acidosis along with
hypokalemia, enteric hyperoxaluria and
malabsorption syndrome, as well as excessive meat
intake.
Normal urinary citrate level > 640 mg/day
Medical Nutrition Therapy: 4 oz. lemon juice diluted with 2 L
water
Standard Medical Practice: oral alkali (K citrate)
52. Calcium Stones and Sodium
Dietary and urinary sodium is directly linked with excretion of
calcium in the urine, so a reduction in sodium excretion will
produce a reduction in calcium excretion, resulting in reduced
risk of developing calculi.
For every 60 mmol (1380mg) increase in urine sodium, the risk of
hypercalciuria rises 1.63 times
Medical Nutrition Therapy: to prevent, keep sodium amounts to
< 100 mmol/day or 2300 mg
With recurring calculi condition, restrict sodium intake
< 50 mmol/day
.
53. Calcium Stones and Potassium
Potassium intake is inversely proportional to
nephrolithiasis risk.
For every 104 mmol/day (4042 mg/day) vs. 74
mmol/day (2895 mg/day), there was a 50% decrease
in renal stone manifestation.
Medical Nutrition Therapy: Advise patients to eat
variety of low oxalate fruits and vegetables
.
54. To Sum It All Up:
Dietary Influence for Calcium
Stone Formation Risk
Increased Risk
Oxalate
Animal Protein
Sodium
Decreased Risk
Calcium
Magnesium
Potassium
Fluid Intake
Fiber
Pyridoxine
56. CALCIUM PHOSPHATE
STONES
Hyperparathyroidism
Ca P
Renal Tubular Acidosis
K CO2
PTH Hormone Promotes renal production of 1-25-dihyroxycholecalciferol – active Vit.D
and also increases absorption of Calcium and decreases Phosphorus absorption from
Kidneys
The largest known kidney stone weighed 1.36 kilograms.
57. PHOSPHATE STONE
USUALLY CALCIUM PHOSPHATE
SOMETIMES CALCIUM MAGNESIUM
AMMONIUM PHOSPHATE OR TRIPLE
PHOSPHATE
SMOOTH MINIMUM SYMPTOMS
DIRTY WHITE
RADIO - OPAQUE
Calcium Phosphate also called ‘Brushite’ appears like Needle shape
under microscope
60. Struvite Stones: Staghorn stone
-Caused bacteria which have a urea splitting enzyme called
urease.
Proteus
Pseudomonas
Klebsiella
Staphylococcus
-Produces struvite: “triple phosphate”, actually a mix of
Mg2+ ammonium phosphate and carbonate apatite
- Struvite will form in urine with pH > 7 due to PO4 poorly soluble
-will not for at normal urine pH (5.85)
- stone fills renal calices and looks like a stag’s horn
Struvite crystaluria
61. Struvite Stones
Under these conditions, struvite stones grow into large
staghorn stones in renal pelvis
Medical Nutrition Therapy: Advise balanced meals
with variety of fruits and vegetables to maintain health,
help fight bacteria
Standard Medical Treatment
Surgical removal
Extracorporeal shockwave lithotripsy
Culture-specific antimicrobials with urease inhibitors
Goal: Prevent and eliminate UTIs through regular screening
and monitoring of urine cultures
62. URIC ACID & URATE STONE
HARD & SMOOTH
MULTIPLE
YELLOW OR RED-BROWN
RADIO - LUCENT (USE
ULTRASOUND)
Under microscope appear like irregular plates or rosettes
pKa of uric acid 5.75 – at this pH 50% of uric acid insoluble.
If pH falls further - uric acid more insoluble
63. Uric acid stones
~6% of all stones
2/3 uric acid waste
outputed by kidney
Urate excretion =
1.5-4.5 mmol/day
pKa = 5.5 (soluble
at 6.5, crystals at 5)
64. Uric Acid Stones
Uric Acid: end product of purine metabolism
Derived from exogenous sources
Produced endogenously during cell turnover
Contributing disease states to uric-acid stones:
Inflammatory bowel disease,
lymphoproliferative and myeloproliferative disorders
due to increased cellular breakdown which causes
purines to be released and so increases uric acid load
65. Uric Acid stones: Uric acid
production
Purines, adenine, guanine
Hypoxanthine
Xantine
Uric Acid pool
2/3 kidney excretion
1/3 gut excreted
Bacterial degradation
NOTE:
All urate is filter through the glomerulus,
but there is 98% resorption in proximal
tubule,
rest excreted.
66. Uric Acid Stones: Risk Factors
Age
sex (M>F)
genetic
metabolic
diet high in purines
Decreased renal NH4 prod.
Decreased fluid intake
increased amb. temp
Increased urate
Decreased pH
<5.5-5.0
Decreased volume
Decreased inhibitors
supersaturation
Urate crystal
Urine
67. Uric Acid Stones
Medical Nutrition Therapy: moderately use foods high
in purines such as:
Organ meats
Anchovies, herring
Animal flesh proteins
Fish, poultry
Standard Medical Practice:
Potassium citrate dissolution therapy
Urine alkalinization (pH 6.0-6.5)
Sodium bicarbonate therapy discouraged
Increases monosodium urate along with calcium
68. CYSTINE STONE
AUTOSOMAL RECESIVE DISORDER
USUALLY IN YOUNG GIRLS
DUE TO CYSTINURIA -
CYSTINE NOT ABSORBED BY TUBULES
MULTIPLE
SOFT OR HARD – can form stag-horns
PINK OR YELLOW
RADIO-OPAQUE
Under microscope appears like hexagonal or benezene
ring – ask for first morning sample
69. Cystine Stones
Autosomal recessive trait
Inborn dysfunction in transport of dicarboxylic acids of
cystine, ornithine, lysine, arginine (sometimes seen as COLA)
1 in 15,000 people in U.S are affected
Normal cystine excretion: < 20 mg/day
> 7.0 urine pH promotes cystine solubility
Medical Nutrition Therapy: increase fluid intake >4 L/day,
decrease sodium, may restrict protein since methionine is
precoursor to cystine
Standard Medical Practice: with medications, keep pH alkaline
24 hrs/day
70. CYSTINE STONE - Management
High Fluid Intake and Alkalanise Urine – dissolve most of
the smaller cystine stones
D-Pencillamine or MPG (Mercaptopropionylglycine) binds
to cystine that is soluble in urine
Side effects of Pencillamine restricts it use – Allergic
rashes, GI problems- Nausea, Vomiting, Diarrhoea
MPG better tolerated
Large obstructive stones – Surgery required first
Cyanide Nitroprusside Calorimeteric Test for detecting Cystinuria. If positive do
amino acid chromatography
pKa of cystine is 8.3, hence alkalinisisation above pH7.5 helps to dissolve the stones
71. Suspect and investigate for RTA
Calcium Phosphate Stone
Recurrent Stones - 2 per year
Bilateral Stones
Medullary Nephrocalcinosis
Hypocitauria
Hypokalemia
Chr. Pyelonephritis
Azotemia
RTA due to defect in urine acidification – due to this supersaturation of Ca.
Phosphate
72. Renal Tubular Acidosis
Type I – or Distal RTA - Low K Cl and Met acidosis.
Urine pH over 6 leads to hypercalciuria, hypocitraturia
( Multiple cyst formation in kidney due to low K over
yrs)
T/t - Give K Cit or Bicarbonate
Type II – or Proximal RTA – Failure to resorb HCO3 in
Proximal Tubule. ( usually associated with Fanconi’s
synd )
Type IV – seen in Diab nephropathy and interstitial renal
ds. Due to parenchymal damage – low GFR – K Cl -
low acid excretion. Urinary lithiasis incidence low – Don’t
make uric acid or Ca. stones
Type III RTA – Hybrid of Type I and II and now considered variant
of Type I or Distal RTA
73. Keep In Mind…
Although a person may
have several risk factors
for the development of
nephrolithiasis,
prevention and
management through
Medical Nutrition
Therapy can deter renal
calculi formations.
74. Evidence-Based Medicine
Become familiar with products that may
be popular, but are not necessarily
scientifically proven for the treatment of
kidney stones:
Cranberry concentrate pills
Wild yam
Flaxseed
Zinc
Copper
Vitamin A
Evening primrose oil
Goldenrod
75. Renal Calculi
Subjective symptoms
Sever pain in the flank area, suprapubic area, pelvis
or external genitalia
If in ureter, may have spasms called “renal colic”
Urgency, frequency of urination
Chills and rigor– As UTI
76. Well, I guess you don’t
have kidney stones after
all.
78. Renal Calculi
Assessment
History and physical exam
Location, severity, and nature of pain
I/O
Vital signs, looking for fever
Palpation of flank area, and abdomen
79. Renal Calculi
Nursing interventions
Primary is to treat pain – usually with opioids
Ambulate
Force fluids, may have IV
Watch for fluid overload
Strain urine – send stone to lab if passed
Accurate I/O
Medicate
80. Investigations for Diagnosis
Urinalysis
urine pH, culture, 24-hr assessment
Serum electrolytes
calcium, phosphate, bicarbonate, uric acid
Blood urea nitrogen
to determine level of renal function
Serum creatinine
to determine level of renal function
Parathyroid hormone
if elevated serum calcium
Stone analysis
if possible
.
82. Investigations for Diagnosis
Plain Abdominal Film/Kidney-Ureter-Bladder View
Assessment of radio-opacity of stone
Allows monitoring calculus progression
Guides shockwave lithotripsy
Un-enhanced Helical Computed Tomography
99% accurate
Provides measurement of stone density
Stones with density > 1000 Housnfield units respond less
well to lithotripsy
83. Case 1. A 32 yr presents with acute R sided abd. colic in casualty that started in
early hrs of morning, he has previous H/O lithuria 4 yrs previously. He has mild
temp. Vomiting and is tender in the RIF.
3. Which investigation at this stage can help in clinching
the diagnosis?
Non contrast spiral or HelicalCT scan – will pick up stone in over
97% of the cases ( 97% specificity, 96% specificity)
12 x 10 mm 7 x 7 mm calculi in lower third Right
Ureter
84. 8. Any Role of Inv like IVU?
• Not Mandatory
• 1in 40,000 patients die due to anaphylactic reaction to contrast
• Useful for radio-lucent stones & to detect
Congenital Anomalies in Urinary tracts
Ultra-sound and Helical CT Scan slowly replacing IVU
85. DD of Radiolucent filling defect on IVU in Ureter or Kidney
Must Know
Uric Acid Calculus
Matrix Calculus
Sloughed Papilla
Blood Clots
TCC
Renal Cysts
Vascular Lesions
Know For Brownie Points
Xanthine Calculus
Hydroxyadenine Calculus
Ephederine Calculus
Infection due to gas forming
Org.
Fungal Ball
Tuberculoma
Malacoplakia
Hypertrophied Papilla
Renal pseudo-tumour
86. Stone Size and rate of passage
Follw-up is 2 MONTHS
Stone size0-4 mm 83%
4-6 mm 60%
greater 6mm 0%
87. Modern Management of Urolithiasis
ESWL
Uretero-renoscopy
Percutaneous Nephrolithotomy
Laparoscopic Approach to stones
Open Ureterolithotomy, Pyelolithotomy or Nephro-pyelolithotomy
is required in less than 1 to 2% of modern stone management
88. Ureteroscopy - Results
Lower ureteric stones -
95 to 97% success with
single ureteroscopy
(Results of Ureteroscopy
better than ESWL)
Mid and Upper Ureteric
stones - 70 to 85%
success with
ureteroscopy
(Results of Ureteroscopy
comparable or similar to
ESWL)
91. DOUBLE J STENTS
DJ Stent made of Silicon or
Poly-urethane
Stents usually inserted
retrogradely over guidewire
The final position of stent
checked with fluroscopy
Antegrade stenting can be
undertaken through
nephrostomy tract
92. DOUBLE J STENTS
Stent Related problems-
Stentitis: irritative
symptoms- dysuria &
frequency due to stent
sitting on trigone of
bladder – in 50%
patients
Forgotten stent :
encrustation
93. TREATMENT (IDEALLY)
MAJORITY : 80 TO 85 % of all stones can be
treated by -
EXTRA - CORPOREAL SHOCK WAVE
LITHOTRIPSY (ESWL)
MINORITY : 15 TO 20 % SHOULD NEED
MINIMALLY INVASIVE SURGERY (PCNL /
URETEROSCOPY)
94. ESWL vs PCNL for renal stones
< 10 mm, ESWL is usually the primary approach
10 - 20 mm, ESWL is still the first-line treatment
Unless factors of composition, location, or renal
anatomy shift the balance toward more invasive but
definitive treatment modalities (PCNL or RIRS)
> 20 mm should primarily be treated by PCNL
Unless specific indications for ureteroscopy are
present (e.g., bleeding diathesis, obesity)
95. EXTRA - CORPOREAL SHOCK WAVE LITHOTRIPSY
(ESWL)
SHOCK WAVES GENERATED UNDER WATER CAN
TRAVEL THROUGH BODY WITHOUT ANY
APPRECIABLE LOSS OF ENERGY. WHEN THEY
ENCOUNTER STONES THE CHANGES IN DENSITY
CAUSES ENERGY TO BE ABSORBED AND REFLECTED
BY THE STONE & THIS RESULTS IN FRAGMENTATION
OF THE STONES.
96. ESWL is a Sound or Acoustic Wave of High Intensity
97. Mechanism of Stone Fragmentation by ESWL
On Front Surface – Compresive or positive
Forces
On Back Surface Of The Stone-
Reflection of Compression Pulse Creates
Negative Or Tensile Wave That Travel
Back Ward Through Calculi
Cavitation – Small air bubbles coalesce
and help in fragmentation
Once Tensile Force Exceeds “ Cohesive
Strength” Of Calculi- Fragmentation
Occurs
98. ESWL- Indications
Urology
Renal Calculus – 2 to 2.5 cms size
Upper Ureteric Calculus
Small Vesical Calculus
Peyronies Ds of Penis
Non-Urology
Pancreatic Calculus
CBD Calculus
Myositis Ossificans
Stents Recommended prior to ESWL for Calculi > 1.5 cms
100. ESWL- FOUR MAIN ELEMENTS
1. ENERGY SOURCE
2. FOCUSING DEVICE
3. COUPLING DEVICE
4. LOCALIZATION DEVICE
ENERGY SOURCE
101. ESWL COMPLICATIONS
Haematuria – is quite common ( short term
antibiotics Recommended )
Incomplete stone Fragmentation &
Obstruction
“Stienstrasse” ( stone street ) usually due to
a large “ Leading fragment”
( Stents Recommended prior to ESWL for
Calculi > 1.5 cm )
102. Steinstrasse ( or Stone Street) – Post
ESWL
Steinstrasse usually due to large leading fragment
103. PCNL Vs OPEN OPERATION
PCNL – short hospital stay
PCNL – Minimum morbidity
PCNL success – Similar to open
operation
The overall cost may not be
different of open and PCNL
operation
LARGE KIDNEY STONE
104. PCNL - Indications
Large Calculi > 2.5cms size
Infected Calculi
Cystine Calculi
Obstructive Uropathies
Failed ESWL
Anatomic Abnormalities
Recurrent Large Calculi after Open
Operation
105. PCNL
Location
Size
Calculi can obstruct the normal
flow of urine anywhere in the
urinary tract. The exact location
of the obstruction is most often
related to the size of the calculi.
Stones over 2cm in diameter and
staghorn calculi often obstruct the
flow of urine at the level of the
renal pelvis and collecting system.
Because of their size and location,
these stones are usually best
managed using PCNL
106. PCNL-TECHNIQUE
Prone position
Under x-ray or Ultra sound guidance
Percutaneous access under taken
Pencil Tipped (18g) needle used to puncture
lower calyx
107. Steps of the Procedure
1. Opacify the Collecting System
2. Establish Percutaneous Access
3. Dilate the Nephrostomy Tract
4. Break up/Remove Calculi
5. Establish Nephrostomy Drainage
116. Establishing Percutaneous
AccessPlace Safety Guidewire
Advance 8/10 French
dilator sheath over
working wire
Remove 8 French
dilator
Place safety wire
through 10 French
sheath; Advance
to bladder
120. Dilating the Tract
Step 3: Advance Working Sheath
Advance sheath over
inflated balloon
Remove inflated balloon
through sheath
Balloon Dilatation
121. Dilating the Tract
Sequential Dilatation
Sequentially advance dilators over
8Fr guiding dilator in 2Fr increments
Place working sheath
122. PCNL TECHNIQUE
STONE REMOVAL -
Saline Irrigation
helps to keep clear
and washes off
small bleeding
points or clots
Small calculi-
Grasped and
Removed
Larger Calculi
fragmented
Percutaneous Nephrolithotomy
123. Removing Calculi
Remove working
wire
Rigid nephroscope
or flexible
nephroscope
Perform Nephroscopy
124. Removing Calculi
Ultrasonic
Laser
Pneumatic
Combination
of ultrasonic
and pneumatic
in one device
Electrohydrauli
c
Perform Lithotripsy
125. Removing Calculi
Swiss LithoClast® Ultra Lithotriptor
• Designed to improve
efficiency of stone
fragmentation
• Suction removes stone
fragments
• Stone catcher captures
stone fragments for
pathology
• Simultaneous ultrasonic &
pneumatic lithotripsy
Stone Catcher
127. ZeroTipTM
Nitinol Basket
Removing Calculi
• Nitinol Construction
• Designed for additional
torqueability and kink
resistance
• Composite Sheath
• Optimizes scope
deflection
• Knotted Basket Tip
• For reliable stone capture
close to the kidney wall
128. GraspitTM
Nitinol Stone Retrieval Forceps
Removing Calculi
• Unique Forcep Design
•Security of a basket,
control of a grasper
• Serrated Inner Wire Edge
•Designed to secure the
stone
• Composite Sheath
•Optimizes scope
deflection
133. Nephroliths: Nephrotomy
Kidney reduced: 20 to 50%
Midline celiotomy
Occlusion of blood supply
Incision on convex surface
Flush ureter and renal pelvis
Reestablish blood flow
Suture renal capsule Vs no suture
134.
135.
136.
137. Nephroliths: Pyelolithotomy
Dilation of renal pelvis
Less effect on renal function
Midline celiotomy
No occlusion of renal blood supply
Dissect peritoneal attachment and
rotate medially
138. Nephroliths: Pyelolithotomy
Incision in renal pelvis and proximal
ureter
Extraction of urolith
Cystoscope 1.9 mm
Flush renal pelvis and ureter
Retrograde catheterization from
bladder
Suture with simple continuous pattern
5-0 monofilament absorbable
QuickTime
139. EXTENDED PYELOLITHOTOMY
PLANE DEVELOPED BETWEEN INTRA RENAL
PELVIS AND OVERLYING PARENCHYMA,WHICH
IS THEN RETRACTED
INCISION INTO THE PELVIS CAN THEN BE
EXTENDED INTO THE NECK OF CALYCES TO
REMOVE A STAGORN CALCULUS
INCISION IS CLOSED WITH ABSORBABLE
SUTURES AND A URETERIC STENT LEFT insitu
141. TOTAL OR PARTIAL
NEPHRECTOMY
NON FUNCTIOINING KIDNEY WITH A
STAGHORN CALCULUS WHICH IS THE SEAT OF
A RECURRENT URINARY SEPSIS
142. TAKE HOME MESSAE
5mm stones are not likely to pass and
require surgical evaluation.
Non contrast helical CT remains the gold
standard for diagnosis.
Work-up after the 1st stone=different
approaches, be patient centered!
ESWL can tx 85% of kidney stones that
need surgical intervention and
ureterorenoscopy often treats the rest
(i.e the more distal stones
143. REFERENCES
BAILEY & LOVE’S- SHORT PRACTISE OF
SURGERY
SABISTON TEXTBOOK OF SURGERY
MASTERY OF SURGERY by Fischer
Urology CAMBELL
Glenn- UROLOGIC SURGERIES
UROLOGY CASE PRESENTATIONS
RECENT ADVANCES- WOLTERS KLUWER