Obstructive Uropathy - Prince of Songkla...

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Obstructive Obstructive Uropathy Uropathy Watid Watid Karnjanawanichkul Karnjanawanichkul

Transcript of Obstructive Uropathy - Prince of Songkla...

Page 1: Obstructive Uropathy - Prince of Songkla Universitymedinfo2.psu.ac.th/surgery/Edu_be_document/document... · Post-obstructive Diuresis ... Causes of obstructive uropathy Anatomic

Obstructive Obstructive UropathyUropathy

WatidWatid KarnjanawanichkulKarnjanawanichkul

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Obstructive Obstructive uropathyuropathy

•• FFunctionalunctional oror anatomicanatomic obstructionobstruction ofof

urinaryurinary flowflow atat anyany levellevel ofof thethe urinaryurinary

tracttract

–– The point of obstruction can be as proximal The point of obstruction can be as proximal

as the calyces and as distal as the urethral as the calyces and as distal as the urethral

meatusmeatus

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Obstructive nephropathyObstructive nephropathy

•• FFunctionalunctional oror anatomicanatomic renalrenal damagedamage

thatthat’’s cause from obstructions cause from obstruction

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ObstructionObstruction

•• Congenital or acquired Congenital or acquired

•• Benign or malignantBenign or malignant

•• Baseline condition of Baseline condition of

the kidneysthe kidneys

•• Partial or completePartial or complete

•• Unilateral or bilateral Unilateral or bilateral

•• Acute or chronicAcute or chronic

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Pathologic changes of obstructionPathologic changes of obstruction

•• lymphatic dilation, lymphatic dilation, interstitial edemainterstitial edema

•• Collecting duct and Collecting duct and tubular dilatation tubular dilatation

•• Widening of Bowman's Widening of Bowman's space, tubular basement space, tubular basement membrane thickening, membrane thickening, cell flattening, and cell flattening, and cytoplasmiccytoplasmic hyalinizationhyalinization

•• Inflammatory cell Inflammatory cell responseresponse

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Pathologic changesPathologic changes

•• Interstitial fibrosis and Interstitial fibrosis and

thickening of the thickening of the

tubular basement tubular basement

membranes membranes

•• Cortical thinning and Cortical thinning and

development of development of

glomerularglomerular crescents crescents

were present at the were present at the

33-- to 4to 4--week intervalweek interval

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PostPost--obstructive obstructive DiuresisDiuresis

•• This occurs mainly after relief of BUO or This occurs mainly after relief of BUO or

obstruction of a solitary kidney, it can obstruction of a solitary kidney, it can

rarely occur when there is a normal, rarely occur when there is a normal,

contralateralcontralateral kidneykidney

•• Normal physiologic response to the Normal physiologic response to the

volume expansion and solute volume expansion and solute

accumulationaccumulation

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Causes of obstructive Causes of obstructive uropathyuropathy

Anatomic abnormalities Anatomic abnormalities

PUV, CBN, stricture urethra, polyp of ureter

Compression from extrinsic masses or processes Compression from extrinsic masses or processes

Reproductive system ; pregnancy, uterine prolapse

GI tract : Crohn’s disease, diverticulitis

GU tract : BPH, CA prostate

Blood vessels : aneurysm, retrocaval ureter

Retroperitoneum : fibrosis, TB, sarcoidosis, lymphoma

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Causes of obstructive Causes of obstructive uropathyuropathy

Functional abnormalitiesFunctional abnormalitiesNB, UPJ obstruction, UVJ obstruction

Mechanical obstructionMechanical obstructioncrystal – renal tubuleBlood clot, renal papillae – renal pelvis, ureterUrolithiasis – renal pelvis, ureter, urethra

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UrolithiasisUrolithiasis

•• EpidemiologyEpidemiology

•• ClassificationClassification

•• PathogenesisPathogenesis

•• PathophysiologyPathophysiology

•• Approach to patientsApproach to patients

•• TreatmentTreatment

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EpidemiologyEpidemiology

•• The lifetime prevalence of kidney stone The lifetime prevalence of kidney stone

disease is estimated at 1% to 15%disease is estimated at 1% to 15%

–– Age, gender, race, and geographic locationAge, gender, race, and geographic location

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AgeAge

•• Stone occurrence is relatively uncommon Stone occurrence is relatively uncommon

before age 20 but peaks in incidence in before age 20 but peaks in incidence in

the fourth to sixth decades of lifethe fourth to sixth decades of life

•• Women show a bimodal distribution of Women show a bimodal distribution of

stone disease, demonstrating a second stone disease, demonstrating a second

peak in incidence in the sixth decade of peak in incidence in the sixth decade of

lifelife

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GenderGender

•• Stone disease typically affects adult men Stone disease typically affects adult men

more commonly than adult womenmore commonly than adult women

–– Two to three times more frequentlyTwo to three times more frequently

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Race/EthnicityRace/Ethnicity

•• Prevalence of stone disease Prevalence of stone disease

–– WhitesWhites

–– Hispanics : 70% of whitesHispanics : 70% of whites

–– Asians : 63% of whitesAsians : 63% of whites

–– African Americans : 44% of whitesAfrican Americans : 44% of whites

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GeographyGeography

•• Higher prevalence of stone disease is Higher prevalence of stone disease is

found in hot, arid, or dry climates such found in hot, arid, or dry climates such

as the mountains, desert, or tropical as the mountains, desert, or tropical

areasareas

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GeographyGeography

•• Worldwide : high stone prevalence Worldwide : high stone prevalence

–– The United States, British Isles, The United States, British Isles,

Scandinavian and Mediterranean countries, Scandinavian and Mediterranean countries,

northern India and Pakistan, northern northern India and Pakistan, northern

Australia, Central Europe, portions of the Australia, Central Europe, portions of the

Malay peninsula, and ChinaMalay peninsula, and China

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PathogenesisPathogenesis

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Stone varietiesStone varieties

•• Calcium calculi 80%Calcium calculi 80%

•• NonNon--calcium calculicalcium calculi–– StruviteStruvite 10%10%

–– Uric acid 5Uric acid 5--10%10%

–– CystineCystine 1%1%

–– XanthineXanthine

–– IndinavirIndinavir

–– Others : SilicateOthers : Silicate

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ClassificationClassification

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Calcium StoneCalcium Stone

1.1.HypercalciuriaHypercalciuria

2.2.HyperoxaluriaHyperoxaluria

3.3.HyperuricouriaHyperuricouria

4.4.HypocitraturiaHypocitraturia

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1.Hypercalciuria1.Hypercalciuria

•• Absorptive Absorptive HypercalciuriaHypercalciuria

•• Renal Renal HypercalciuriaHypercalciuria

•• ResorptiveResorptive HypercalciuriaHypercalciuria

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Absorptive Absorptive hypercalciuriahypercalciuria

Serum Pi 1:25 (OH)2 D3Non-vitamin D factors

Jejunal calcium absorption

Serum Calcium (high normal)

Filtered calcium

Urinary calcium excretion

PTH

Renal tubular reabsorption

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Renal Renal HypercalciuriaHypercalciuria

Renal calcium leak

Serum calcium

PTH

1:25 (OH)2 D3

Intestinal calcium absorption

Functional tubular defect

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ResorptiveResorptive HypercalciuriaHypercalciuria

• Hyperparathyroidism

• Excessive PTH-dependent bone resorption

• Enhanced intestinal absorption of calcium

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2.Hyperoxaluria2.Hyperoxaluria

•• Primary Primary hyperoxaluriahyperoxaluria

•• Enteric Enteric hyperoxaluriahyperoxaluria

•• DietaryDietary hyperoxaluriahyperoxaluria

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Primary Primary hyperoxaluriahyperoxaluria

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Enteric Enteric HyperoxaluriaHyperoxaluria

•• Most common cause of Most common cause of hyperoxaluriahyperoxaluria

•• Associated with chronic Associated with chronic diarrhealdiarrheal statesstates

–– FFatat malabsorptionmalabsorption resultsresults inin sponificationsponification ofof

fattyfatty acidsacids withwith divalentdivalent cationscations

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Dietary Dietary HyperoxaluriaHyperoxaluria

•• Overindulgence in oxalateOverindulgence in oxalate--rich foodsrich foods

–– Nuts, chocolate, brewed tea, spinach, Nuts, chocolate, brewed tea, spinach,

broccoli, strawberries, and rhubarb broccoli, strawberries, and rhubarb

•• OxalobacterOxalobacter formigenesformigenes,, anan oxalateoxalate--

degradingdegrading intestinalintestinal bacteriumbacterium

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3.Hyperuricosuria3.Hyperuricosuria

•• HyperuricosuriaHyperuricosuria increases urinary levels increases urinary levels

of monosodium of monosodium urateurate, which in turn , which in turn

promotes calcium oxalate stone promotes calcium oxalate stone

formationformation

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4.Hypocitrauria4.Hypocitrauria

•• Citrate is an important inhibitor that can Citrate is an important inhibitor that can

reduce calcium stone formation reduce calcium stone formation

•• Reduces urinary saturation of calcium salts Reduces urinary saturation of calcium salts

by by complexingcomplexing with calcium with calcium

•• Directly prevents spontaneous nucleation Directly prevents spontaneous nucleation

of calcium oxalateof calcium oxalate

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CitrateCitrate

•• AcidAcid--base state is the primary determinant base state is the primary determinant

of urinary citrate excretionof urinary citrate excretion

•• Metabolic acidosis reduces urinary citrate Metabolic acidosis reduces urinary citrate

levels secondary to enhanced renal levels secondary to enhanced renal

tubular tubular reabsorptionreabsorption and decreased and decreased

synthesis of citrate in synthesis of citrate in peritubularperitubular cellscells

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Renal Tubular AcidosisRenal Tubular Acidosis

•• RTA is a clinical syndrome characterized RTA is a clinical syndrome characterized

by metabolic acidosis resulting from by metabolic acidosis resulting from

defects in renal tubular hydrogen ion defects in renal tubular hydrogen ion

secretion and urinary acidificationsecretion and urinary acidification

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RTARTA

•• ThereThere areare threethree typestypes ofof RTARTA

(1, 2 (1, 2 andand 4)4)

•• RTA occurs as a result of impairment RTA occurs as a result of impairment

of net excretion of acid into the urine of net excretion of acid into the urine

((type 1type 1) ) or of or of reabsorptionreabsorption of of

bicarbonate bicarbonate ((type 2type 2))

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RTARTA

•• The most common type of stone The most common type of stone

associated with distal RTA is associated with distal RTA is calcium calcium phosphatephosphate as a result of as a result of hypercalciuriahypercalciuria,,

hypocitraturiahypocitraturia,, andand increasedincreased urinaryurinary pHpH

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Uric acid StoneUric acid Stone

•• All mammals, except All mammals, except humans and humans and DalmatiansDalmatians, synthesize the enzyme , synthesize the enzyme uricaseuricase, ,

which catalyzes the conversion of uric acid which catalyzes the conversion of uric acid

to to allantoinallantoin, the end product of , the end product of purinepurine

metabolism metabolism

•• Because Because allantoinallantoin is 10 to 100 times more is 10 to 100 times more

soluble in urine than uric acid, humans are soluble in urine than uric acid, humans are

prone to uric acid stone formationprone to uric acid stone formation

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Relationship between Relationship between undissociatedundissociated

uric acid, total uric acid, and uric acid, total uric acid, and

urinary pHurinary pH

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Uric acid StoneUric acid Stone

•• The three main determinants of uric acid The three main determinants of uric acid

stone formation are low pH, low urine stone formation are low pH, low urine

volume, and volume, and hyperuricosuriahyperuricosuria

•• The most important The most important pathogeneticpathogenetic factor factor

is is low urine pHlow urine pH

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PathophysiologyPathophysiology

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CystineCystine StoneStone

•• CystineCystine stonesstones areare rarerare,, occurringoccurring inin thethe

UnitedUnited StatesStates andand EuropeEurope withwith anan

incidenceincidence ofof onlyonly 11 inin 1,0001,000 toto 11 inin 17,00017,000–– InIn childrenchildren,, cystinuriacystinuria isis thethe causecause ofof upup toto

10%10% ofof allall stonesstones

•• AutosomalAutosomal recessive recessive

–– Two genes involved in the disease have been Two genes involved in the disease have been identified, identified, SLCSLC33AA11 and and SLCSLC77AA99

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Infection StoneInfection Stone

•• Magnesium ammonium phosphate Magnesium ammonium phosphate hexahydratehexahydrate ((MgNHMgNH44POPO44 •• 6H6H22O)O)

•• IInfectionnfection withwith ureaseurease--producingproducing bacteriabacteria

isis a a prerequisiteprerequisite forfor thethe formationformation ofof

infectioninfection stonesstones

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Infection StoneInfection Stone

•• The most common The most common ureaseurease--producing producing pathogens are pathogens are ProteusProteus,, KlebsiellaKlebsiella,,PseudomonasPseudomonas,, and Staphylococcus and Staphylococcus speciesspecies

withwith Proteus mirabilisProteus mirabilis thethe mostmost commoncommon

organismorganism associatedassociated withwith infectioninfection stonesstones

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StruviteStruvite StoneStone•• Infection stoneInfection stone

–– Female > Male (2:1)Female > Male (2:1)

–– RadiopaqueRadiopaque: : StaghornStaghorn calculicalculi

•• Treatment requires eradication of Treatment requires eradication of

infection and stone removalinfection and stone removal

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Miscellaneous StonesMiscellaneous Stones

•• XanthineXanthine and and DihydroxyadenineDihydroxyadenine StonesStones

•• Ammonium Acid Ammonium Acid UrateUrate StonesStones

–– Laxative abuse, recurrent urinary tract Laxative abuse, recurrent urinary tract

infection, recurrent uric acid stone infection, recurrent uric acid stone

formation, and inflammatory bowel diseaseformation, and inflammatory bowel disease

•• Matrix StonesMatrix Stones

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MedicationMedication--Related StonesRelated Stones

•• Calcium stoneCalcium stone

–– Loop diuretic Loop diuretic ((furosemidefurosemide, , bumetanidebumetanide)), ,

acetazolamideacetazolamide, , topiramatetopiramate, and , and

zonisamidezonisamide

•• Ephedrine, Ephedrine, TriamtereneTriamterene, , GuaifenesinGuaifenesin, ,

Silicate, Silicate, IndinavirIndinavir, Ciprofloxacin , Ciprofloxacin

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Approach to the patientsApproach to the patients

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Evaluation of stone formersEvaluation of stone formers

•• Patients presented with acute flank painPatients presented with acute flank pain

–– Loin painLoin pain

–– VomittingVomitting

–– Mild feverMild fever

•• Patients with established Patients with established nephrolithiasisnephrolithiasis

(metabolic evaluation)(metabolic evaluation)

–– Medical management to prevent recurrence Medical management to prevent recurrence

after a 1after a 1stst stone episode is not most stone episode is not most

effectiveeffective

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Indications for a Metabolic Stone Indications for a Metabolic Stone

EvaluationEvaluation

•• Recurrent stone formersRecurrent stone formers

•• Strong family history of stonesStrong family history of stones

•• Intestinal disease (chronic diarrhea)Intestinal disease (chronic diarrhea)

•• Pathologic skeletal fracturePathologic skeletal fracture

•• OsteoporosisOsteoporosis

•• HxHx of UTI with calculiof UTI with calculi

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Indications for a Metabolic Stone Indications for a Metabolic Stone

Evaluation Evaluation

•• Personal Personal HxHx of goutof gout

•• Infirm healthInfirm health

•• Solitary kidneySolitary kidney

•• Anatomic abnormalitiesAnatomic abnormalities

•• Renal insufficiencyRenal insufficiency

•• Stone composed of Stone composed of cystinecystine, uric acid , uric acid

or or struvitestruvite

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Dietary ModificationDietary Modification

•• High fluid intakeHigh fluid intake

•• Decrease intake of animal proteinDecrease intake of animal protein

•• Normal calcium intakeNormal calcium intake

•• Restrict salt intakeRestrict salt intake

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Dietary ModificationDietary Modification

•• Decrease dietary oxalateDecrease dietary oxalate

•• Cranberry juiceCranberry juice

•• Ascorbic acidAscorbic acid

•• Potassium & magnesiumPotassium & magnesium

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Acute flank painAcute flank pain

•• HistoryHistory

–– Family history of Family history of nephrolithiasisnephrolithiasis

–– Previous history of Previous history of nephrolithiasisnephrolithiasis

–– Recent dehydrationRecent dehydration

–– Recurrent UTIRecurrent UTI

–– Recurrent flank pain with N/VRecurrent flank pain with N/V

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Acute flank painAcute flank pain

•• Physical examinationPhysical examination

–– Flank, testicular or labial tendernessFlank, testicular or labial tenderness

–– No rebound tendernessNo rebound tenderness

–– Normal or mildly decreased bowel soundNormal or mildly decreased bowel sound

–– FeverFever

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Acute flank painAcute flank pain

•• Lab investigationLab investigation

–– CBCCBC

–– UA : UA : hematuriahematuria, pH, Crystal, pH, Crystal

–– Imaging : Imaging :

•• Plain KUB : initial screening Plain KUB : initial screening

•• IVP : obstruction, anatomical abnormalities IVP : obstruction, anatomical abnormalities

•• USG : nonUSG : non--opaque stone, obstruction opaque stone, obstruction

•• CT scan : nonCT scan : non--opaque stone, opaque stone, obstuctionobstuction

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Pain Pain ManagamentManagament

•• Treatment should be Treatment should be stratedstrated with with

NSAIDsNSAIDs

–– Inhibition of prostaglandin synthesisInhibition of prostaglandin synthesis

–– Reduce collecting system pressureReduce collecting system pressure

–– Reduction in renal blood flowReduction in renal blood flow

•• Narcotic analgesicsNarcotic analgesics

–– Rescue pain is not controlled adequately Rescue pain is not controlled adequately

with with NSAIDsNSAIDs or adjunct to or adjunct to NSAIDsNSAIDs therapytherapy

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Surgical Management Surgical Management

of of UrolithasisUrolithasis

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IntroductionIntroduction

•• PCNL, URS, ESWL has almost PCNL, URS, ESWL has almost

eliminate openeliminate open stone surgerystone surgery (OSS)(OSS)

•• Goal: Maximal stone clearance with Goal: Maximal stone clearance with

minimal morbidity minimal morbidity

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Renal calculiRenal calculi

Optional treatment :Optional treatment :

1.1. ESWLESWL

2.2. PCNLPCNL

3.3. Retrograde ureteroscopic intrarenal Retrograde ureteroscopic intrarenal

surgery (RIRS)surgery (RIRS)

4.4. Sandwich techniqueSandwich technique

•• PCNL+ESWLPCNL+ESWL

•• RIRS + ESWLRIRS + ESWL

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Simple renal calculiSimple renal calculi

•• 8080--85 % success by ESWL85 % success by ESWL

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ESWLESWL

•• Poor result factorsPoor result factors

1.1.Large renal calculi (>22.2 mmLarge renal calculi (>22.2 mm22))

2.2.Stone within dependent or obstructed Stone within dependent or obstructed

portion of the collecting systemsportion of the collecting systems

3.3.Stone compositionStone composition

––Calcium oxalate monohydrateCalcium oxalate monohydrate

––BrushiteBrushite

4.4.ObesityObesity

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Nonstaghorn calculi, ESWLNonstaghorn calculi, ESWL

•• ComplicationComplication

–– SteinstrasseSteinstrasse

•• Stone > 3 cm (8%)Stone > 3 cm (8%)

•• Success rateSuccess rate

–– < 10 mm< 10 mm 79.9% 79.9%

–– 1010--20 mm20 mm 64%64%

–– > 20 mm> 20 mm 53.7%53.7%

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Staghorn calculiStaghorn calculi

•• Pelvic stone + 2 extended Pelvic stone + 2 extended calycealcalyceal

groupsgroups

•• Most : Most : StruviteStruvite stonestone

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Staghorn calculiStaghorn calculi

•• Staghorn stoneStaghorn stone

–– 10 year mortality10 year mortality

•• Untreated stoneUntreated stone 28%28%

•• Treated stoneTreated stone 7.2%7.2%

–– CRFCRF

•• Untreated stoneUntreated stone 36%36%

•• Treated stoneTreated stone 28%28%

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Surgical managementSurgical management

1.1. Open stone surgeryOpen stone surgery

•• Stone free rateStone free rate 85%85%

•• Stone recurrence Stone recurrence 30% (6yr)30% (6yr)

2.2. PCNL+/PCNL+/-- ESWLESWL

•• Stone free rateStone free rate 85%85%

3.3. ESWLESWL

•• Stone free rateStone free rate 51.2%51.2%

•• Auxiliary procedure 30.5%Auxiliary procedure 30.5%

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Surgical managementSurgical management

GuidelineGuideline

•• PCNL+/PCNL+/-- ESWL ESWL

–– First line management First line management

of staghorn calculiof staghorn calculi

•• ESWL, OSSESWL, OSS

–– Not to be first line Not to be first line

managementmanagement

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Renal stone 1-2 cm

Lower pole All other sites

ESWL or PCNL ESWL

PCNLESWL

> 2 cm< 1 cm

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Ureteric stoneUreteric stone

•• Width of stone is the most importance Width of stone is the most importance factor of spontaneous passagefactor of spontaneous passage–– < 4 mm : 80%< 4 mm : 80%

–– 44--6 mm : 59%6 mm : 59%

–– > 6 mm : 21%> 6 mm : 21%

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Proximal ureteric stoneProximal ureteric stone

•• Stone < 1cmStone < 1cm–– ESWLESWL 84%84%

–– URSURS 56%56%

•• Stone > 1 cmStone > 1 cm

–– ESWLESWL 72%72%

–– URSURS 44%44%

•• ComplicationComplication–– ESWLESWL 4%4%

–– URSURS 11%11%

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Proximal ureteric stoneProximal ureteric stone

•• Stone < 1cmStone < 1cm

–– ESWLESWL

•• Stone > 1 cmStone > 1 cm

–– ESWLESWL

–– URSURS

–– PCNLPCNL

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Distal ureteric stoneDistal ureteric stone

•• Not be used as a primary approachNot be used as a primary approach

–– Blind basketBlind basket

–– OSSOSS

•• Acceptable optionAcceptable option

–– ESWLESWL

–– URSURS

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Ureteral calculus stone location

Any size

ESWL in situor ureteroscopic treatmentUreteroscopic treatment

or ESWL in situ

ESWL in situ

> 1.5 cm< 1.5 cm

Stone size

Proximal ureter Distal ureter

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Ureteric stoneUreteric stone

•• Laparoscopic ureterolithotomyLaparoscopic ureterolithotomy

–– Failed ESWL / URSFailed ESWL / URS

–– Stone > 1.5 cmStone > 1.5 cm

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MethodMethod

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ResultResult

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ResultResult

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Bladder calculiBladder calculi

•• 5% of all urinary calculi5% of all urinary calculi

•• Risk factorsRisk factors

–– BOOBOO

–– NeurogenicNeurogenic bladderbladder

–– FBFB

–– Bladder Bladder diverticulumdiverticulum

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Bladder calculiBladder calculi

•• CompositionComposition

–– Struvite stoneStruvite stone

–– Calcium oxalateCalcium oxalate

–– Uric acid stonesUric acid stones

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TreatmentTreatment

•• CystolitholapaxyCystolitholapaxy

–– ContraindicationContraindication

•• Small bladder Small bladder

capacitycapacity

•• Multiple stonesMultiple stones

•• > 2 cm> 2 cm

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TreatmentTreatment

•• Small stonesSmall stones•• EHLEHL

•• PneumaticPneumatic

•• HolmiumHolmium

•• Large stonesLarge stones•• CystolithotomyCystolithotomy

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Knowledge

•• Smith's General Urology Smith's General Urology -- 17th Ed17th Ed. (. (2008)2008)

•• CampbellCampbell--Walsh Urology Walsh Urology –– 9th Ed. (2007)9th Ed. (2007)