power point

1. DISCUSS THE AETIOPATHOGENESIS
AND TREATMENT OF UROLITHIASIS
Dr Sanusi A.A
Urology unit
Dept of surgery
JUTH

2. Outline
 Introduction
 Definition
 Epidemiology
 Classification
 Aetiopathogenesis
 Clinical presentation
 History
 Physical examination
 Investigation

3. Outline
 Treatment
 Prevention
 Peculiarity
 Conclusion
 References

4. Introduction
 Urinary stone disease/ calculus disease of
urinary tract
 It is a problem that has plagued humans since
antiquity
 Urinary stones have been seen in remains of
mummified Egyptians since 4800BC
 They can be found anywhere in the urinary
tract
 They display significant variations in
morphology

5. Epidemiology
 It has a worldwide distribution
 Prevalence is high in mountainous areas, deserts, &
tropical areas of the world
 Highest prevalence in India, Pakistan & middle east
 Incidence: 7—34/100 000(Nig); 2-3/100 (Western
Europe)
 M/F ratio-3:1
 Race : Whites>Blacks
 Peak incidence: 3rd –5th decades
 Bimodal incidence in female

9. Classification
 BASED ON: -
 Anatomic Location
 Nephrolithiasis
 Ureteric calculi
 Vesical calculi
 Prostatic calculi
 Urethrolithiasis

10. Classification
 Composition
 Oxalate stones
 Phosphate stones
 Uric acid & Urate stones
 Cystine stones
 Xanthine Stones

11. Classification
 Based on radiological properties
 Radio opaque- oxalate, phosphate, cystine
 Radiolucent- urate, xanthine, matrix
 Based on number
 Single
 multiple

12. Classification
 Oxalate stones (60%)
 Mainly calcium oxalates
 Formed in acidic urine
 Hard, irregular, spiculated
 Usually single
 Yellow– dark red
 Radio-opaque

13. Classification
 Phosphate stones (30%)
 Usually calcium phosphate /Others,(Ammonium,
Magnesium & or combined)
 Smooth
 Dirty white
 Formed in alkaline urine
 May take the shape of the structure in which it is
found. e.g. staghorn calculus
 Radio-opaque

14. Classification
 Uric acid & Urate stones
 Usually multiple, hard & smooth
 Yellow to purple
 Radio-lucent
 Found more in the bladder

15. Classification
 Cystine stone
 Multiple( may aggregate 2 form stag horn)
 Soft
 Yellow changes to green on exposure to light
 Radio-opaque

18. Risk factors
 Family history
 Genetic
 Diet
 Socio-economic factors
 Occupation
 Sedentary life style
 Climate
 Stasis
 Infection
 Medications

19. Aetiopathogenesis
• Supersaturation Theory
• Nucleation and crystal growth Theory
• Crystal Inhibition Theory
• Fixed particle Theory
• Matrix Theory

20. Aetiopathogenesis
 Supersaturation Theory
 The central event in the formation of stone is
supersaturation of urine
 Supersaturation depends on urinary pH, ionic strength,
solute concentration, and complexation
 Concept of conc. product (CP), solubility product (Ksp),
formation product (Kfp)
 Three major states of saturation in urine:
undersaturated, metastable, and unstable

22. Aetiopathogenesis
 Nucleation and crystal growth Theory
 Calculus originate from crystal or foreign body
immersed in supersaturated urine
 Magnesium and citrate inhibit crystal aggregation
 Crystallization can potentially occur when (CP) > (Ksp)
 In the presence of urinary inhibitors, precipitation
occurs only when supersaturation exceeds solubility
by 7 to 11 times

23. Aetiopathogenesis
 Crystal Inhibition Theory
 Calculi form owing to the absence or low
concentration of natural stone inhibitors
 E.g. pyrophosphates, citrate, Mg, Tamm-Horsfall
protein, uropontin, Nephrocalcin
 No absolute validity

24. Aetiopathogenesis
 Matrix Theory
 Non crystalline component (2-10%)
 Actual role unknown
 Nidus for crystal aggregation
 Inhibitory role
 An innocent bystander

25. Aetiopathogenesis
 Fixed particle Theory
 Presupposes an anchoring site to which crystals bind
 Oxalate-induced injury to renal tubular epithelial
cells
 Exact mechanism of oxalate-induced cell injury is
not known

26. Clinical presentation
 Asymptomatic.
 Accidental findings in the course of assessment of
an individual for some other pathological conditions
 Sometimes even for ordinary medical exams
 Symptomatic
 Acute
 Chronic
 Acute on chronic

27. Clinical presentation
 Major symptoms
 Pain
 Dysuria
 Haematuria
 Others
 LUTS
 Passage of stones
 Recurrent UTI
 Acute retention
 Features of renal impairment

28. Clinical presentation
 Minor symptoms
 Constitutional Changes.
 Fever
 Headache
 Loss of appetite
 Nausea and vomiting

29. Evaluation
 History
 Physical examination
 Investigations
 Laboratory
 Imaging

30. Investigations
 Laboratory
 Urinalysis
 Urine m/c/s
 Blood chemistry- ca, protein, phosphorus, uric acid,
creatinine, urea, ALP, PTH assay
 24 hr urine: volume, Ca, Mg, Phos., uric acid, oxalate
cystine, citrate, Na, & mean pH

31. Investigations
 Imaging
 Plain Abdominal X-ray/ K U B
 Ultrasound scan
 I.V.U
 CT scan (Non contrast spiral CT- gold standard)
 Urethrocystoscopy
 Retrograde Pyelography

33. IVU

34. Treatment
 Emergency presentation
 Analgesics, anti-spasmodics
 Antibiotics if there is evidence of infection
 Relief of obstruction
 Ureteral stent
 Percutaneous nephrostomy
 Adequate hydration
 When acute attack subsides
 Detail evaluation
 Specific treatment

35. Treatment
 Elective presentation
 General measures
 Watchful waiting
 Dietary control
 Medical
 Copious fluid intake
 Treat associated medical conditions
 Dietary control
 Use of drugs
 Surgical

36. Treatment: choice
 Stone factors
 Stone size
 Number
 composition
 Location
 Associated obstruction, hydronephrosis,
pelviureteric junction obstruction, calyceal
diverticulum

37. Treatment: choice
 Patient’s factors
 Obesity
 Body habitus/ deformity
 Infection
 Coagulopathy
 Elderly, juvenile
 Renal failure, solitary / transplanted kidney
 Pregnancy, urinary diversion
 Expectation and preference

38. Treatment: choice
 Institutional factors
 Equipment
 Personnel
 Cost

39. Treatment –General measures
 Liberal oral fluid intake
 Reduce animal protein=0.8-1.0/g/kg/day
 Reduce intake of oxalate rich foods
 Reduce Na intake =2-3g/day or 80-100mEq/day
 Reduce dairy product
 Avoid stone provoking drugs -calcitriol,
probenecid

40. Treatment: Watchful waiting
 At presentation, 66-75% of calculi are in the ureter,
of which 80% are in distal ureter
 10-15% of calculi are bilateral
 75-80% of calculi pass Spontaneously
 Indicated in calculi of <5mm
 Special Cases e.g. pregnancy

41. Treatment: Medical
 Involves Chemolysis & MET or combination
 Chemolysis involves use of oral or parenteral dissolution
agents, that alter urinary pH
 Uric acid, Cystine & Struvite stones are amenable to such
Rx
 E.g. Potassium citrate or Sodium citrate can be used to
alkalinize urine to pH 7.0-7.5 & cause dissolution of Uric
acid Stone
 Uric acid lowering medication

42. Treatment: Medical
 Medical Expulsive therapy involves use of certain
drug that relaxes tone of ureter
 Calcium blockers & alpha blockers are rec. by
EAU
 Specific e.g are Nifedipine, Tamsulosin,
Terazosin, & Doxazosin

43. Treatment: Surgical
 Indication for active removal
 Intractable pain
 Obstruction
 Symptomatic stone more > lcm in diameter in the
pelvis or calyx. It is unlikely to pass
 A small stone that causes repeated colic or
haematuria but shows no sign of passage on X-ray
 Infection

44. Treatment: Surgical
 Non invasive procedures
 Extra-Corporeal shock wave lithotripsy-ESWL
 Electromagnetic
 Piezoelectric
 Minimally invasive procedures
 Intra-corporeal lithotripsy
 Electrohydraulic
 Laser
 Ultrasonic
 Ballistic

45. Treatment: Surgical
 Minimally invasive procedures
 Percutaneous Nephrolithotomy-PCNL
 Ureteroscopy + Stone Extraction
 Endoscopic cystolitholapaxy

46. ECSWL

47. PCNL

48. Treatment: surgical
 Open surgery
 Approaches include;
 Pyelolithotomy
 Nephrolithotomy
 Nephrectomy
 Ureterolithotomy
 Cystolithotomy
 Urethrolithotomy if impacted

49. Impacted urethral stone

50. Prevention
 Increased fluid intake.
 Alkalinise urine for urate stones
 Acidify urine for calcium stones
 Identify predisposing factor espeacially
metabolic and treat e.g. gout

51. Peculiarity
 Cost
 Availability of facilities
 Late presentation

52. Conclusion
 Calculus dx quite common
 Long term follow-up is quite difficult
 Thus, medical mgt. Often difficult to practice
 Minimal access procedure for calculus removal not
readily available
 Hence, open surgery remains a regular means of
intervention

53. Conclusion
 Mgt of Urinary Calculi has undergone
tremendous revolution over the years
 Advances in treatment has outpaced
understanding of the aetiology
 It is hoped that modern approaches to its mgt
would be readily available to our teeming
population soonest

54. References
 Klufio G.O; Mbonu O.O; Kidneys and ureters in Badoe
E.A. Principle and practice of surgery including
pathology in the tropics, 4th ed. 2008; 45:853-858
• Christopher G.F. The kidneys and ureters, in Bailey and
Love’s short practice of surgery, 26th ed. 2013; 75:1292-
1298
• Freddie H. The urinary bladder, in Bailey and Love’s
short practice of surgery, 26th ed. 2013; 76:1320-1322
• Ian E. Urethral and penis, in Bailey and Love’s short
practice of surgery, 26th ed. 2013; 78:1367

55. References
 Marshall L.S; Urinary stone disease, in Smith’s General
Urology,17th ed. 2008; 16:264-277
 Margaret S.P, Yair L.; Urinary Lithiasais: Etiology,
Epidemiolgy, and Pathogenesis, in Campbell-Walsh
urology 10th ed. 2012; 45:1257-1286
 Michael N.F et al, Evaluation and Medical Management
of Urinary Lithiasis, in Campbell-Walsh urology 10th ed.
2012; 46:1287-1323
 Brian R.M, James E.L; Surgical Management of Upper
Urinary Tract Calculi, in Campbell-Walsh urology 10th
ed. 2012; 48:1357-1410

56. Thank you