![Test Procedure Observation
1- pH
Sample + 1 drop of universal
indicator
Yellow- red:
Acidic
Green: Neutral
Blue: Alkaline
2-Carbonate Sample + 2 drops of 2N HCL Effervescence
3-Oxalate Sample mixed with equal
portion of resorcinol +1 drop
of conc. Sulphuric acid
Dark blue green
color
4-Phosphate Sample + mixture of [2 drops
of cobalt chloride + 2 drops
of Na CN ]+ 1 drop of 10N
NaOH
Blue color
5-Calcium Sample + 2 drops of H2O + 2
drops of 2N HCL + 5 drops
Gelatinous PPt.](https://image.slidesharecdn.com/seminarrenalstoneon24-170206025912/85/Seminar-renal-stone-on-24-10-16-45-320.jpg)
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Similar to Seminar renal stone on 24.10.16 (20)
Seminar renal stone on 24.10.16
- 1. EVALUATION OF RENAL STONE IN CHILDREN Presented By- DR. AZMERY SAIMA DR. RAKHI MAITRAYEE BHOWMIC PHASE A ( NEONATOLOGY) Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka.
- 2. Case scenario • A 15 year old boy admitted in hospital with the complaints of severe left flank pain , haematuria for 10 days. But patient has no fever, gave history of inadequate fluid intake. Family history of nephrolithiasis positive.
- 3. INTRODUCTION Kidney Stones, also known as renal calculus or nephrolith, are small, hard deposits of mineral and acid, salts on the inner surfaces of the kidneys. If stones grow to sufficient size they can cause blockage of the ureter.
- 4. • Urolithiasis- stone in urinary tract. • Nephrolithiasis- stone in renal tissue. • Nephrocalcinosis- deposition of calcium in the substance of the kidney.
- 5. EPIDEMIOLOGY • Urinary lithiasis in children is related to genetic, climatic, dietary & socioeconomic factors. • The incidence is increasing : in 1996 the rate of symptomatic nephrolithiasis was 7.9 in 10000, whereas in 2007 it was 18.5 in 10000 . • Approximately 7% of urinary calculi occur in children younger than 16 year of age.
- 6. EPIDEMIOLOGY • The prevalence of pediatric urolithiasis in developed countries had fallen following improved socioeconomic condition, but currently is increasing. This may be explained by an increase in diagnosis secondary to improved diagnostic technique.
- 7. INCIDENCE Urinary calculi are more common in men than in women. (3:1) Incidence of urinary calculi peaks between the 3rd and 5th decades of life. 80% of stones under 2mm in size 90% of stones pass through the urinary system spontaneously There is seasonal variation with stone occurring more often in the summer months.
- 8. STONE FORMATION Highly concentrated urine constituents crystallize and harden to form calculi. Kidney stones form when urine contains more crystal- forming substances - such as calcium, oxalate and uric acid. At the same time, urine may lack substances that prevent crystals from sticking together, creating an ideal environment for kidney stones to form. The crystals get deposited on the nucleus and continue to grow. These can some times adhere to the renal papillae.
- 9. Inhibitors and promotors of stone formation INHIBITORS Inhibits crystal Growth - Citrate Magnesium Pyrophosphate Zinc Inhibits crystal Aggregation Glycosaminoglycans Tamm- Horsfall Protein
- 10. PROMOTERS Bacterial Infection Anatomic Abnormalities – PUJ obst. Altered Ca and oxalate transport in renal epithelium. Prolonged immobilisation. Increased uric acid levels - taking increased purine subs– promotes crystalisation of Ca and oxalate
- 11. Stone formation • Stone formation depends on four factors: 1. Matrix 2. Precipitation-crystallization 3. Epitaxy 4. Absence of inhibitors of stone formation in the urine
- 13. TYPES OF KIDNEY STONES Calcium oxalate Calcium phosphate Struvite Uric acid Cystine
- 16. Calcium stones: Most kidney stones are calcium stones, usually in the form of calcium oxalate and calcium phosphate. Oxalate is a naturally occurring substance found in food. Some fruits and vegetables, as well as nuts and chocolate, have high oxalate levels.
- 17. Uric Acid: This type of kidney stone is more common in men than in women. They can occur in people with gout or those going through chemotherapy. Struvite: This type of stone is found mostly in women with urinary tract infection. These stones can be quite large and cause urinary obstruction. Cystine: Cystine stones are rare. They occur in both men and women who have the genetic disorder cystinuria. Other: Other, rarer types of kidney stones also can occur. Such as xanthine, dihydroadenine stone, indinavir etc.
- 18. RISK FACTORS HIGH MINERAL CONTENT IN DRINKING WATER DEHYDRATION FAMILY OR PERSONAL HISTORY DIETARY INTAKE BEING OBESE
- 19. PATHOPHYSIOLOGY • Slow urine flow, resulting in super saturation of the urine. • Damage to the lining of the urinary tract • Decreased inhibitor substances in the urine that would otherwise prevent super saturation and crystalline aggregation.
- 20. Approach to diagnosis of renal stone
- 21. Approach to renal stone 1. Detailed history 2. Clinical examination 3. Relevant Investigations
- 22. HISTORY • Age – uncommon in children. • Sex- more common in male (3:1) • Geography -More in southeast Asia. • Climatic & geographic factors • Occupation – sedentary lifestyle.
- 23. HISTORY… Presentation is variable. • Children may present initially with- loin pain (50%),abdominal pain haematuria features of UTI, N, V dysuria, urgency, frequency may be asymptomatic
- 25. • Birth history- PT (12-64%), LBW, diuretics, duration of oxygen therapy. • Family history of nephrolithiasis, consanguinity • Past illness – similar type illness, IBD, Cystic fibrosis, malignancy. • Dietary history-Fluid intake, vitamin & mineral suplementation, tea, coffee, dairy products, spinach, beet, peanuts. • Personal history- immobility, bowel habit (cr. Diarrhoea). • Drug history-Loop diuretics, corticosteroid, is geeting chemotherapy.
- 26. • An underlying metabolic abnormality – symptoms of thirst polyuria, anorexia, muscle cramps, abdominal & bone pain • Evaluation of growth & development, bone structure, blood pressure.
- 27. Presentation • Factors –Size of stone –Location of stone –Degree of obstruction –Presence of infection –Presence/absence of normal contralateral kidney
- 29. Renal stone: • 1.Recurrent flank pain or renal colic occurs in 40-75% of children or Abdominal pain • 2.Gross or Microscopic hematuria in 33- 90% of children • 3.Repeated attack of UTI • 4.Occasionally the stone may be silent & leads to obstructive uropathy .
- 30. Ureteric Calculus 1. Always of Renal Origin 2. Commonly of elongated shape 3. Can get impacted at 3 constrictions of ureter 4. Can cause: Obstruction Hydronephrosis Infection Ureteral Stricture 5. C/F: Colicky Pain (from loin to tip genitalia) Hematuria, dysuria, frequency, strangury Tenderness in iliac fossa
- 31. Bladder Calculus 1. Primary vesical calculus: • occurs in sterile urine • Comes down from kidney through ureter and gets enlarged in bladder (usually oxalate stone). • Can irritate bladder mucosa causing hematuria 2. Secondary vesical calculus: • Occurs in presence of infection (commonest bladder stone) • Usually phosphate stone, occurs in bladder only
- 32. Urethal stone: • Dysuria • Inability to void/difficulty voiding. • Present with terminal hematuria • It is uncommon to pass urethral calculus without symptoms
- 33. Investigations for Urolithiasis: • 1.Imaging Plain X-ray Ultrasonography IVU CT abdomen
- 34. • URINE for Routine analysis(including & specific gravity) Culture Spot specimen: Ca, protein, uric acid, oxalate, citrate ,Mg, creatinine. 24hr urine: Volume, protein, creatinine, Na, Ca, Mg, oxalate, phosphorus, uric acid, citrate, cystine. • Stone analysis. P H
- 35. BLOOD for • Urea • Creatinine • Electrolytes • PH • HCO3 • Ca • Phosphorus • Uric acid • Citrate • Cystine • CBC
- 36. Imaging: Plain X-ray KUB • Not useful – Radioluscent stone – Stone <4mm – Lies over sacrum/bony structures • Bowel gas can obscure its efficacy • Cannot differentiate – Stones – Calcified LN • Sensitivity: 50-70%
- 38. Imaging: KUB Ultrasound • Sensitivity to detect renal calculi ~95% (complement KUBXR) • Very sensitive to detect obstruction and radioluscent stone,Hydronephrosis • Non-invasive • May miss small stone (<5mm) and ureteral stone
- 39. Imaging: IVU • Provide anatomical and functional informations • Size and location of the stone • Presence and severity of obstructions • Renal and ureteral abnormalities
- 40. IVU:
- 41. CT Scan Renal Stone On CT almost all stones are opaque(has 96% sensitivity& specificity), but vary considerably in density. 1. calcium oxalate +/- calcium phosphate: 400-600HU 2. struvite (triple phosphate): usually opaque but variable 3. uric acid: 100 - 200HU 4. cysteine: opaque 5. HIV medication related stones (indinavir) difficult to visualize
- 42. Urine analysis:
- 43. Normal urinary excretion of important constituents: Constit uent 24hrs excretion Ca Less than 4mg/Kg Protein Less than 100mg/m2 Oxalate Less than 2mg/Kg Mg More than 0.8mg/Kg Uric acid Less than 35mg/kg Cystine Below 10yrs :less than 13 mg/1.73m2 Above 10yrs :30-50 mg/1.73m2 Citrate More than 320 mg/1.73m2 Creatini ne Newborn: 8-10mg/Kg Child: 15-20mg/Kg
- 44. Method of stone analysis
- 45. Test Procedure Observation 1- pH Sample + 1 drop of universal indicator Yellow- red: Acidic Green: Neutral Blue: Alkaline 2-Carbonate Sample + 2 drops of 2N HCL Effervescence 3-Oxalate Sample mixed with equal portion of resorcinol +1 drop of conc. Sulphuric acid Dark blue green color 4-Phosphate Sample + mixture of [2 drops of cobalt chloride + 2 drops of Na CN ]+ 1 drop of 10N NaOH Blue color 5-Calcium Sample + 2 drops of H2O + 2 drops of 2N HCL + 5 drops Gelatinous PPt.
- 46. 6- Cystine Sample + 2 drops of NaOH 10% + 1 drop of amm. Hydroxide 25% + 2 drops of Na CN allow to stand for 5 min. + few crystals of sodium nitroprusside Red color 7- Ammonium salts Sample+ 2 drops NaOH 10% + 5 drops of cobalt chloride Blue color 8-Uric acid Sample + 2 drops of NaOH mix. + 3 drops of phosphotungestic acid Blue color 9- Magnesium Sample + 2 drops of NH4OH 25% + 2 drops Gelatinous white PPt.
- 47. How to Investigate Urolithiasis??Urine - RME - 24 hour urine collectio n - Urine C+S Blood - CBC - Renal Profile Imaging - KUB X- ray - KUB Ultrasoun d - IVU Plan for Intervention - DTPA If IVU contraindicate d - CTU
- 48. Algorithm for the investigation of renal calculi: Stone Hypercalciuria Hyperoxaluria(primary/enteri c) Hypocitraturia Increased urinary cystine(cystinuria) Hyperuricaemia(IEM,Diuretic ) Hyperuicosuria(IEM,TLS,Chr. diarrhea) Infection Passed In urina ry tract Mg NH4 PO4 Paedia tric urologi Hypercalcemia Metabolic acidosis(DRTA,PRTA) Hypokalaemia(RTA,Bartter’s ) Hypochloremia Hypomegnesaemia Captu red Ca phosphat e Ca OxalateCysti ne Uric acid Not captur ed Metabolic evaluation Not captured
- 49. Hypercalciuria: Hypercalcaem ia Hypophosphatasia vit D excess Immobilization malignancy hyperparathyroidis m Yes N o N o Metabolic acidosis Metabolic alkalosis N o Yes Yes Rickets,GF , aminoacid uria, glycosuria , acidosis Hyperchlor aemia,urina ry p H 6 Proximal RTA,Fanconi’s Syndrome,Tubulo- interstitial disorder Distal RTA Bartter’s syndrome,loop diuretics Idiopathic hypercalciuria, immobilization , Juvenile chronic arthritis Dent’s disease Medullary sponge kidney Haematuria,UTI,dilated tubules on IVP Low mol. Wt. proteinuria,f am his Electroly tes, urinalysi s NAD
- 50. Case:Siam,6months old boy presented with passage of sand like substance during micturition and not growing well since his 2months of age.
- 51. Nephrocalcinosis • Refers to renal parenchymal calcification. The calcification may be dystrophic or metastatic. 1.With dystrophic calcification, there is deposition of calcium in necrotic tissue. This type of parenchymal calcification occurs in tumors, abscesses, and hematomas. 2.Metastatic nephrocalcinosis occurs most often with hypercalcemic states caused by hyperparathyroidism, renal tubular acidosis, and renal failure. Metastatic nephrocalcinosis can be • further categorized by the location of calcium deposition as cortical or medullary.
- 52. Causes of Nephrocalcinosis • Causes of cortical nephrocalcinosis include 1. Acute cortical necrosis 2. Chronic glomerulonephritis 3. Chronic hypercalcemic states ethylene glycol poisoning, sickle cell disease, and rejected renal transplants • Causes of medullary nephrocalcinosis include 1. Hyperparathyroidism (40%) 2. Renal tubular acidosis (20%) 3. Medullary sponge kidney bone metastases, chronic pyelonephritis, cushing’s syndrome, hyperthyroidism, malignancy, renal papillary necrosis, vitamin D excess, and Wilson’s disease.