Seminar renal stone on 24.10.16
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Transcript of Seminar renal stone on 24.10.16
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.
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.
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.
• Urolithiasis- stone in urinary tract.• Nephrolithiasis- stone in renal tissue.• Nephrocalcinosis- deposition of calcium in the substance of the kidney.
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.
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.
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.
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.
Inhibitors and promotors of stone formationINHIBITORSInhibits crystal Growth - Citrate Magnesium Pyrophosphate ZincInhibits crystal Aggregation Glycosaminoglycans Tamm- Horsfall Protein
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
Stone formation• Stone formation depends on four factors:1. Matrix2. Precipitation-crystallization3. Epitaxy 4. Absence of inhibitors of stone
formation in the urine
TYPES OF KIDNEY STONES Calcium oxalate
Calcium phosphate
Struvite
Uric acid
Cystine
Fig: staghorn calculi
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.
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.
RISK FACTORSHIGH MINERAL CONTENT IN DRINKING WATER
DEHYDRATION
FAMILY OR PERSONAL HISTORY
DIETARY INTAKE
BEING OBESE
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.
Approach to diagnosis of renal stone
Approach to renal stone1. Detailed history 2. Clinical examination3. Relevant Investigations
HISTORY
• Age – uncommon in children.• Sex- more common in male (3:1)• Geography -More in southeast Asia.• Climatic & geographic factors• Occupation – sedentary lifestyle.
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
• 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.
• An underlying metabolic abnormality –
symptoms of thirst polyuria, anorexia, muscle cramps,
abdominal & bone pain• Evaluation of growth & development, bone structure, blood pressure.
Presentation• Factors
–Size of stone–Location of stone–Degree of obstruction–Presence of infection–Presence/absence of normal contralateral kidney
Clinical feature:
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 .
Ureteric Calculus
1.Always of Renal Origin
2.Commonly of elongated shape
3.Can get impacted at 3 constrictions of ureter
4.Can cause: ObstructionHydronephrosisInfectionUreteral Stricture
5.C/F:Colicky Pain (from loin to tip genitalia)
Hematuria, dysuria, frequency, strangury
Tenderness in iliac fossa
Bladder Calculus1.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
Urethal stone:• Dysuria
• Inability to void/difficulty voiding.
• Present with terminal hematuria
• It is uncommon to pass urethral calculus
without symptoms
Investigations for Urolithiasis:• 1.Imaging
Plain X-ray
Ultrasonography
IVU
CT abdomen
• 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.
PH
BLOOD for• Urea
• Creatinine
• Electrolytes
• PH
• HCO3
• Ca
• Phosphorus
• Uric acid
• Citrate
• Cystine
• CBC
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%
X-ray findings:
75% radiopaque
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
Imaging: IVU• Provide anatomical and functional informations
• Size and location of the stone
• Presence and severity of obstructions
• Renal and ureteral abnormalities
IVU:
CT Scan Renal StoneOn 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
Urine analysis:
Normal urinary excretion of important constituents:Constituent
24hrs excretion
Ca Less than 4mg/KgProtein Less than 100mg/m2
Oxalate
Less than 2mg/Kg
Mg More than 0.8mg/KgUric 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
Creatinine
Newborn: 8-10mg/KgChild: 15-20mg/Kg
Na More than 3000mg/1.73m2
Phosphorus
Less than 1100mg/1.73m2
Method of stone analysis
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
of 10N NaOH add gradually.
Gelatinous PPt.
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
Na2 PO4 0.1M
Gelatinous
white PPt.
How to Investigate Urolithiasis??Urine- RME- 24 hour
urine collection
- Urine C+S
Blood- CBC- Renal
Profile
Imaging- KUB X-
ray- KUB
Ultrasound
- IVU
Plan for Intervention- DTPA
If IVU contraindicated- CTU
Algorithm for the investigation of renal calculi:
Stone
HypercalciuriaHyperoxaluria(primary/
enteric)Hypocitraturia
Increased urinary cystine(cystinuria)
Hyperuricaemia(IEM,Diuretic)
Hyperuicosuria(IEM,TLS,Chr.diarrhea)Infection
Passed
In urina
ry tract
MgNH4 PO4
Paediatric urologist
HypercalcemiaMetabolic
acidosis(DRTA,PRTA)Hypokalaemia(RTA,Bartt
er’s)Hypochloremia
Hypomegnesaemia
Captured
Ca phospha
teCa
OxalateCystine
Uric acid
Not captured
Metabolic evaluation
Not captured
Algorithm for investigation of Hypercalciuria:Hypercalcae
mia
Hypophosphatasia
vit D excessImmobilization
malignancyhyperparathyroid
ism
Yes
No
No
Metabolic acidosis
Metabolic alkalosis
No
Yes
Yes
Rickets,GF,
aminoaciduria,
glycosuria,
acidosisHyperchloraemia,urinary pH
6
Proximal RTA,Fanconi’s
Syndrome,Tubulo-interstitial disorder
Distal RTA
Bartter’s syndrome,loop diureticsIdiopathic
hypercalciuria, immobilization ,Juvenile chronic
arthritisDent’s diseaseMedullary sponge
kidneyHaematuria,UTI,dilated
tubules on IVP
Low mol. Wt.
proteinuria,fam his
Electrolytes,
urinalysis NAD
Case:Siam,6months old boy presented with passage of sand like substance during micturition and not growing well since his 2months of age.
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.
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.