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Management Of Acute Renal Injury In Pediatrics

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Lecture given byProf Sonia Elsharkawy Head of pediatric department Suez canal university at our Port Said fifth neonatology conference

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Management Of Acute Renal Injury In Pediatrics

  1. 1. Management Of Acute Renal Injury In Pediatrics Prof Sonia Elsharkawy Head of pediatric department Suez canal university
  2. 2. Objectives
  3. 3. Acute renal failure. • •DDeeffiinniittiioonn ooff AARRFF.. • Classification of ARF. • Causes of ARF. • Symptoms & sings Of ARF. • Diagnosis Of ARF.& prevention
  4. 4. Indications and goals for acute renal replacement therapy • Modalities for renal replacement therapy – Peritoneal dialysis – Intermittent hemodialysis – Continuous renal replacement therapy (CRRT) Special issues related to the infant
  5. 5. TThhee PPrroobblleemmaattiicc DDeeffiinniittiioonn ooff AARRFF • The Conceptual Definition of Acute Renal Failure: – “Sudden loss of renal function resulting in the loss of the kidneys’ ability to regulate electrolyte and fluid homeostasis”
  6. 6. TThhee PPrroobblleemmaattiicc DDeeffiinniittiioonn ooff AARRFF • Pediatric AKI definition: a moving target • Infants – Cr in the first few weeks of life may reflect maternal values • Children – Low baseline Cr makes 0.2-0.3 changes in Cr significant – Varying muscle mass • Adolescents – Similar to adults
  7. 7. ARF • Pre renal (functional) • Renal-intrinsic (structural) • Post renal (obstruction)
  8. 8. ARF Pirouz Daeihagh, M.D.Internal medicine/Nephrology Wake Forest University School of Medicine. Downloaded 4.6.09
  9. 9. Causes of ARF Pre-renal Renal Post-renal Absolute Glomerular hypovolaemia (RPGN) Pelvi-calyceal Relative hypovolaemia Tubular (ATN) Ureteric Reduced cardiac output Interstitial (AIN) VUJ-bladder Reno-vascular occlusion Vascular (atheroemboli) Bladder neck-urethra
  10. 10. ARF Pre renal •Decreased renal perfusion without cellular injury – 70% of community acquired cases – 30% hospital acquired cases
  11. 11. ARF Intrinsic • Acute tubular necrosis (ATN) – Ischaemia – Toxin – Tubular factors • Acute interstitial Necrosis (AIN) – Inflammation – oedema • Glomerulonephritis (GN)
  12. 12. ARF Post renal • Post renal obstruction • Obstruction to the urinary outflow tract Blocked catheter – Malignancy
  13. 13. Contrast-Induced ARF • Prevalence • Less than 1% in patients with normal renal function • Increases significantly with renal insufficiency
  14. 14. Contrast-Induced ARF • Risk Factors • Renal insufficiency • Diabetes mellitus • Multiple myeloma • High osmolar (ionic) contrast media • Contrast medium volume
  15. 15. Contrast-induced ARF Clinical Characteristics • Onset - 24 to 48 hrs. after exposure • Duration - 5 to 7 days • Non-oliguric (majority) • Dialysis - rarely needed • Urinary sediment - variable • Low fractional excretion of Na
  16. 16. Contrast-induced ARF Prophylactic Strategies • Use I.V. contrast only when necessary • Hydration • Minimize contrast volume • Low-osmolar (nonionic) contrast media • N-acetylcysteine.
  17. 17. PPeeddiiaattrriicc MMooddiiffiieedd RRIIFFLLEE---- ddeeffiinniittiioonn GFR per Schwartz equation: GFR= Ht (cm) X constant / serum creat (mg/dl) Pediatric Modified RIFLE Criteria CrCl Urine output Risk GFR decrease by 25% <0.5ml/kg/hour for 8 hours Injury GFR decrease by 50% <0.5ml/kg/hour for 16 hours Failure GFR decrease by 75% or GFR<35ml/min/1.73m 2 Ackan-Arikan et al: Kid Int 2010 <0.3 ml/kg/hour for 24 hours or anuric for 12 hours Loss Persistent ARF > 4 weeks End stage End Stage Renal Disease (>3 months)
  18. 18. Acute Kidney Injury AKI can be prevented by early recognition and treatment of the underlying cause, for example: -Early treatment of infections/sepsis – Early treatment/prevention of dehydration – Correcting hypovolaemia
  19. 19. Monitoring use of drugs such as NSAIDs and ACE inhibitors, especially if a patient is acutely unwell • Taking care with at-risk patients who need iodinated contrast agents with scans
  20. 20. BIOMARKERS
  21. 21. Biomarkers ffoorr AAccuuttee KKiiddnneeyy IInnjjuurryy • Ideally AKI would have a biomarkers like myocardial infarction (i.e. troponin-1) • Currently no Troponin-I like marker to identify the site or severity of injury, although various markers are being evaluated
  22. 22. – Kidney Injury Molecule (KIM-1) – Neutrophil gelatinase-associated lipocalcin (NGAL) – IL-18 – Cystatin C (Changes in SCr may be a very late indicator of renal injury)
  23. 23. AKI in the ICU • Treatment of acute kidney injury (AKI) is principally supportive -- renal replacement therapy (RRT) indicated in patients with severe kidney injury. • Goal: optimization of fluid & electrolyte balance
  24. 24. Observations and assessment Use an early warning score that recognises and responds to deterioration and acute illness Staff should have competencies in: • Monitoring • Measurement • Interpretation
  25. 25. Neonatal Renal Failure In term neonates, renal failure is suspected when the plasma creatinine concentration is greater than 15 mg/L, for at least twenty four to forty eight hours, while maternal renal function is normal
  26. 26. Incidence  Precise incidence and prevalence of ARF in the newborn is unknown , 6%- 24% (Andreoli, 2013).  In developing countries, the incidence and epidemiology of acute renal failure in newborns was 3.9% of 1.000 live births and 34.5% of 1.000 newborns admitted to the neonatal unit (Andreoli, 2013).
  27. 27. The mortality of acute renal failure is still very high (30%- 60%) (Drukker & Guingard, 2012).
  28. 28. Etiology  Variety of congenital, developmental, and acquired conditions (Mercado-Deane et al, 2012).  Prenatal injury/vascular damage: - Maternal - Congenital renal diseases  Postnatal: 1- Prerenal: - Decreased true intravascular volume - Decreased effective intravascular volume 2- Intrinsic: -ATN -Interstitial nephritis 3- Postrenal (obstructive)
  29. 29. Management  IImmmmeeddiiaattee MMeeaassuurreess:: 11-- volume trials. 2- Diuretics 3- Dopaminergic (Vasoactive) Agents  CCoonnsseerrvvaattiivvee ttrreeaattmmeenntt..  RReennaall rreeppllaacceemmeenntt tthheerraappyy  RReennaall TTrraannssppllaannttaattiioonn
  30. 30. Indications for Renal Replacement • Volume overload • Metabolic imbalance • Toxins (endogenous or exogenous) • Inability to provide needed daily fluids due to insufficient urinary excretion
  31. 31. Goals of Renal Replacement • Restore fluid, electrolyte and metabolic balance • Remove endogenous or exogenous toxins as rapidly as possible • Permit needed therapy and nutrition • Limit complications
  32. 32. R R T Includes: •Traditional intermittent hemodialysis, • Peritoneal dialysis • Variety of other intermittent and continuous therapy, •Renal transplant
  33. 33. Indications to start RRT • Anuria – oliguria(diuresis <200 ml in 12 hr) • Severe metabolic acidosis(pH<7.10) • Hyperazotemia(BUN> 80mg/dl) or creatinine >4mg/dl • Hyperkalemia K >6.5mEq/l • Clinical signs of uremic toxicity
  34. 34. • Severe dysnatremia Na<115 or Na>160mEq/l • Hyperthermia (>40 deg.C without response to medical therapy) • Anasarca or severe fluid overload • Multiple organ failure with renal dysfunction and /SIRS, sepsis, or septic shock with renal dysfunction
  35. 35. BUT • The optimal timing of RRT for AKI is not defined • Timing of renal replacement therapy initiation in acute renal failure: a meta-analysis
  36. 36.  Meta-analysis of randomized trials, early RRT was associated with a nonsignificant 36% mortality risk reduction (RR, 0.64; 95% confidence interval, 0.40 to 1.05; P = 0.08)  In cohort studies, early RRT was associated with a statistically significant 28% mortality risk reduction (RR, 0.72; 95% confidence interval, 0.64 to 0.82; P < 0.001). • Seabra VF, Balk EM, Liangos O, Sosa MA, Cendoroglo M, Jaber BL. Am J Kidney Dis. 2012;52:272–284
  37. 37. when IInniittiiaattee RRRRTT EEmmeerrggeennttllyy Life-threatening changes in fluid Electrolyte Acid-base balance Uremic complications: pericarditis, pleuritis, encephalopathy, coagulopathy Kidney Disease: Improving Global Outcomes (KDIGO), 2012
  38. 38. Technique and modalities
  39. 39. Technique and modalities • All RRT consist of blood purification by having the blood flow through SPM. • Blood flow into hollow fibers composed by biocompatible synthetic materials.
  40. 40. • Wide range of substances( water , urea,and low, middle and high mol.wt. solutes)allow the blood across such membranes by diffusion (solutes) and by convection(solute and water)
  41. 41. Modalities for Renal Replacement • Hemodialysis. • Peritoneal dialysis. • Continuous renal replacement therapy (CRRT) • Heamofiltiration. • Renal replacement.
  42. 42. Principles of dialysis • Dialysis = diffusion = passive movement of solutes across a semi-permeable membrane down concentration gradient – Good for small molecules • (Ultra)filtration = convection = solute + fluid removal across semi-permeable membrane down a pressure gradient (solvent drag) – Better for removal of fluid and medium-size molecules Faber. Nursing in Critical Care 2009; 14: 4 Foot. Current Anaesthesia and Critical Care 2005; 16:321-329
  43. 43. Principles of dialysis  Hemodialysis = solute passively diffuses down concentration gradient  Dialysate flows countercurrent to blood flow.  Urea, creatinine, K move from blood to dialysate  Ca and bicarb move from dialysate to blood.  Hemofiltration: uses hydrostatic pressure gradient to induce filtration / convection plasma water + solutes across membrane.  Hemodiafiltration: combination of dialysis and filtration.
  44. 44. Intermittent hemodialysis (IHD) • Oldest and most common technique • Primarily diffusive treatment: blood and dialysate are circulated in countercurrent manner • Best for removal of small molecules • typically performed 4 hours 3x/wk or daily
  45. 45. Continuous RRT Introduced in 1980s • involve either dialysis (diffusion-based solute removal) or filtration (convection-based solute and water removal) treatments in a continuous mode with slower rate of solute or fluid removal • CRRT includes continuous hemofiltration, hemodialysis and hemodiafiltration, all of which can be performed using arteriovenous or venovenous extracorporeal circuits.
  46. 46. Peritoneal dialysis Considerations for Infants ADVANTAGES • No vascular access • No extracorporeal perfusion • Simplicity • ? Preferred modality for cardiac patients? DISADVANTAGES • Infectious risk • Leak • ? Respiratory compromise?
  47. 47. Intermittent hemodialysis Considerations for Infants ADVANTAGES • Rapid particle and fluid removal; most efficient modality • Does not require anticoagulation 24h/d DISADVANTAGES • Vascular access • Complicated • Large extracorporeal volume • Adapted equipment • ? Poorly tolerated
  48. 48. Pediatric CRRT: Vicenza, 1984
  49. 49. CRRT for Infants: A Series of Challenges • Small patient with small blood volume • Equipment designed for bigger people • No specific protocols • Complications may be magnified • No clear guidelines • Limited outcome data
  50. 50. Potential Complications of Infant CRRT • Volume related problems • Biochemical and nutritional problems • Hemorrhage, infection • Thermic loss • Technical problems • Logistical problems
  51. 51. Role of RRT in different clinical situations • Sepsis • Congestive heart failure •Miller's Anesthesia, 7th ed. 2009
  52. 52. RRT in congestive heart failure • Slow continuous ultrafiltration (SCUF) effective for fluid removal in decompensated CHF.. Costanzo et al J Am Coll Cardiol 2010 49:675-683.
  53. 53. Discontinuation of RRT • Until “evidence of recovery of kidney function” – Improved UOP in oliguria – Decreasing creatinine – Creatinine clearance minimum 12 mL/min, some say 20 mL/min
  54. 54. Thanks!

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