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Acute renal failure in children,causes, investigation andmanagement,
- 2. AKI is also defined as Increased in serum creatinine > 0.3mg/dl from baseline within 48 hrs OR Increased serum creatinine >1.5 times base line within the previous 7 days OR Urine volume < 0.5ml/kg/hr
- 3. INCIDENCE OF AKI 2-5% of all hospitalized patients >25% in critically ill infants and children
- 10. PATHOGENESIS PRE-RENAL AKI: Decreased effective circulatory volume leading to inadequate renal perfusion and a decreased GFR Absence of structural kidney disease If renal hypoperfusion is reversed , renal function returns to normal If hypoperfusion is sustained , intrinsic renal parenchymal damage can develop
- 11. INTRINSIC RENAL AKI Renal parenchymal damage including sustained hypo-perfusion Hypoxic/Ischemic injury and nephrotoxic insult leading to acute tubular necrosis(ATN) mechanism including alteration in intrarenal hemodynamics , tubular obstruction, and passive back leak of glomerular filtrate across inujred tubular cells into peritubular capillaries
- 12. POST RENAL AKI Obstruction of urinary tract due to Congenital conditions including posterior urethral valve,uretero pelvic junction obstruction. Other causes 1. Hemorrhagic cystitis 2. Neurogenic bladder 3.Relief of obstruction results in recovery of renal function except renal dysplasias or prolonged urinart tract obstruction
- 20. CBC Anemia (Dilutional or Hemolytic ) Leucopenia Thrombocytopenia Eosinophillia SLE, Renal vein thrombosis, HUS SLE ,Sepsis SLE , Renal vein thrombosis, Sepsis,HUS Interstitial Nephritis to hypersensitivity reaction
- 21. LABORATORY FINDINGS Raised serum urea and creatinine Arterial blood Gases (metabolic acidosis) Electrolyte imbalance ( hyperkalemia , hyperphosphatemia and hypocalcemia) Urine routine examination( WBC, WBC cast, RBC, proteins, eosinophills and granular cast) Low C3 (SLE, PIGN,membranoproliferative GN) ASO titer ANA, ANCA ,Anti GBM
- 22. URINARY INDICES PRE RENAL AKI Elevated urine specific gravity(>1.020) Elevated urine osmolality(U Osm>500 mOsm/kg) Low urinary sodium (20mEq/L) Fractional excretion of sodium(<1%) INTRINSICS AKI Specific gravity <1.010 Low urine osmolality <350 mOsm/kg High urine sodium >40mEq/L Fractional excretion of Na>2%
- 23. Chest Radiography (pulmonary congestion, or pleural effusion) Renal ultrasonography( hydronephrosis, hydroureter) Renal Biopsy
- 27. 1.Administration of isotonic saline 20ml/kg over 30 mints 2. Hypovolemic patient usually void within 2 hr of resuscitation, failure to do suggests intrinsic or post renal AKI 3. Severe hypovolemia may require additional fluid boluses In the presence of blood loss or hypoproteinemia colloid containing solutions required Hypotension due to sepsis requires vigorous fluid resuscitation and continuous vasopressors infusion Diuretic therapy: After adequacy of blood volume Furosemide (2-4mg/kg) IV single dose Bumetanide (0.1mg/kg) alternative If no improvement in urine output then continuous diuretic infusion needed If no response to diuretic challenge, then diuretic should be discontinued and fluid restriction is essential
- 28. Patient with normal intravascular volume should be limited to 400ml/m2/24 hrs ( insensible losses) plus amount of fluid equal to urine output for that Extra-renal fluid losses should be replaced for ml with appropriate fluids Patient with hypervolemic state-can require further fluid restriction omitting replacement of insensible losses, losses, urine output and extra renal losses Fluid intake, urine and stool output, body weight and serum chemistries should be monitored on daily basis Mannitol effective in prevention of pigment induced AKI (Hemoglobin, Myoglobin)
- 40. GI
- 45. Thank You