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Prof. Rai Muhammad Asghar Department of Pediatrics
Rawalpindi Medical College
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Acute Renal Failure
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Acute Renal Failure:. Clinical Syndrome
Acute Renal Failure: * Clinical Syndrome * Sudden deterioration in renal Function * Inability of kidneys to maintain fluid and electrolytes homeostasis * 2-3% children, 8% neonates
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Paediatric-Modified Rifle (Prifle) Criteria
Estimated CCI Urine Output Risk eCCI decrease by 25% < 0.5mL/kg/hr for 8 hr Injury eCCI decrease by 50% < 0.5mL/kg/hr for 16 hr Failure eCCI decrease 75% or eCCI <35 ml/min/1.73m2 < 0.3mL/kg/hr for 24 hr or anuric for 12 hr Loss Persistent failure >4 wk End-Stage End-stage renal disease (persistent failure >3 mo)
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Acute Renal Failure Stage I Stage II Stage III
Rise in serum creatinine >150% Stage II Rise in serum creatinine > 200% Stage III Rise in serum creatinine > 300%
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Classified into 3 categories. 1- Prerenal ARF. 2- Intrinsic Renal ARF
Classified into 3 categories Prerenal ARF 2- Intrinsic Renal ARF 3- Postrenal ARF
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Pathogenesis and Causes Prerenal ARF * Diminished effective circulating arterial volume * Inadequate renal perfusion * Decreased GFR * No evidence of kidney damage
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Causes of Prerenal ARF. 1- Dehydration. 2- Hemorrhage. 3- Sepsis
Causes of Prerenal ARF 1- Dehydration 2- Hemorrhage Sepsis Hypoalbuminemia Cardiac Failure
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Intrinsic Renal ARF. Renal parenchymal damage
Intrinsic Renal ARF * Renal parenchymal damage * Sustained hypoperfusion / ischemia
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Causes of Intrinsic Renal ARF. 1- Glumerulonephritis
Causes of Intrinsic Renal ARF 1- Glumerulonephritis * Post streptococcal * Lupus nephritis * Henoch-schonlein purpura * Membranoproliferative * Anti-glomerular basement membrane nephritis
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Causes of Intrinsic Renal ARF (cont). 2- Hemolytic uremic syndrome
Causes of Intrinsic Renal ARF (cont) 2- Hemolytic uremic syndrome Acute Tubular Necrosis Renal vein thrombosis Rhabdomyolysis Acute interstitial nephritis Tumor lysis Syndrome
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Postrenal ARF. Obstruction of urinary tract. Causes
Postrenal ARF Obstruction of urinary tract Causes Posterior urethral valves Ureteropelvic junction obstruction Urolithiasis Tumor 5- Hemorrhagic cystitis Neurogenic bladder
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Clinical Manifestation Depends upon the cause
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Diagnosis Detailed History Physical Examination
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Investigations. 1- Blood urea / creatinin. 2- Electrolytes
Investigations Blood urea / creatinin 2- Electrolytes CBC, platelet count 4- Urine RE 5- C3 6- ASO titer 7- X-ray chest 8- Renal ultrasonography Renal Biopsy
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Urinary Indices. Urinary Indices. Prerenal ARF
Urinary Indices Urinary Indices Prerenal ARF Intrinsic ARF Specific gravity > < Urine osmolality >500 mOsm\kg <350mOsm\kg Urine Sodium <20mEqIL >40mEqIL Fractional Excretion Na<1% >2%
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Treatment. Depends upon cause / complication. Bladder catheterization
Treatment Depends upon cause / complication Bladder catheterization (relieve obstruction & monitor urine output)
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Volume Resuscitation. If no evidence of volume overload /
Volume Resuscitation If no evidence of volume overload / cardiac failure Isotonic saline 20ml/kg over 30 minutes Severe hypovolemia require additional fluid boluses Hypovolemic patient voids within 2 hours
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Diuretic therapy. Exclude hypovolemia. Mannitol 0. 5g / kg
Diuretic therapy * Exclude hypovolemia * Mannitol 0.5g / kg *Furosimide 2-4mg/kg * Continuous diuretic infusion * dopamine 2-3mcg / kg / min
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Fluid requirements. 400ml / m2 / 24 hrs
Fluid requirements * 400ml / m2 / 24 hrs Plus Fluid equal to urine output * Replace extra renal fluid loss ml for ml * Fluid restriction in hypervolemic patients * Daily monitor for fluid intake, urine & stool output, body weight & serum chemistries
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Hyperkalemia (>6mEq / l). Leads to cardiac arrhythmia & cardiac
Hyperkalemia (>6mEq / l) *Leads to cardiac arrhythmia & cardiac arrest * Peaked T wave, wide QRS, ST segment depression * Stop exogenous sources of K+ * Calcium gluconate 10% 1ml/kg * Sodium bicarbonate 1-2mEq / kg IV * Regular insulin 0.1U/kg with 50% dextoxe solution 1ml/kg over 1hr * Kayexalate 1g/kg * B-adrenergic agonist * Dialysis
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Metabolic acidosis. Due to retention of hydrogen ions,
Metabolic acidosis * Due to retention of hydrogen ions, phosphate & sulphate * Treat if severe (PH<7.15, Serum bicarbonate <8mEq/l) * Correct partially (PH to 7.20) * Oral sodium bicarbonate
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Hypocalcemia. Treat by lowering serum phosphorus
Hypocalcemia * Treat by lowering serum phosphorus * Do not give I/V calcium except if tetany * Low phosphorus diet * Phosphate binder (calcium carbonate, Ca acetate)
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Hyponatremia. Mainly dilutional. Fluid restriction
Hyponatremia * Mainly dilutional * Fluid restriction * I/V 3% NaCl if seizures or <120mEq / l * mEq NaCl required = 0.6 X Wt (kg) X[ S.Na +(mEq/l)]
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GIT Bleeding. Uremic platelet dysfunction. Increased stress
GIT Bleeding * Uremic platelet dysfunction * Increased stress * Heparin exposure * Give H2 blocker (Ranitidine)
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Hypertension. Diuretic. Isradipine. 05 -0. 15mg/kg/24hrs. Amlodipine
Hypertension * Diuretic * Isradipine mg/kg/24hrs * Amlodipine mg/kg/24hrs * Propranolol 0.5 – 8mg/kg/24hrs * Labetalol 4-40mg/kg/24hrs
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Neurogenic Symptoms. Headache, Seizures, Lethargy. I/V Diazepam
Neurogenic Symptoms * Headache, Seizures, Lethargy * I/V Diazepam * Treat precipitating cause
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Anemia. Generally mild. Hemodilution
Anemia * Generally mild * Hemodilution * Packed red blood cells if Hb <7g/dl * Use fresh, washed RBCs
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Nutrition. Restrict Na+, K+ & Phosphorus. Protein restriction
Nutrition * Restrict Na+, K+ & Phosphorus * Protein restriction * Parentral hyperalimentation
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Dialysis. Indications. Volume overload with hypertension
Dialysis Indications * Volume overload with hypertension refractory to diuretics * Persistent Hyperkalemia * Severe metabolic acidosis * Neurological symptoms * BUN > mg/dl * Calcium /Phosphorus imbalance with hypocalcemic tetany
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Types of dialysis 1- Intermittent hemodialysis Peritoneal dialysis Continuous renal replacement therapy
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Prognosis. Depends entirely on underlying disease
Prognosis * Depends entirely on underlying disease * AGN has very low mortality (<1%) * ARF related to multiorgan failure has high mortality (>90%) * Recovery is likely if ARF due to HUS, ATN, AIN or tumor lysis syndrome * Recovery is unusual when ARF due to rapidly progressive GN, bilateral renal vein thrombosis, bilateral cortical necrosis
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Thank You
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