Pediatric Acute Kidney Injury AKI

Pediatric Acute Kidney Injury AKI PowerPoint PPT Presentation


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AKI. Formerly referred to as acute renal failureAbrupt reduction in kidney function measured by decline in GFRResults in disturbancesImpaired nitrogenous waste excretionLoss of H2O

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Pediatric Acute Kidney Injury AKI

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1. Pediatric Acute Kidney Injury (AKI) Heather Stewart, MD Internal Medicine-Pediatrics Nephrology Fellow UNC Kidney Center September 13, 2010

2. AKI Formerly referred to as acute renal failure Abrupt reduction in kidney function measured by decline in GFR Results in disturbances Impaired nitrogenous waste excretion Loss of H2O & electrolyte regulation Loss of acid-base regulation Contributing factor in morbidity & mortality of critically ill

3. A Common, Serious Problem Present in 5% of all hospitalized patients, & up to 30% of ICU patients Incidence is increasing at an alarming rate Mortality rate >50% in dialyzed ICU patients 25% of ICU dialysis survivors progress to ESKD within 3 years

4. Clinical Approach to AKI: Pre-, Intra-, and Post-Renal

6. Pathophysiology: Newborn Embryogenesis completed by 35th wk resulting in 0.6-1.2 million nephrons per kidney Immaturity limits kidney fxn Hemodynamic changes @ birth Increased risk of hypovolemia b/c lg insens. losses

7. Pathophysiology: Newborn RBF increases after birth b/c renal vasc resist decreases & systemic BP increases As a proportion of CO, RBF inc from 2 to 4% in fetus 1wk of life 10% adult 20% Dec ability to compensate for significant hemodynamic changes

8. Pathophysiology: Newborn Limited Urine concentrating ability Concentration inc from 400 mosm/kg in 1st few days to 1200 mosm/kg at 1yr of age Low CM solute gradient Decreased cAMP in response to ADH Short Loop of Henle Interference by PGs Inc risk of volume depletion

9. Epidemiology Retrospective review est. a yearly incidence for AKI 0.8 /100,000 This is about 1/5 of that seen in adults Incidence rising with inc availability of advanced technology Txplt: BM, Liver, Heart CHD surgery Care of VLBW infants

10. Etiology: Newborn Perinatal asphyxia Prerenal Dz & ATN Renal Vasc Thrombosis RAT RVT Nephrotoxins Urological abnormalities

11. Etiology: Newborn Perinatal asphyxia Most common cause Diminished RBF due to hypovol/hypotension Preglomerular vasoconstriction Increased catechols, adenosine, & angiotensin Postglomerular vasodilatation – dec GFR Activated RAAS and inc ADH – salt & H20 retention with oliguria

12. Etiology: Newborn Renal Vascular Thrombosis RAT Assoc with UAC placement Thrombi can partially occlude abd Ao thus dec renal perfusion embolize to renal artery => infarction & inc renin => HTN RVT – incidence 2.2/100,000 live births Palpable flank mass accompanied by HTN & dec UOP; hematuria (gross or micro) Thrombocytopenia, anemia, leucocytosis, DIC

13. Etiology: Newborn Renal & Urinary Tract Abnml Polycystic kidney disease AD (1:400–1:1000) or AR Multicystic Dysplastic kidneys Renal agenesis Bilateral (1 in 4000) – Potter Sequence Unilateral (1 in 550)– inc incidence of Mullerian duct defects Urinary tract obstruction – bilat/unilat hydro PUV Severe UPJ

14. Etiology: Children Volume depletion Bleeding, GI, burns Heart failure, shock, *cirrhosis Dec effective circulating volume Vascular RAT, RVT, HUS, *Vasculitis *Glomerular Nephrotoxins/AIN Urologic abnormalities

15. Presentation: Newborn History: Prenatal conditions – oligo- or polyhydramnios; renal abnml noted on antenatal US; and antenatal medications Neonatal conditions – prematurity, perinatal asphyxia, RDS, sepsis, UAC, Rx administration, volume depletion, delayed 1st UOP, abnml urine stream in males PxEx: Edema, BP, enlarged/absent kidneys, distended bladder, dysmophic features (myelomeningocele, anal atresia, PBS, facial/limb deformities)

16. Presentation: Newborn Oligoanuria No UOP by 48hrs of age or dec UOP (less than 1 ml/kg/hr) Elevated Cr >1.5mg/dL or increasing by at least 0.2-0.3 mg/dL per day Azotemia BUN >50mg/dL Lab abnmls hypoNa, hyperK, met acidosis, hyperPhos, hypoCa

17. Presentation: Children History: AGE, hemorrhage, sepsis, decreased oral intake Bloody diarrhea w/ oliguria (<500ml/1.73m2/day) or anuria – HUS Pharyngitis or impetigo – PIGN Hemoptysis and renal impairment – Pulm-Renal Syndrome (Wegner’s, Goodpasture’s) Trauma/crush injury – rhabdomyolysis Exposure to nephrotoxins – aminoglycosides, amphotericin-B, chemotherapy Rx PxEx: Tachycardia, dry MM, sunken eyes/fontanel, orthostatic BP, decreased skin turgor Edema – nephrotic syndrome, heart failure, liver failure Skin findings – purpura, petechiae, malar rash, maculopapular – HSP/SLE, AIN

18. Common Nephrotoxic Agents Antimicrobial agents Aminoglycosides Amphotericin B Acyclovir Foscarnet Pentamidine Chemotherapeutic agents Cisplatin Mitomycin C Streptozocin Vasoactive drugs NSAIDS ACE inhibitors CSA, Tacrolimus, Rapamycin Radiocontrast agents Colloidal agents Dextran 40 Hydroxyethyl starch

19. Diagnosis of AKI is Often Delayed Elevation in serum Cr - current gold standard Normal serum Cr varies widely with age, gender, diet, muscle mass/metabolism, medications (Bactrim, Cimetidine), and hydration status Serum Cr can take several days to reach a new steady state Up to 50% of kidney function may be lost before serum Cr even begins to rise

20. Evaluation Serum chemistries Na, K, CO2, Cr, Ca, Phos, Albumin CBC Polycythemia or thrombocytopenia => RVT Microangiopathic hemolytic anemia assoc with thrombocytopenia => HUS Eosinophilia => AIN Urine Urinalysis with microscopy Urine lytes (Na, Cr, Urea in Lasix use) Other Aminoglycoside levels Uric acid if TLS suspected C3, C4, dsDNA, ANA, ANCA, ASO

21. Evaluation Renal Imaging RUS: 1 or 2 kidneys, echogenicity, renal size, obstruction VCUG: to assess for obstructive uropathy +/- VUR in newborns wit h renal anomalies

22. Evaluation: Serum Creatinine Normal ranges: Newborn 0.3-1.0 mg/dL Declines to infant values* - 1wk in term infants & 2-3wks in preterm infants *Infant 0.2-0.5 mg/dL Child 0.3-0.7 mg/dL Adolescent 0.5-1.0 mg/dL Even if value remains in normal range a sequential inc in Cr concentration strongly suggests a dec in GFR. Certain Rx – Cimetidine, Bactrim Renal dosing in AKI assume eGFR <15 ml/min/1.73m2

23. AKI Indices Pre-Renal ATN UNa Children < 10 > 10 Neonates <20-30 >30 Spec Grav > 1.018 <1.010 Urine/Serum Cr >40 <40 FeNa Children < 1% > 2% Neonates < 3% > 3% * low FeNa not unique to Pre-renal – nml tub fxn but low GFR like acute GN, vasculitis, acute obstruction Urine Osmolality > 500 < 350 Sediment normal active

25. Urinalysis

26. Urine Sediment

27. Urine Sediment

28. Management Fluids Hyperkalemia Metabolic Acidosis Hypocalcemia & hyperphosphatemia Hyponatremia Nutrition Hypertension

29. Management: Intravascular Volume Fluids Place foley catheter Fluid challenge - Isotonic saline 10-20 ml/kg (+) response (> 1ml/kg/hr) indicates pre-renal cause (-) response indicates intrinsic cause Prevent fluid overload - restrict D5W or D10W with bicarbonate to replace insensible losses (approx 1/3 of maintenance) Replace urine losses with ½ NS Lasix (1-5mg/kg) for signs of overload Discontinue fluids/TPN with K

30. Management: Intravascular Volume Diuretics Loop - Bolus vs Drip Bolus short onset of duration of action Multiple doses (if not effective) likely to cause ototoxicity Drip Continuous superior to bolus due to metabolism, less drug needed (Martin et al, CCM 1994 22:1323) 26 Post-Op Cardiac Neonates 1mg/kg q4hrs vs 0.1 mg/kg/hr gtt UOP similar but gtt had less drug & more consistent UOP (Luciani et al, Ann Th Sg 1997 64:1133)

31. Management: Intravascular Volume Diuretics Augmentation of Loop with addition of Thiazide Augment loop diuretics by delivering more Cl to the distal tubule by blunting Na reaborption Fiser et al, Kid Int 1994 46:482 IV thiazide vs Control to augment loop in 10 adults with AKI Thiazide addition resulted in sig improvement in UOP 5mg/kg/dose q6 Diuril followed by Lasix IV q6 or Lasix gtt

32. Management: Intravascular Volume Albumin good or bad? Finfer et al, NEJM 2004 350:2247 ~7000 adults with hypovolemia randomized to NS or 4% albumin No difference in AKI or need for dialysis BUT NS group received 1.3 times greater volume to restore hemodynamics Volume excess may be a negative indicator of survival in AKI

33. Management: Intravascular Volume Dopamine ‘Renal-dose’ dopamine (0.5 to 3-5 mcg/kg/min) Increases RBF by promoting vasodilatation & may improve UOP by promoting naituresis Not shown to alter course of renal failure Not proven to convert oliguric to non-oliguric AKI No effect in decreasing need for dialysis or improving survival in patients with AKI Bellomo et al, Lancet 2000 36:2139 RCT that revealed no change in survival b/w Dopamine and placebo Complications: tachycardia, arrhythmias, & myocardial ischemia

34. Management: Hyperkalemia “C BIG K Die” Calcium gluconate (from pharmacy) or Calcium chloride (on crash cart) Bicarbonate/beta-agonist (Albuterol) Insulin + Glucose Kayexalate Diuretic (Lasix) EKG changes: peaked T waves, flattened P waves, inc PR interval, widening of QRS, bradycardia, SVT/VT, and Vfib

35. Management: Hyperkalemia

36. Management: Acidosis Impaired acid excretion + increased acid production from underlying condition Administration where max resp compensation is adequate and/or acidosis is contributing to hyperK Plasma bicarb falls below 15 meq/L or arterial pH < 7.25

37. Management: Acidosis Correction estimated by HCO3 dose = (16-measured HCO3)(0.4)(wgt in kg) Or empirically give HCO3 at dose of 1-2 meg/kg Avoid rapid correction – HTN, fluid overload, intracranial hemorrhage If (+) hypoCa correct this 1st b/c HCO3 will decrease ionized Ca – tetany or SZ

38. Management: hypo-Ca, Hyper-Phos, & hypo-Na hypo-Ca: generally not treated unless symptomatic or hypoCa is severe Hyper-Phos: lowering Phos tends to raise Ca Restrict dietary Phos Use Ca-carbonate for Phos binding hypo-Na: typically assoc from H2O intake that cannot be excreted Restrict free H2O “Hot salt” if Na <120 meq/L & symptoms

39. Management: HTN Prevent by avoiding fluid overload Diuretics if responsive Vasodilators usually drug of choice Nitroprusside, Labetalol, or Nicardipine gtt Intermittent IV doses of Hydralazine or If taking po oral minoxadil or hydralazine

40. Management: Nutrition AKI assoc w/ marked catabolism Balance of volume and components Enteral preferred (Nepro, RenaCal, etc.) over central Consider the following with TPN Volume High Dextrose, low rates; 20% lipids Components AA~ 1-1.5 gm/kg No K, Phos

41. Traditional Indications for Kidney Support in AKI “AEIOU” Severe metabolic acidosis unresponsive to bicarbonate therapy Electrolyte disturbance despite medical therapy; Refractory or severe hyperkalemia Intoxication/Ingestions (i.e. lithium, ASA) Overload - Diuretic unresponsive hypervolemia Uremic complications pericarditis

42. Dialysis Modalities Intermittent hemodialysis Continuous therapies Continuous hemofiltration Continuous hemodialysis Continuous hemodiafiltration Peritoneal dialysis

43. Dialysis Machines at UNC

44. Dialysis Modalities

45. Choice of Modality Influenced by age, size, and medical comorbidities of patient Availability of access placement HD/CRRT are technically challenging in neonates PD preferred in neonates Safe, effective, technically simpler, less expensive Can be initiated after catheter placed & ~3days after major abd surgery (i.e. NEC)

46. Timing of Dialysis in AKI

47. Timing of CVVH in AKI (adults)

48. Adverse Outcomes Associated with RRT Delay in recovery of kidney function Access related complications Infection Hemorrhage Thrombosis Vascular injury Circuit associated complications Bio-incompatibility Anticoagulation-associated complications

49. Adverse Outcomes Associated with RRT Hemodynamic compromise Electrolyte and metabolic complications Errors in compounding fluids Not common here as we use standard dialysate at UNC Acid-base disturbances Thermal balance Electrolyte and nutrient depletion Hypokalemia Hypophosphatemia Vitamins and micronutrients Amino acids

50. Prognosis Highly dependent on underlying etiology, age of patient, and clinical presentation AKI neonates (review) Oliguric AKI mortality as high as 60% CHD & Uro abnml mortality up to 86% Children (retrospective) > 3 system organ failure assoc with more than 50% mortality

51. To infinity and beyond . . . although it may be light-years away.

52. Need for AKI Biomarker(s) The paucity of early biomarkers has crippled our ability to institute therapy Need early biomarkers for improved understanding, early treatment, and better outcomes

53. Towards a Kidney Troponin

54. Urinary Biomarkers

55. Urinary Biomarkers NGAL Covalently bound protein to gelatinase from human neutrophils Expressed in low levels in diverse human tissues Induced in injured tissues including kidney tubular cells Increases in the blood & urine within 2-4 hrs after injury Easily detected in urine

56. Urinary Biomarkers Studies Support NGAL as Biomarker of AKI in the following: Pediatric Cardiac Surgery Pediatric Contrast Induced Nephropathy Adult Emergency Room Patients NGAL increases in CKD Better marker in pediatric than adult patients Very stable in the urine Rapid ELISA

57. Urinary Biomarkers: Clinical Performance

58. Urinary Biomarkers: Clinical Performance

59. Urinary Biomarkers in the Diagnosis of AKI Post-Cardiac Surgery

60. Urinary Biomarkers: Confounding Factors

61. Role of Biomarkers in AKI Early prediction & diagnosis of AKI (before inc in serum Cr) Identify the primary locationof injury (proximal tubule, distal tubule, interstitium, vasculature) Pinpoint duration (AKI, CKD) and severity Identify the etiology of AKI (ischemic, septic, toxic, combination)

62. Take Home Points

63. Take Home Points: Prevention Recognizing whom is at risk Unrecognized CKD in pediatrics as it is “silent” due to interstitial disease – assoc with polyuria & tendency for dehydration NPO for procedures Exposure to Nephrotoxins (i.e. NSAIDs, Contrast, Abx, etc.) NAC may be beneficial Bicarb may be beneficial Watch for 2ndry electrolyte changes – Met Alk can induce hypo-Ca Close monitoring of serum levels of nephrotoxic drugs Removing vasodilators ahead of time (i.e. ACEi, ARBs) Hydration, Hydration, Hydration -- Adequate fluid repletion in hypovolemia Aggressive hydration & alkalinization of urine prior to chemotherapy Preventive therapy for post-ischemic ATN is uproven “Renal-dose” Dopamine, Mannitol, Lasix gtt

64. Take Home Points: Management Volume status Hyperkalemia: Therapy “C BIG K Die” Acidosis HTN Nutrition Dialysis: Indications “AEIOU”

65. Take Home Points: Prognosis depends on etiology, age of patient, clinical presentation, and status of patient Hypotension & the need for inotropes during dialysis are significant poor predictors for patient survival

66. Take Home Points: Future Developments Current clinical tests do not allow early detection of cases at a time when interventions may have the biggest effects Urinary biomarkers under development show great promise – of these NGAL is the most advanced Longer term, clinical outcome studies needed to validate utility & validity of AKI biomarkers

69. Extra Info for Review AKI in the ICU RIFLE & AKIN Criteria CIN NAC, HCO3 AIN

70. Acute Kidney Injury in the ICU

72. The Rifle Criteria

74. Albanese et al, Chest 2004 14 adults with septic shock (SS) to 10 adults with head injury (HI) without sepsis Goal to keep MAP > 70mmHg Avg dose in SS 1.3 mcg/kg/min Avg UF increased from 14 to 121 ml/hr Cr drop from 280 to 170 mmol/L/24hrs Avg dose in HI 0.3 mcg/kg/min Avg UF increased from 97 to 117 ml/hr Cr rise from 90 to 105 mmol/L/24hrs

75. Radiocontrast-Induced Acute Kidney Injury Induces renal vasoconstriction and direct cytotoxicity via oxygen free radical formation Risk factors: Renal insufficiency - Diabetes Advanced age - > 125 ml contrast Hypotension Usually non-oliguric ARF; irreversible ARF rare

76. Contrast-Induced Nephropathy (CIN) Most common definitions absolute increase in serum creatinine level of 0.5 to 1 mg/dL (0.044 -0.088 mmol/L) within 48-72 hours 25% increase in serum creatinine level within 48-72 hours Accounts for 12% of cases of acute kidney injury Marker for increased mortality

77. Contrast Induced Nephropathy Incidence may be decreasing over the last 10 years – 15% to 7% (Bartholomew BA et al. Am J Cardiol 2004;93:1515-1519). 2003-80 million doses of iodinated contrast administered worldwide 2004 – United States 3.3 million coronary angiograms 25.7 million contrast-enhanced CT scans 2 million conventional angiograms

78. N-acetylcysteine > 20 published studies, most underpowered, with conflicting results 11 meta-analyses demonstrate increased heterogeneity among trials May have a small effect on the measurement of serum creatinine (lowers SCr a mean of 0.06 mg/dL), further complicating interpretation of data Use in moderate to high risk patients is reasonable

79. Interventions to Limit Risk of CIN Many trials on both isotonic bicarbonate, iso- vs. low-osmolar contrast, and N-acetylcysteine with mixed results There remains a need for well-powered randomized controlled trials to establish the optimal preventative regimen Should use measures GFR rather than creatinine Urinary biomarkers markers may help determine best preventive strategy

80. Interventions to Limit Risk of CIN-Key Points Optimize the effective circulating volume Delay studies in patients with volume depletion, circulatory collapse or decompensated congestive heart failure when possible Optimize congestive heart failure when possible Hydration with isotonic saline or sodium bicarbonate 1-1.5 ml/kg/hr starting 3-12 hours prior to the study and continuing for at least 12 hours after the study in moderate risk patients

81. Interventions to Limit Risk of CIN-Key Points N-acetylcysteine 600-1200 mg twice daily starting one day prior to and twice daily on the day of the study is reasonable Use minimal volumes of low osmolar or iso-osmolar non-ionic contrast

82. Etiology of Acute Interstitial Nephritis (AIN)

83. Clinical Features of AIN

84. Liquid Gold

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