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11 Turman Management Of Acute Renal Failure In Picu

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  • 1. Management of Acute Renal Failure Martin Turman, MD, PhD
  • 2. Acute Renal Failure
    • Definition: Sudden deterioration in the ability of the kidneys to maintain fluid, solute or electrolyte homeostasis
    • Common in PICU patients (10-20%)
    • Greater than 50% mortality
    • ARF in PICU patients has an independent and significant impact on mortality
  • 3. ARF: Causes and mortality
    • Primary renal disease: 33%
      • Hemolytic uremic syndrome: 88%
      • Obstructive uropathy
      • Renal vein/artery thrombosis
      • Primary glomerulonephritis (RPGN)
    • Overall mortality: 6%
    • Most primary renal diseases develop RF gradually and do not need emergent dialysis
  • 4. Extrarenal causes of ARF: 67% of total
    • Overall mortality: 62%!!
    • In third world: V/D/D-induced ATN most common cause of ARF
    Data pooled from Ped. Nephrol. 7:703, 8:334, 6:470, and 7:434
  • 5. ARF: Risk factors for mortality
    • Multi-organ failure
    • Bacterial Sepsis
    • Fungal sepsis
    • Hypotension/vasopressors
    • Ventilatory support
    • Initiation of dialysis late in hospital course
    • Oliguria/anuria: with oliguric ARF, mortality is > 50% compared to < 20% with non-oliguric ARF
  • 6. Best cure is to prevent
    • Have a high index of suspicion for reversible factors - volume depletion, decreasing cardiac function, sepsis, urinary tract obstruction
    • Be sure patient is well-hydrated when exposing patient to nephrotoxic drugs
  • 7. Anticipate problems
    • Avoid worsening the ARF
      • Adjust medicines for renal insufficiency
      • Avoid nephrotoxins if possible
      • Avoid intravascular volume depletion (especially in third-spacing or edematous patients)
  • 8. Case #1
    • ET is a 3 year old who presented with abdominal pain and vomiting for 3 days. He underwent surgery for intussuception.
    • Post-operatively he had oliguria. BUN and creatinine were 80 and 2.5. Sodium was 145.
    • Two 5 cc/kg fluid boluses had minimal effect on urine output. He had anasarca with severe periorbital and pedal edema.
  • 9. How do you proceed from here?
    • General approach to ARF – what is the 1 st question to ask in the DDx?
    • Is it pre-renal, renal or post-renal?
    • What labs help you decide this?
    • BUN:Cr ratio and fractional excretion of sodium (FE-Na)
    • What labs do you need to calculate the FE-Na?
    • urine lytes + urine creatinine near same time as serum lytes to calculate
  • 10. Prerenal azotemia
    • Decreased effective circulatory volume
      • Hypovolemia
        • GI losses (V/D, ileostomy, NG drainage)
        • Hemorrhage (trauma, GI bleeding)
        • Cutaneous losses (burns)
        • Renal losses (diabetes insipidus or mellitus)
      • Loss of fluids from intravascular space
        • Third spacing
        • Septic (capillary leak) or anaphylactic shock
        • Hypoalbuminemia (Neph syndrome, protein-losing enteropathy)
  • 11. Prerenal azotemia
    • Decreased local blood flow to kidney
      • Renal artery stenosis or RVT
      • Drug-induced renal vasoconstriction
        • cyclosporin, tacrolimus
      • Hepatorenal syndrome
    • Diminished cardiac output
      • Congestive Heart Failure
      • Arrythmias, tamponade, etc.
      • Cardiovascular surgery
  • 12. Postrenal Failure
    • Kidney stone (usually UVJ)
    • Ureteropelvic junction (UPJ) or UVJ obstruction
    • Bladder: &quot;prune belly&quot;; neurogenic bladder; fungus ball
    • Urethra: posterior urethral valve; foreign body
    • Iatrogenic: obstructed Foley; narcotics
  • 13. Intrinsic Acute Renal Failure
    • Acute tubular necrosis
      • Prolonged prerenal azotemia of any cause
    • Nephrotoxin-induced (aminoglycosides; amphotericin)
    • Primary glomerular diseases
      • Hemolytic uremic syndrome
      • All other forms of glomerulonephritis (RPGN)
    • Intra-renal obstruction: rhabdomyolysis, tumor lysis syndrome
  • 14. Evaluation of ARF - 1
    • In history, seek clues regarding secondary causes - symptoms of CHF, liver disease, sepsis, systemic vasculitis, prodromal bloody diarrhea; birth asphyxia
    • Check for symptoms of primary renal disease - UTI sx, gross hematuria, flank pain, Hx of strept infection, drug exposure (esp. CSA, aminoglycosides and amphotericin for renal toxins or narcotics for bladder dysfunction)
  • 15. Evaluation of ARF - 2
    • During exam, look for secondary causes
      • Causes of decreased effective circulatory volume - CHF, ascites, edema, sepsis
      • Signs of systemic illness - (vasculitis, SLE, HSP): rash, arthritis, purpura
      • Signs of RVT and obstructive uropathy: enlarged kidneys or bladder - CHECK FOLEY; Give Narcan
  • 16. Evaluation for ARF - 3
    • Lytes, BUN, Cr; CBC with platelets (HUS)
    • UA: hematuria, myoglobinuria, proteinuria, RBC casts, eosinophils
    • Urine indices
    • Renal US (with Doppler flow to rule out renal vein thrombosis)
    • RPGN evaluation: anti-DNase B, C3, ANA, Anti-GBM, ANCA, renal biopsy
  • 17. Urinary indices in ARF 40 U/P Cr 20 PR ATN FE-Na 1% 2% FE-Na = (U/P Na ÷ U/P Creatinine ) *100 Adopted from J. Crit. Illness 4:32 500 U-osm 350 PR ATN 40 U-Na 20 PR ATN PR ATN
  • 18. Use of FE-Na
    • FE-Na < 1: Decreased effective blood volume; ATN 2 o to myo- or hemo-globinuria or contrast dye; sepsis sometimes, CSA, acute glomerulonephritis, hepatorenal syndrome
    • FE-Na > 2: ATN, chronic GN, diuretics, salt-wasting nephropathy
    • Unpredictable: Obstructive or reflux nephropathy, normal people
  • 19. Back to Case #1 (intussuception)
    • ET had no proteinuria and small hematuria on urinalysis. A FE-Na was 0.1%. A serum albumin was 2.2.
    • Thus, he had pre-renal azotemia because of loss of intravascular fluid secondary to hypoalbuminemia and third spacing.
    • After receiving 25% albumin and further fluid resuscitation his UOP and Creatinine normalized.
  • 20. Clinical Case #2
    • S.E. is a 10 year-old with acute lymphocytic leukemia receiving chemotherapy
    • Has fever, neutropenia and thrombocytopenia
    • UOP is 1.2 cc/kg/hour
    • On clinical exam she has very moist mucus membranes
    • BUN and creatinine are 110 and 0.7. Albumin is 3.5
  • 21. Assessment of case #2
    • Is she in renal failure?
      • Creatinine is normal, so NO!
    • Why is BUN so high?
  • 22. Use of plasma BUN: Cr ratio
    • In pre-renal BUN:Cr > 20 usually
    • However, BUN may be increased disproportionately with blood products, excess amino acids in TPN, GI or other bleed; increased catabolism (treatment with steroids, fever).
  • 23. Clinical Case #3
    • CE is a 15 yo male who presented with URI symptoms, then headache, vomiting, abdominal pain, knee pain, edema, and a purpuric rash on his legs. He had not voided for 24 hours.
    • What is diagnosis?
      • HSP
  • 24. Physical exam and labs
    • BP was 152/94. He had anasarca. Heart and lung exams were normal.
    • A urinalysis revealed hematuria and proteinuria. BUN and Creatinine were 76 and 8.0. Albumin was 3.1
    • He has aggressive HSP nephritis
  • 25. Fluid management in ARF
    • This kid weighs 70 kg. What percent “maintenance” should you run his IV at?
      • NO FLUIDS - Hep-lock it!! He’s fluid overloaded and hypertensive – he doesn’t need any fluid
    • How were the maintenance calculations derived? – What goes into the formula?
      • Insensibles + UOP = maintenance
  • 26. Fluid management in ARF
    • If this kid had an albumin of 1.0 and mucus membranes were very dry, what fluids would you give him?
      • Bolus of NS like any other dehydrated kid – but cautiously
    • Now you have the kid euvolemic by exam but still has no UOP. He’s NPO though, so what fluid rate should you run now?
      • Insensibles + UOP = maintenance (i.e. about ¼ to 1/3 of a normal kid’s maintenance or 400 cc/M2)
  • 27. Management of ARF - Volume status
    • Water balance
      • &quot;Maintenance&quot; is IRRELEVANT in ARF!!!
      • If euvolemic, give insensibles + losses + UOP
      • If volume overloaded, they don't need anything (except the minimum for meds and glucose)
        • concentrate all meds; limit oral intake
      • Need frequent weights and BP, accurate I/O
      • Insensibles = 30 cc/100 kcal or 400cc/M 2 /day
      • If has any UOP, Lasix + zaroxolyn may help with fluid overload
  • 28. Hypertension
    • Could be from volume overload or from intrinsic renal disease
    • If has volume overload, need to directly vasodilate (calcium channel blockers, clonidine, nicardipine drip, nitropruside, etc.)
    • If intrinsic renal disease, ACE may work also
    • Goal is to prevent stroke, congestive heart failure
  • 29. Back to Case #3 (nephritis)
    • K+ 6.5,
    • Bicarb 14
    • Calcium 5.8, Phosphorus 9.3
    • Hematocrit 30.3%, Platelets 280K
  • 30. Hyperkalemia
    • With ARF, K + will increase and will be worsened by infection, hemolysis, acidosis
    • DON'T IGNORE A HIGH K + just because the specimen is hemolyzed especially in a patient who could easily be hyperkalemic
    • How can you tell if it is “real”?
      • check EKG for peaked T waves, widened QRS
    • It’s real. What’s the first thing to do?
      • Emergently stabilize membranes with calcium to prevent arrhythmia
  • 31. Hyperkalemia
    • What’s next?
      • Shift K + intracellularly with:
        • insulin (+ glucose to prevent hypoglycemia)
        • bicarbonate infusion
        • albuterol (SQ/aerosol)
      • Check IV fluids to ensure no intake
    • What happens to ionized calcium level as you correct the acidosis?
      • Increases albumin binding so ionized calcium decreases
    • What’s the third step?
      • Remove from body with Lasix, Kayexalate, dialysis
  • 32. Hypocalcemia and hyperphosphatemia
    • Ca +2 x PO 4 > 60-70 is risk for metastatic calcification, including in the cardiac conduction system
    • Often are reciprocal: as PO 4  Ca + 
    • Sx of hypocalcemia: irritability, tetany, sz
    • If hypoalbuminemic:
      • check ionized Ca or
      • correct (0.8 increase of Ca for each 1.0 of albumin below 4)
  • 33. Hypocalcemia and hyperphosphatemia
    • Reduce PO 4 with calcium acetate if can swallow pills, calcium carbonate if needs liquid
    • Diet restriction
    • Avoid exogenous PO 4 : Fleet's, carafate, TPN
  • 34. Acidosis
    • Correct if bicarbonate is < 15
    • Acidosis makes the kids feel terrible
    • BUT...
      • watch sodium and fluid overload
      • watch lowering ionized calcium levels (by increasing binding of calcium to albumin)
  • 35. Anemia and uremic bleeding
    • Anemia results from lack of renal erythropoietin production + increased loss
    • Underlying disorder may also cause hemolysis (DIC, HUS, SLE) or decreased RBC production (sepsis, leukemia)
    • Uremic PLT's do not function well, so have increased bleeding: treat with cryo-precipitate and DDAVP (causes transient improvement in PLT function; estrogen
  • 36. Indications for renal replacement therapy
    • Volume overload
      • Pulmonary edema, CHF, refractory HTN
      • NOT for peripheral edema, esp. with cap. leak
    • Hyperkalemia
    • Hyperphosphatemia/Hyperuricemia in TLS
    • Uremic side-effects:  mentation, sz, pericarditis, pleuritis
    • Need to maximize nutrition
  • 37. Modes of renal replacement therapy
    • CVVH, CVVD, CVVDHF - gentle, but slower than hemodialysis; need large lines and heparin
    • Peritoneal dialysis - also gentle and don't need heparinization but slow and catheter may leak or not work
    • Hemodialysis - very fast, but need big lines and systemic heparinization; causes hemodynamic instability and uremic dysequilibrium symptoms
  • 38. Unproven or controversial treatments
    • Diuretics could decrease tubular obstruction by helping to &quot;flush out&quot; casts
      • BUT, may worsen electrolyte problems
      • May cause ototoxicity
    • 126 post-op heart adult patients given Lasix drip
      • Creatinine  -fold higher! (Lassnigg, JASN 11:97,2000)
    • Still consider if patient is volume overloaded or has hyperkalemia
  • 39. Unproven or controversial treatments
    • &quot;Renal dose&quot; dopamine could increase renal perfusion, esp. with concurrent norepinephrine
      • Works in animal models, BUT:
      • May depress respiratory drive
      • May trigger arrythmias
      • Induces a state of “hypopituitarism”
      • It’s an added expense
      • No conclusive clinical studies demonstrating benefit
  • 40. Effect of low-dose Dopamine on ARF Adopted from Alkhunaizi & Schrier, Am J Kidney Dis 28:315
  • 41. Are there any new treatments?
    • MANY in vitro and animal studies of ARF demonstrate improvement with various factors
      • Glycine, thyroxine, anti-intercellular adhesion molecule-1 (ICAM-1), platelet-activating factor (PAF) antagonist, various growth factors, etc.
  • 42. New potential therapies
    • Growth factors
      • Insulin-like growth factor (IGF-1), epidermal growth factor, hepatocyte growth factor
        • May help in recovery from ARF by improving regeneration, by protecting cells from injury or facilitating their recovery
        • IGF-1 trial - failed to decrease need for dialysis
        • GH for critically ill patients WORSENED outcome
  • 43. New potential therapies
    • Calcium channel blockers
      • Most studies demonstrate benefit post transplant
      • One small study demonstrates improved GFR after malaria-induced ARF
      • Conflicting results with contrast-induced ARF
      • Large meta-analysis showed no prospective placebo-controlled studies have shown benefit – only poorly designed studies did.
    • CVVH to remove cytokines, etc. for patients with systemic inflammatory response syndrome
  • 44. New potential therapies
    • Endothelin antagonists for ATN
      • Remarkably effective in animal models
      • Humans with radiocontrast nephrotoxicity:
        • Multicenter trial
        • ET antagonist given 30 min before contrast
        • Agent EXACERBATED renal insufficiency
  • 45. New potential therapies
    • Atrial natriuretic peptide (ANP)
      • ANP dilates afferent & constricts efferent
        • Leads to increased GFR
      • Inhibits vasoconstrictors (endothelin, etc.)
      • Improves outcome in animals with ATN
  • 46. New potential therapies
    • Anaritide trials
      • 504 patients with oliguric and non-oliguric ARF (NEJM 336:828, 1997)
        • Improved dialysis-free survival in oliguric patients (27% vs. 8%)
        • Worsened outcome for non-oliguric ARF (59% vs. 48%)
      • 222 patients (AJKD 36:767, 2000) with oliguric ARF – NO benefit (21% vs. 15%)
  • 47. &quot;The great tragedy of Science - the slaying of a beautiful hypothesis by an ugly fact.&quot; T.H. Huxley (1825-1895) Collected Essays
  • 48. The End Any questions???

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