11 Turman Management Of Acute Renal Failure In Picu
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Transcript of 11 Turman Management Of Acute Renal Failure In Picu
Management of Acute Renal Failure
Martin Turman, MD, PhD
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
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
Extrarenal causes of ARF: 67% of total
Post-op heart or other heart
failure 32%
Sepsis 17%
Cancer related14%
Liver transplant or
failure16%
Trauma6%
Other15%
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
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
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
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)
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.
How do you proceed from here? General approach to ARF – what is the 1st
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
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)
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
Postrenal Failure
Kidney stone (usually UVJ) Ureteropelvic junction (UPJ) or UVJ
obstruction Bladder: "prune belly"; neurogenic bladder;
fungus ball Urethra: posterior urethral valve; foreign
body Iatrogenic: obstructed Foley; narcotics
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
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)
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
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
Urinary indices in ARF
500
U-osm
350
PR
ATN
40
U/P Cr
20
PR
ATN
40
U-Na
20PR
ATN
FE-Na
1%
PR
ATN
2%FE-Na = (U/PNa ÷ U/PCreatinine ) *100
Adopted from J. Crit. Illness 4:32
Use of FE-Na
FE-Na < 1: Decreased effective blood volume; ATN 2o 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
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.
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
Assessment of case #2
Is she in renal failure?– Creatinine is normal, so NO!
Why is BUN so high?
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).
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
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
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
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)
Management of ARF - Volume status
Water balance – "Maintenance" 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/M2/day
– If has any UOP, Lasix + zaroxolyn may help with fluid overload
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
Back to Case #3 (nephritis)
K+ 6.5, Bicarb 14 Calcium 5.8, Phosphorus 9.3 Hematocrit 30.3%, Platelets 280K
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
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
Hypocalcemia and hyperphosphatemia
Ca+2 x PO4 > 60-70 is risk for metastatic calcification, including in the cardiac conduction system
Often are reciprocal: as PO4 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)
Hypocalcemia and hyperphosphatemia
Reduce PO4 with calcium acetate if can swallow pills, calcium carbonate if needs liquid
Diet restriction Avoid exogenous PO4: Fleet's, carafate,
TPN
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)
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
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
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
Unproven or controversial treatments
Diuretics could decrease tubular obstruction by helping to "flush out" 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
Unproven or controversial treatments
"Renal dose" 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
Effect of low-dose Dopamine on ARF
Source Type of Study Severity Efficacy
Lindner Established ARF Mod-severe Yes
Graziani Established ARF Mod-severe Yes
Lumlertgul Established ARF Severe No
Lumlergul Established ARF Moderate Yes
Duke Established ARF Mild No
Weisberg Prophylaxis IVC Chronic No
Adopted from Alkhunaizi & Schrier, Am J Kidney Dis 28:315
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.
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
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
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
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
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%)
"The great tragedy of Science - the slaying of a beautiful hypothesis by an ugly fact."
T.H. Huxley (1825-1895) Collected Essays
The End
Any questions???