Transcript ARF

Acute Renal Failure:
A Review
Bradley J. Phillips, M.D.
Burn-Trauma-ICU
Adults & Pediatrics
Renal Function and Failure

Overview
 Renal Physiology
 Trauma and Renal Function
 Initial management of Oliguria
 Acute Renal Failure

Key Management Issues
Glomerular
Architecture
Physiology in Normal State
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Renal blood flow (RBF)
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20-25% cardiac output
distribution
• 85% outer cortical
• 15% inner cortex outer
medulla
• <1% inner medulla
Physiology in Normal State
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Glomerular filtration
 20% of plasma filtered as cell-free and protein-free
 normal GFR 125 ml/min
 calculate
• most accurate - insulin

completely filtered/neither secreted or absorbed
• good estimation - creatinine
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(Cr Urine / Cr Plasma) x urine (ml/min)
Glomerular Component Functions
Proximal Convoluted Tubule
60-80% reabsoprtion of H2O,
Na, Cl, K, HCO3
100% glucose/amino acids
Distal Convoluted Tubule
20% reabsoprtion of H2O
Renin/Aldosterone Effect
Loops of Henle
20% of H2O (descending), 25% Na,
Cl, K, Large amounts HCO3, Mg, Cl
Secretion of H ions, Active Na
Reabsorption
Collecting Ducts
reabsoprtion of H2O,
ADH effect
Renal Physiology after Trauma
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Class I Hemorrhage (10-15%)
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Class II Hemorrhage (15-30%)
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autoregulation maintains GFR
exceeds autoregulation
vasoconstriction at afferent & efferent
GFR decreases by 50-60%
Class III Hemorrhage (30-40%)
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GFR decreases to less than 20%
resuscitation relieves vasocontriction over hours to days,
afferent then efferent arterioles
Oliguria after Trauma
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Rapid replenishment of the circulatory volume and
cardiac output
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at least 3-4 L for every 1 L of blood loss
Factors
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general anesthetic
• loss of renal autoregulation
• loss of systemic vasoconstriction
Key Management Issue
IV Fluid Resuscitation
Renal Function and Trauma
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Postresuscitative oliguria
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even if MAP and CO restored
persistant for several hours secondary to renal arteriole vasoconstriction
shifting of fluid from plasma to interstitial space secondary to depletion
during hypotension/hypovolemia
Postresuscitative polyuria
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usually transient
not excessive (< 250 cc for 30-45 mins, < 3 hrs)
“wash out” effect of inner medulla
use other parameters ( i.e. HR, base deficit)
Postoperative Fluid Sequestration
Obligatory extravascular sequestration
 Phase II (Lucas, Resuscitation of the Injured Patient: Three Phases of Resuscitation, Surg Clin North Am, 1977)
 Lasts 12-36 hours
 Clinical signs
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tachycardia
reduced pulse pressure
oliguria
weight gain
some respiratory insufficiency
Hormoral effect - ADH, aldosterone
Fluid Mobilization Phase
Phase III - mobilization and diuresis
 Water added to plasma faster than excreted
 “Postresuscitation Hypertension”
 Renal blood flow still remains decreased
 Caution with diuretics
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role in post elective surgery in elderly patient with CHF
avoid in trauma patients
can precipitate oliguria/renal dysfunction
Mechanical Ventilation and Fluid Therapy
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Reduce renal blood flow
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even if zero PEEP
PEEP reduces RBF more
additional fluid may be required to maintain UOP
Acid-Base Balance
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Hemorrhagic shock
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increased lactate acidosis
metabolic acidosis persistent after intravascular volume repleted (hours)
• cell metabolism
• impaired renal excretion of acids
Renal acid excretion
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absorb Na/HCO3, excrete PO, NH3
normal excrete 70-80 mEq /day
can excrete 4-5x normal with severe acidosis
depends on GFR and RBF
Renal Response to Sepsis
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Hyperdynamic state
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increased CO, increased RBF, decreased SVR, expanded ECF
volume, increased UOP
“inappropriate polyuria”
• vasodilators of sepsis
• “wash out” effect
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Hypodynamic state
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later stages of severe sepsis
decreased CO, increased SVR, decreased GFR and RBF
Key Management Issue
IV Fluid Resuscitation
PEARL: Check Urine Na.
If less than 10 meq/L…???
Acute Renal Failure

Mortality in posttrauma = 50- 60%
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acute oliguric > 90%
contrast nonoliguric < 20%
Terminology
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ARF - sudden, severe deterioration
• rule of thumb - Cr increasing > 1.0 mg/dL/day
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Acute tubular necrosis (ATN) - form of ARF
Oliguria: UOP less than 400 ml/d
• 500 mOsm daily solute concentrated to 1200 mOsm/kg
Anuria: UOP less than 50 ml/d
Nonoliguric renal failure
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progressive azotemia despite UOP > 400 ml/d
High-output renal failure
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acute renal insufficiency with UOP > 4 L/d
Acute Renal Failure
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Etiology
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severe and prolonged hypotension
severe sepsis
massive blood transfusions
compartment syndrome
myoglobinuria/hemoglobinuria
radiocontrast
aortic cross clamping (> 30 minutes)
drug-induced
postinfectious glomerulonephritis
Contributing factors
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age
pre-existing renal vascular disease
pre-existing renal insufficiency
Myoglobinuria/hemoglobinuria
Muscle necrosis or RBC destruction
 Hypotension significant increase risk of ATN
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Skeletal muscle (per kg of tissue)
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can occur even if renal perfusion well maintained
40-45 meg K
730 ml of H2O
23 mmol of PO4
4 g myoglobin ( takes 100-150 mg/dL to discolor urine)
Severe crush injury/muscle ischemia causes hyperkalemia,
hyperphosphotemia,azotemia, hypocalemia, DIC, hypotension, and
myoglobinuria
Predictors of ARF ?

Vivino G. Antonelli M. Moro ML. Cottini F. Conti G. Bufi M. Cannata F.
Gasparetto A. Risk factors for acute renal failure in trauma patients.
Intensive Care Medicine. 24(8):808-14, 1998 Aug
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prospective, consecutive 153 trauma patients
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CPK > 10,000, PEEP > 6, hemoperitoneum
Loun B. Astles R. Copeland KR. Sedor FA. Adaptation of a quantitative
immunoassay for urine myoglobin. Predictor in detecting renal
dysfunction. American Journal of Clinical Pathology. 105(4):479-86, 1996
Apr.
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urine assay for myoglobinuria
levels > 20,000 mcg/L
Key Management Issue
Administer IV Fluid Resuscitation
and
Maintain UOP > 100 cc/hr
Rhabdomyolysis
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Treatment
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volume, volume, volume!!!
• shock and rhabdomyolysis = renal failure
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maintain UOP > 100 - 200 cc/hr
? role or sodium bicarbonate
• precipitation of myoglobin urine pH < 5.6
• check urine pH
• consider if UOP marginal or severe hyperkalemia
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mannitol (avoid lasix if possible)
• volume expander, mild diuretic, free radical scavenger
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follow CPK levels (most sensitive)
Drug-Induced ARF
Pathogenesis depends on drug
 Predisposing factors
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volume depletion
age
pre-existing renal disease
prolonged therapy
other nephrotoxic agents
Drug-Induced ARF
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Antibiotics
 aminoglycosides (most publicized)
• however use of cephalosporins and clindamycin potentate nephrotoxicity
amphotericin B
 vancomycin
 PCN can cause hypersensitivity nephritis
 Limit nephrotoxicity
 low trough
 ? once a day dosing (proven to limit ototoxicity)
 avoid NSAIDS
 avoid combination of nephrotoxic antibiotics
 avoid hypotension
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Radiocontrast-Induced Nephropathy
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Incidence as high as 13%
Mechanisms
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direct toxicity
renal ischemia (vasoconstriction)
intratubular obstruction
immunologic abnormality
Clinical
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serum Cr elevation within 24 hours
serum Cr peak day 3-5
renal function normally returns by 10 days
hemodialysis seldom needed
Key Management Issue
Administer IV Fluid Resuscitation
Only IV fluid hydration has been shown to reduce incidence of IV
contrast nephropathy (not lasix or dopamine).
Should maintain UOP 12 hours before and 24 hours post procedure
Classification of ARF
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Prerenal azotemia
 inadequate renal perfusion
 characterized by low urine Na/high urine Cr
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Postrenal azotemia
 complete obstruction bilateral ureteral or lower urinary tact
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Acute tubular interstitial nephritis
 usual drug-induced
 signs of hypersensitivity (check urine eosinophils)
 renal biopsy
ARF - Clinical Changes
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Increase serum Cr (> 1 to 1.5 mg/dL/d)
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Increase BUN (exceeds > 25 mg/dL/d)
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directly related to decreased GFR
related to decreased GFR and reabsorption
Hyponatremia
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intake fluids > UOP (particularly hypotonic solutions)
increased endogenous water
increased loss of urine sodium
ARF - Clinical Changes
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Hyperkalemia
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Metabolic acidosis
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reduced excretion from decreased GFR
impaired renal tubules secretion
faster if muscle protein breakdown due to ischemia or injury
accelerated protein catabolism
decreased excretion of acid load
Other electrolytes
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hyperPO4, hyperMg
hypoCa
Differential Diagnosis
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Postrenal azotemia
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rule out urinary tract obstruction
Prerenal azotemia
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hypovolemia
cardiac failure
Hypovolemia
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Renal response to decreased blood flow
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normal - conserve H20 and Na
ARF - impaired ability to concentrate/conserve
Differentiation of Pre-renal vs ARF
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renal failure index
RFI = Urine Cr / Plasma Cr
< 1.0 prerenal azotemia
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fractional excretion of sodium
FE = (U Na/P Na) / (U Cr/P Cr) x 100
< 1.0 prerenal azotemia
SIMULATANEOUS SPOT PLASMA & URINE SAMPLES
Urinalysis
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Prerenal azotemia
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Obstructive uropathy
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unremarkable
unremarkable
Glomerular disease
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heavy proteinuria
sterile pyuria
mild microhematuria
casts (granular/WBC)
? eosinophils
Key Management Issue
Fluid Challenge !!!!!
RULE OUT HYPOVOLEMIA
1. test response to fluid challenge at least 500 to 1,000 cc
(15-30 minutes)
2. consider CVP or pulmonary artery monitoring
Treatment of ARF
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Diuretics
 after hypovolemia ruled out
 if given soon after onset of oliguria may convert to nonoliguric renal dysfunction (better prognosis)
 types
• mannitol
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osmotic diuretic decrease proximal Na reabsorption
dose: 25 g IV bolus
• lasix
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inhibits active Na transport in loop of Henle
dose: 20-40 mg IV initial, then double every 30 minutes if no
response (max dose 500 mg)
• dopamine (low dose, 1-3 ug/kg/min)
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effects partially due to inhibition of ADH
Sodium and Water Balance
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Fluid restriction is important treatment of ARF
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careful to maintain perfusion
problem sometimes with initial hemodialysis
Fluid requirements
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GI and renal loss plus 500 cc
accurate daily weights and I/O’s
Metabolic Acidosis
Hypercatabolic generation of acid loads
 Produces anion gap
 Best treated with reducing catabolism or
hemodialysis, not sodium bicarbonate
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Hemodialysis
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Indications
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refractory pulmonary edema
hyperkalemic crisis
uremic complications
severe metabolic acidosis
A
Acidosis
E
Electrolyte disturbance
I
Intoxication
O
Overload
U
Uremia
Y
Why not
Hemodialysis
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Ultrafiltration
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indicated in hemodynamically unstable patients
continuous venovenous (CVVH) or arteriovenous (CAVH)
filtrate removal of 500-800 ml/hr
require often some heparinization
Hemodialysis
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rapid correction of uremia, fluid overload, electrolyte disturbances, and
acidosis
“prophylactic” dialysis probably beneficial
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added benefit by providing for adequate calories and protein
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ARF - Special
Consideration/Complication
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Adjustment of medications
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Coagulopathy
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platelet dysfunction in aggregation
• treatment with DDAVP (0.3 ug/kg)
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low antithrombin III levels
• microvascular thrombosis
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Hyperkalemia
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increased with blood transfusions, acidosis, and hyperosmolemia
(ie treatment with diuretics)
usual treatment (glucose + insulin, calcium IV)
avoid kayexelate (Na exchange for K)
ARF - Special
Consideration/Complication
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Anemia
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reduced EPO levels
contributing factors include GI blood loss and
hemodialysis (i.e. hemolysis)
treatment with recombinant EPO/Fe replacement
Stress gastritis
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more than 20% of ARF patients
treatment
• AlOH antacids (also treats hyperphosphotemia)
• H2 blockers
ARF - Special
Consideration/Complication
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Pericarditis (uremia)
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with or without pleuritis
presence of chest pain or friction rub
some with fever with or without leukocytosis
treatment with hemodialysis
Nutritional support
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problems
• insulin resistance
• negligible free water and urea clearance
• ? high energy requirement
ARF - Special
Consideration/Complication
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Nutritional support
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treatment
• minimize free water
• do not restrict protein if needed unless unable to clear with
hemodialysis
Outcomes of ARF
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Oliguric ARF
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expect return of renal function in 3 weeks
if enter diuretic phase, likelihood of survival greatly increased
older patients progress to chronic renal failure much more often
Non-oliguric ARF
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increasing secondary earlier and aggressive fluid resuscitation and
conversion with diuretics
easier to manage than oliguric
only few require dialysis
much lower mortality
Questions ?