Transcript Acute Kidney Injury Jeffrey Coughenour, MD, FACS Medical Director, Surgical Critical Care

Acute Kidney Injury
Jeffrey Coughenour, MD, FACS
Medical Director, Surgical Critical Care
Acute Kidney Injury
• More than 35 definitions exist in literature
• Based on:
– Serum creatinine, urine output, BUN, renal
replacement therapy
• RIFLE Criteria proposed in 2002
Acute kidney injury in the intensive care unit: An update and primer for the
intensivist
Dennen P Crit Care Med 2010 Jan;38(1):261-75
RIFLE Criteria
AKIN Diagnostic Criteria
• Abrupt onset (within 48 hours) including:
– Absolute increase in SCr ≥ 0.3 mg/dL OR
– Percentage increase in SCr ≥ 50% OR
– Reduction in urine output (< 0.5 mL/kg/hr x6)
• Requires two SCr values within 48 hours
• AKIN Stage 1-3 correlates with RIFLE risk,
injury, and failure
Incidence
• Approximately 7% of all hospitalized patients
• 65-70% of critically ill patients
– RIFLE Stage F 10-20% of ICU admissions
• AKI requiring RRT: Mortality range 50-70%
• Sepsis most common cause
RIFLE criteria for acute kidney injury are
associated with hospital mortality in critically ill
patients: a cohort analysis
Hoste EA Crit Care 2006;10(3):R73. Epub 2006 May 12
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5,383 admissions
67% of all ICU admissions met AKI criteria
45% developed AKI after ICU admission
Mortality
– No AKI 5.5%, maximal RIFLE stage increased to
8.8%, 11.4%, 26.3% respectively
Defining the contribution of renal dysfunction
to outcome after traumatic injury
Harbrecht BA Am Surg 2007 Aug;73(8):836-40
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3,968 patients with ISS ≥ 14
167 (4%) developed SCr > 2
Mortality 2.9% vs. 34.1%
Hospital LOS 10.9 vs. 29.1
Ventilator days 2.4 vs. 12.7
AKI and Mortality
• Independent risk factor
• “AKI appears to increase the risk of developing
severe non-renal complications that lead to
death”
• Respiratory failure 20.7% vs 57.4%
• ICU mortality 14% vs 42.8%
• In-hospital mortality 7% vs 34%
Causes of AKI
Top 5
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Sepsis
Major surgery
Low cardiac output
Hypovolemia
Medications
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Other common causes
Cardiopulmonary
bypass
IAH-ACS
Trauma
Rhabdomyolysis
Obstruction
Risk Factors
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Nephrotoxic medications
Radiographic imaging dye
Gadolinium
Trauma: Age > 60, higher ISS, multiple
transfusions, GCS < 10, PEEP < 6 OR 2.89, PEEP
> 6 OR 20.7, hemoperitoneum OR 11.9
Prevention
Primary prevention best, often unpredictable
• Contrast-induced nephropathy
– Give fluid, NAC, low volume non-ionic or isoionic
contrast agent
• Albumin after large-volume paracentesis or
SBP (day 1 and 3) may decrease incidence of
AKI
Secondary Prevention
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Recognize underlying risk factors
Maintain renal perfusion
Avoid hyperglycemia
Avoid nephrotoxins
Acute Oliguria
“Lack of urine output in the acutely hypovolemic patient is renal success,
not renal failure”
Oliguria
• Urine output less than 400 mL/day
• Should be accompanied by:
– Increase in serum Cr ≥ 0.5 mg/dL above baseline
– Increase in serum Cr ≥ 50% above baseline
– Reduction in creatinine clearance ≥ 50%
– Severe renal dysfunction requiring some form of
renal replacement therapy
Prerenal Disorders
• Represents 50% of acute oliguric renal failure
• UNa < 20 mEq/L, FENa < 1%
Hypovolemia
Severe cardiac dysfunction
Loss of vascular tone
Renal vasoconstriction agents (NSAIDs)
Reduction in GFP (ACE-inhibitors)
Intrinsic Renal Disorders
• Impaired glomerular filtration, renal tubular
dysfunction, or both
• UNa > 40 mEq/L, FENa > 2%
• Described as three entities:
– Acute glomerulonephritis
– Acute tubular necrosis (most common)
– Acute interstitial nephritis
Acute Tubular Necrosis
• Ischemia and inflammatory cell injury
• Slough of tubular epithelial cells into lumen
• Obstructed proximal tubule creates backpressure decreases filtration
• Tubules and adjacent parenchyma involved
Postrenal Disorders
• Obstruction of urinary flow
– Collecting system
– Ureters
– Bladder outlet
• Acute—prerenal values (<20, <1%)
• Chronic—renal values (>40, >2%)
• Uncommon
Clinical Application
“This too shall pass– just like a kidney stone”
Serum Creatinine
• Standard surrogate measure of GFR
• Affected by non-renal factors common in the
ICU (variable secretion, volumes of
distribution)
• Late marker of AKI
– Rise in SCr = ~ 50% loss of function
Renal Ultrasound
• Confirm number of kidneys
• Rule out obstruction
• Evaluate degree of chronicity if baseline lab
values are unknown
• Measure degree of volume depletion (IVC)
Urine Microscopy
• Urine Microscopy
– Examination of sediment, easy, cost-effective
• Abundant tubular epithelial cells (ATN)
• White cell casts (interstitial nephritis)
• Pigmented casts (myoglobinuria)
If unrevealing, urinary sodium determination
may be helpful
Urine Sodium
• In the setting of oliguria, urine sodium below
20 mEq/L usually indicates a prerenal
disorder
• Elevated urine sodium can occur when a
prerenal disorder is superimposed on intrinsic
renal dysfunction (or diuretic therapy)
One of the most reliable parameters to
determine difference: FENa
FENa
• FENa < 1% = Prerenal disorder
• FENa > 2% = Intrinsic renal disorder
Optimize Central Hemodynamics
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CVP 6-8 mmHg
CO low? Push CVP 10-12 mmHg
Still low? Cardiac contractility measurement
Consider inotropic support agent
– Dopamine 5 mcg/kg/min
– Dobutamine 5 mcg/kg/min
– Goal CI above 3 L/min/m2
Stroke Volume Variability
Edwards Lifesciences, Irvine, CA
Stroke Volume Variability
• Correlation with “gold standard” of PAC
debated
• Requires 100% mechanical ventilation
• Interference
– Spontaneous respirations
– Arrythmia
Avoid Fluid Overload
• SOAP study subset; 1,120 patients with AKI
• Association with positive fluid balance and
increasing mortality
• Mean fluid balance differed between survivors
and non-survivors
• Patients requiring RRT, increase in fluid
balance 64.6% vs. 44.8% mortality
Payen, Crit Care Med 2008
Maintain Perfusion
• To prevent or mitigate injury, especially with
compromised autoregulation
• Volume
• Inotropic or vasopressor support
• Target MAP ≥ 65 generally accepted
Improving Perfusion
If oliguria persists despite adequate filling
pressure and flow…
• No evidence to support low-dose dopamine
• Mixed results with fenoldopam
Diuretics in AKI
• Studies conflicting re: affect on mortality
• No findings to support
– Shortened duration of AKI
– Reduced need for RRT
– Improved outcomes
• Furosemide
– Less than 10% of bolus dose reaches tubule lumen
– Continuous infusion may be preferred method of
delivery, 1-9 mg/hr rates reported
Hyperglycemia
• Decreased incidence of AKI and requirement
for RRT with tight glucose control
Tight blood glucose control is renoprotective in critically ill patients
Schetz M, Vanhorebeek I, Wouters PJ, Wilmer A, Van den Berghe G
J Am Soc Nephrol 2008 Mar;19(3):571-8 Epub 2008 Jan 30
Nutrition
• Malnutrition associated with increased
mortality
• Prealbumin renally excreted, may falsely
elevate in AKI
• AKI patients are hypercatabolic
• Consensus recommendation: 20-30
kcal/kg/day and 1.5 gm/kg/day protein
Treatment
“Last week I would've given a kidney to anyone in this office. I would've
reached right into my stomach and pulled it out for them. But now, no. I
don't have the relationship with these people that I thought I did. I hope
they ask, so they can hear me say, "Uh, no, I only give my organs to my real
friends. Go get yourself a monkey kidney.“
--Michael Scott, The Office
Treatment
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CRRT Continuous renal replacement therapy
SCUF Slow continuous ultrafiltration
CVVH Continuous venovenous hemofiltration
CVVHD Continuous venovenous hemodialysis
Classic Indications for RRT
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A—acidosis
E—electrolyte disturbances
I—intoxication
O—overload
U—uremia
Criteria for Initiation
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Non-obstructive oliguria
Severe acidemia
Hyperkalemia
Uremic end-organ involvement
Severe dysnatremia
Hyper- or hyponatremia
Overdose with dialyzable drug
Therapeutic Goal
Fluid removal
Urea clearance
Hyperkalemia
Metabolic acidosis
Cerebral edema
Hemodynamics
Preferred Therapy
Stable
Intermittent UF
Unstable
SCUF
Stable
Intermittent HD
Unstable
CRRT
Stable
Intermittent HD
Unstable
Intermittent HD
Stable
Intermittent HD
Unstable
CRRT
Stable
CRRT
Unstable
CRRT
Adapted from Continuous Renal Replacement Therapy,
John Kellum, Oxford Press 2009
Intermittent vs. Continuous
• Conflicting outcome data
• Recent meta-analysis demonstrated no
difference in mortality
• What about renal recovery?
– 2 studies—CRRT improved recovery
– 4 studies—No difference
– No definitive data
Continuous RRT
• Approximates “normal physiology”
– Slow correction of metabolic disturbances
– Volume removal better tolerated
• Goals
– Maintain fluid, electrolyte balance, acid/base,
prevent further renal damage, provide renal
support pending recovery
Discontinuation of CRRT
• No consensus in nephrology or critical care
literature
• UOP most important predictor of successful
discontinuation
– Greater than 400 mL/24 hrs without diuretics or >
2300 mL/24 hrs with diuretics, ≥ 80% chance of
success
Discontinuation of continuous renal replacement therapy: a post hoc analysis
of a prospective multicenter observational study
Uchino S Crit Care Med 2009 Sep;37(9):2576-82
Transition—CRRT to IHD
• No data
– Hemodynamically stable
– No vasopressor support
– Need to mobilize patient ?
– Need machine for more critically ill patient ?
Summary
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AKI is a common, complex condition
Etiology often multifactorial
Can be functional or structural
“Acute kidney injury” replaces “acute renal
failure”
• Small changes in SCr associated with adverse
outcomes
– Short and long-term increase in morbidity and
mortality
Summary
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Diagnosis frequently delayed
SCr poor marker of function in critically ill
AKI increases risk of CKD
AKI accelerates progression from CKD to ESRD
Volume overload is associated with worse
outcomes