Transcript Acute Kidney Injury in the Critically Ill

Acute Kidney Injury in the Critically Ill
Stephanie Davidson, ACNP-BC
Vanderbilt University Medical Center
Medical Intensive Care Unit
Objectives
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Brief pathophysiology review
Name the 3 types of acute kidney injury
Review contrast nephropathy and its treatments
Discuss necessary diagnostic tests
Discuss treatment modalities for the 3 types of acute
kidney injury
Epidemiology
• Acute Kidney Injury (AKI) – occurs in up to 20% of
ICU patients
– 25% will require RRT
– 5% of general hospital population
• AKI is usually multifactorial
– Sepsis
– Hypotension
– Drugs
• Mortality rate up to 80%
Pathophysiology
• Blood flows from renal arteries and is delivered to
the glomeruli
• Glomeruli form ultrafiltrate  delivered to renal
tubules
– Nearly free of protein and blood elements
• Tubules reabsorb and secrete solute and/or water
from ultrafiltrate
• Final tubular fluid (urine) leaves kidneys and drains
into renal pelvis to ureters, bladder, then urethra
Pathophysiology
• Urine volume indicated kidney perfusion
• Urine specific gravity and osmolality
(concentrating ability) indicate tubular
function
Definition
• Lack of consensus definition in the past
• Acute Dialysis Quality Initiative (ADQI) created
– RIFLE criteria
– Graded risks of injury
– Has been validated in variety of critically ill populations
• Acute Kidney Injury Network (AKIN)
– Modified RIFLE criteria
– Diagnostic and staging criteria for injury
– Acute Kidney Injury to describe all levels of injury
Bellomo et al.,Critical Care 2004, 8:R204-R212
RIFLE Criteria
Creatinine/GFR
OR
UOP
Risk
1.5-fold ↑ in Cr OR
GFR ↓ by 25%
< 0.5 ml/kg/hr x 6 hrs
Injury
2-fold ↑ in Cr
GFR ↓ by 50%
OR
< 0.5 ml/kg/hr x 12 hrs
Failure
3-fold ↑ in Cr
GFR ↓ by 75%
OR
< 0.5 ml/kg/hr x 24 hrs
OR
Anuria x 12 hrs
Loss
Complete loss of function > 4
weeks (needs RRT)
ESRD
Complete loss of function > 3
months
AKIN Criteria
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Based on abrupt (48 hr) increases
⬆ Cr of ≥ 0.3 mg/dl from baseline
OR
⬆ in Cr of ≥ 50%
OR
Oliguria ( < 0.5mg/kg/hr x 6 hrs or more)
✴✴Exclude obstruction if UOP is basis for diagnosis
✴✴Optimize volume status, then apply criteria
Mehta, R, et al. Crit Care, 2007; 11:R31
Risk Factors for AKI
• age > 75 yrs
• chronic kidney disease (CKD, eGFR < 60
mls/min/1.73m2)
• Cardiac failure
• Atherosclerotic peripheral vascular disease
• Liver disease
• Diabetes mellitus
• Nephrotoxic medications
Complications of AKI
Metabolic
CV
Neuro
Metabolic
acidosis
Fluid
overload
Hyper K+
HTN
Hypo Ca++
Arrhythmias Seizures
Hyperphos
Pericarditis
Heme
GI
Infectious
Neuropathy Anemia
N&V
UTI
Dementia
GI bleeding IV catheter
sepsis
Coag
anomalies
Pneumonia
hyper
uremic
Marini, J & Wheeler, A, Critical Care Medicine, 2010
Types of AKI
• Pre-renal
– Hypoperfusion (shock, cirrhosis, CHF)
– Volume depletion (GI bleed, dehydration)
• Intra-renal
– Acute interstitial nephritis (drug induced)
– Acute tubular necrosis
– Tumor Lysis Syndrome
• Post renal
– obstruction
Tests and Formulas
• FENa - fractional excretion of sodium
• Can help differentiate prerenal from ATN
– Measures percentage of filtered Na that is excreted
– If <1%: prerenal, if >1%: ATN
– Not accurate if pt has received diuretics
– (PCr x UNa)/ (PNa x UCr) x 100%
– Na = mEq/L Cr = mg/dl
• Feurea – fractional excretion of urea
– Better estimation if pt has had diuretics
– (serumCr x urineUrea)/ (serumUrea x urineCr) x 100%
– all units in mg/dl
Tests and Formulas
• Urine to plasma creatinine ratio
– Estimates tubular water resorption
– Creatinine in filtrate is equal to that of plasma
– Urine Cr increases as water, not Cr, is reabsorbed
Prerenal
AKI
Postrenal
AKI
ATN
AIN
Etiology
Dehydration,
hypoperfusion
Obstruction
Ischemia,
nephrotoxins
Allergic rxn;
drug rxn
Serum BUN:Cr
ratio
> 20:1
> 20:1
< 20:1
< 20:1
Urine Na
(mEq/L)
< 20
Variable
> 20
Variable
FeNa
< 1%
Variable
> 1%
Variable
Urine osms
(mosm/kg)
>500
< 400
250 - 300
Variable
Urinary
sediment
Hyaline casts
Nml or red
Muddy brown
cells, white
casts, renal
cells, or crystals tubular casts
White cells,
white cell casts,
+/- eosinophils
Common Diagnostics
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Urinalysis
Serum BUN/Cr
Urine Na+
FENa or FEurea
Urine osmolality
Urine to plasma Cr ratio
Urine volume
• Renal ultrasound
– Gold standard
– Will show obstructions,
hydronephrosis, kidney
size
• Consider CT abd/pelvis
• Consider 24 hr urine
collection
Prerenal Failure
• R/T hypoperfusion and incomplete compensatory mechanisms
• Causes:
– Hypovolemia: dehydration, hemorrhage, diuretics, GI losses
– Edematous states: cirrhosis, CHF
– Renal artery stenosis, hepatorenal syndrome, compartment
syndrome with elevated intraabdominal pressures
• Results:
– Kidney is normal: glomeruli, tubules and interstitium intact
– Untreated can lead to ischemia
– Can occur is MAP <60 for >30minutes; worse if patient is
hypoxic
Compensatory Mechanisms
Systemic hypoperfusion
Preservation of blood flow
BUT
Kidneys secrete renin and
ADH
Renal vasoconstriction
decreases renal flow and GFR
Arterial and venous
vasoconstriction
Untreated = persistently
decreased MAP and GFR
Prerenal Treatment
• Treat underlying problem
– GI losses
– CHF/cirrhosis (intravascularly dry)
• Attempt to reverse oliguria
– Fluid challenge
– Over 20-30 min; repeat if needed  monitor UOP
– Use crystalloid solution, 15-30ml/kg x1
– Avoid if pt has s/s volume overload
– Lasix challenge: one dose of 1mg/kg
• Consider invasive monitoring
– CVP
Intrarenal Failure
Tubular
Disorders
Interstitial
Nephritis
Glomerulonephritis
and small vessel
vasculitis
-ATN
-Tumor lysis
syndrome
-Contrast
Nephropathy
-Drug induced
allergy
-uncommon
cause of AKI in
ICU patients
ATN
• Sudden decline in GFR, accumulation of nitrogenous
wastes, and dysregulation of electrolytes and acidbase balance
• Causes:
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Prerenal if delayed treatment
Hypotension
Sepsis
Tumor lysis syndrome
Nephrotoxic substances
• Drugs: aminoglycosides, amphotericin, cyclosporine, ACEi, NSAIDs
• Ethylene glycol/methanol
Prerenal
AKI
Postrenal
AKI
ATN
AIN
Etiology
Dehydration,
hypoperfusion
Obstruction
Ischemia,
nephrotoxins
Allergic rxn;
drug rxn
Serum BUN:Cr
ratio
> 20:1
> 20:1
< 20:1
< 20:1
Urine Na
(mEq/L)
< 20
Variable
> 20
Variable
FeNa
< 1%
Variable
> 1%
Variable
Urine osms
(mosm/kg)
>500
< 400
250 - 300
Variable
Urinary
sediment
Hyaline casts
Nml or red
Muddy brown
cells, white
casts, renal
cells, or crystals tubular casts
White cells,
white cell casts,
+/- eosinophils
ATN Treatment
• Treat underlying cause
– Sepsis, hypotension, ischemia, drugs
• Avoid volume overload
• Nonoliguric renal failure has better outcomes than
oliguric
• Monitor for hyperkalemia and treat
• Monitor acid-base status (BMP)
ATN Treatment
• Consult nephrology
– Courtesy and evaluate for possible RRT
• Monitor for AEIOU of HD
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A = acidosis/alkalosis
E = electrolyte disturbances
I = Intoxications (methanol, ethylene glycol, salicylate)
O = overload (volume)
U = uremia
If any of these exist or are refractory, pt may need dialysis
-Decision when to start hemodialysis is difficult and cannot be guided by a
single objective measure
-Delaying until patient is symptomatic could increase risk of harm and/or
death
Tattersall, J., et al, Neph. Dial. Transplant (2011). 26(7):2082-2086
Contrast-Induced Nephropathy
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Evaluate risk vs. benefit of test
Occurs within 72 hrs of contrast given
Can resolve within 5 days
Prevent with fluid
– 0.9% saline: 1mL/kg x 12 hrs pre and post procedure
– Isotonic bicarb: same dosing
– No consensus on which is better
• No evidence for NAC (mucomyst)
• Consider holding ACE-I/ARB and metformin prior to
contrast
AIN
• Drug induced allergic reaction in the renal interstitium
• Common drugs: PCN, cephalosporins, sulfonamides,
quinolones, rifampin, thiazides, furosemide, NSAIDs,
allopurinol, cimetidine
• Oliguria and rising serum creatinine often only indicators
– ¼ of patients will have eosinophilia
– ⅔ of patients will have eosinophiluria
• Discontinue offending drug, consider steroids
Marini, J & Wheeler, A, Critical Care Medicine, 2010
Prerenal
AKI
Postrenal
AKI
ATN
AIN
Etiology
Dehydration,
hypoperfusion
Obstruction
Ischemia,
nephrotoxins
Allergic rxn;
drug rxn
Serum BUN:Cr
ratio
> 20:1
> 20:1
< 20:1
< 20:1
Urine Na
(mEq/L)
< 20
Variable
> 20
Variable
FeNa
< 1%
Variable
> 1%
Variable
Urine osms
(mosm/kg)
>500
< 400
250 - 300
Variable
Urinary
sediment
Hyaline casts
Nml or red
Muddy brown
cells, white
casts, renal
cells, or crystals tubular casts
White cells,
white cell casts,
+/- eosinophils
Post Renal Failure
• Less than 10% of AKI cases
• High suspicion if abrupt stop in flow or decreased UOP
• Causes:
– Renal calculi/clots
– Prostatic hypertrophy
– Ureteral stone
– Rhabdomyolysis
• Check renal ultrasound- hydronephrosis, renal obstruction
• Consider CT of abd/pelvis
• Treat underlying cause
Prerenal
AKI
Postrenal
AKI
ATN
AIN
Etiology
Dehydration,
hypoperfusion
Obstruction
Ischemia,
nephrotoxins
Allergic rxn;
drug rxn
Serum BUN:Cr
ratio
> 20:1
> 20:1
< 20:1
< 20:1
Urine Na
(mEq/L)
< 20
Variable
> 20
Variable
FeNa
< 1%
Variable
> 1%
Variable
Urine osms
(mosm/kg)
>500
< 400
250 - 300
Variable
Urinary
sediment
Hyaline casts
Nml or red
Muddy brown
cells, white
casts, renal
cells, or crystals tubular casts
White cells,
white cell casts,
+/- eosinophils
Outcomes and Prognosis
• AKI patients associated with
– Increased hospital and long term mortality
– Longer hospital LOS
– Increased costs
• AKI patients requiring HD
– Extremely high risk for CKD
– 10% may go on to develop ESRD
**Importance to have post-discharge follow up with
nephrologist
Waikar, S. & Bonventre, J., Harrison’s Principles of Internal Medicine, 2012.
References
Bellomo, R, et al. Acute renal failure-definition, outcome measures, aminal
models fluid therapy and information technology needs: the Second
International Consensus Conference of the Acute Dialysis Quality
Initiative (ADQI) Group. Crit Care 2004; 8:R 204.
Erdbruegger, U. and Okusa, M. (2012). Etiology and diagnosis of acute
tubular necrosis and prerenal disease. Retrieved from
www.uptodate.com.
Esson, M. and Schrier, R. (2002). Diagnosis and Treatment of Acute Tubular
Necrosis. Annals of Internal Medicine, 137: 744-752
Fink, M., Abraham, E., Vincent, J.L., and Kochanek, P. (2005). Textbook of
Critical Care (5th ed.). Philadelphia, PA: Elsevier Saunders.
Levin, A, et al. Improving outcomes from acute kidney injury: report of an
initiative. Am J Kidney Dis. 2007; 50:1.
References
Lewington, A. and Kanagasundaram, S. (2011). Summary of clinical practice
guidelines for acute kidney injury. Retrieved from
www.renal.org/Clinical/GuidelinesSection/AcuteKidneyInjury.aspx
McPhee, SJ and Papadakis M. (2008). Current Medical Diagnosis and
Treatment. Tierney Jr, Lawrence (Ed.). New York, NY: McGraw Hill
Medical.
Neesh, P., Nadim, M., An overview of drug-induced acute kidney injury.
Critical Care Medicine, 2008; 36: No 4 (suppl).
Palevsky, P. (2012). Definition of acute kidney injury (acute renal failure).
Retrieved from www.uptodate.com.
Post, T. and Rose, B. (2012). Diagnostic approach to the patient with acute or
chronic kidney disease. Retrieved from www.uptodate.com.
Ricci, A., Cruz, D., and Ronco, C. (2008). The RIFLE criteria and mortality in
acute kidney injury: A systematic review. Kidney International, 73, 538546
References
Tattersall, J., et al. When to start dialysis: updated guidance following
publication of the Initiating Dialysis Early and Late (IDEAL) Study.
Nephrol. Dial. Transplant (2011) 26(7). 2082-2086.
Waikar S.S., Bonventre J.V. (2012). Chapter 279. Acute Kidney Injury. In Longo
D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J (Eds),
Harrison's Principles of Internal Medicine, 18e. Retrieved August 16, 2014
fromhttp://accessmedicine.mhmedical.com/content.aspx?bookid=331&S
ectio nid=40727068.