L20: AKI Flashcards
Acute renal failure
refers to severe AKI which requires dialysis
AKI diagnosis
One of the following
- Increase in serum creatinine by >.3 mg/dL in 48 hours
- Increase in serum creatinine 1.5X baseline within last 7 days
- Urine output*
Prerenal AKI
decreased renal perfusion
Intrinsic renal AKI
acute tubular necrosis
Postrenal AKI
obstructive
Prerenal disease can be caused by
True volume depletion Hypotension (Shock, Aggressive HTN tx) Edema Selective renal ischemia (Bilateral renal artery stenosis) Medications affecting GFR
Medications affecting GFR
NSAIDS
ACE-I
Intrinsic renal disease can be caused by
Renal ischemia: from any severe prerenal disease
Sepsis: hypotension→ release of cytokines and activation of neutrophils
Nephrotoxins
Risk of AKI from IV contrast
Pre-existing renal disease: rare in normal renal function
Volume depletion
Repeated doses of contrast
DM, CHF, age
Nephrotoxic drugs to avoid for 48 hours after IV contrast
NSAIDS
Metformin
Nephrotoxins that may cause AKI
Rhabdomyolysis→ Heme pigments Cisplatin HIV meds IVIG Mannitol IV contrast Aminoglycosides
Causes of postrenal AKI
Bilateral obstruction:
Prostatic disease: hyperplasia or cancer
Metastatic cancer
Neurological disease: neurogenic bladder→ urinary retention
Obstructive BPH tx
foley catheter
Nonoliguric
> 400 mL/24 hours
Oliguric
<400 mL/24 hours
Anuric
<100 mL/24 hours
Make sure urine from a urinalysis
Is at room temperature within 2 hours of collection (or refrigerated then rewarmed)
Foley catheter: get sample “fresh” from tubing, not bag
Pathognomonic for acute tubular necrosis
muddy brown casts
Normal serum creatinine levels by gender
Male: .6-1.2 mg/dL
Female: .5-1.1 mg/dL
How is serum creatinine related to GFR?
Inverse relationship
ex: doubled serum creatine would represent a halved GFR
Prerenal fractional excretion of sodium (FENa)
<1%
Intrarenal fractional excretion of sodium (FENa)
> 2%
fractional excretion of sodium (FENa) is between 1-2%
could be either prerenal or intrarenal causes
when is fractional excretion of sodium (FENa) unreliable
diuretics
fractional excretion of sodium (FENa) calculation
(Urine Na/Serum Na)/ (Urine Cr/Serum CR) x 100%
Would diagnose post-renal cause of AKI if seen on ultrasound
hydronephrosis
Indication for renal biopsy
To provide more definitive diagnosis when there is no clear explanation of AKI:
Creatinine is markedly elevated/significantly worsens
May allow therapeutic intervention to prevent end stage renal disease
Contraindications for renal biopsy
Bleeding diathesis
Pyelonephritis
Renal tumor
Solitary native kidney
When is dialysis indicated for AKI?
Life-threatening complications
Volume imbalance, metabolic acidosis, hyperkalemia, hypocalcemia, hyperphosphatemia, uremia, AMS (severe AKI)
Fluid challenge
if fluid causes an increase in urine, the cause of AKI is prerenal
Signs/symptoms of volume depletion
History of fluid loss: N/V
Hypotension, tachycardia, oliguria
How to do a fluid challenge
1-3 L of .9 NS
Reassess
How might a patient become volume overloaded?
Initial presentation
~OR~
Fluid retention from IV therapy + decreased ability to secrete sodium and water
Volume overload treatment
Diuretics
I+Os
What can volume overload eventually cause?
Fluid retention→ pulmonary edema→ respiratory failure
If diuretics don’t increase urine output in a volume overloaded patient
stop diuretics
start dialysis
Causes of metabolic acidosis
Excretion of acid and regeneration of bicarb impaired + Low GFR
Diarrhea→ lost bicarb→ worsens
Sepsis, trauma, multi-organ failure (lactic/keto acids)
For whom is dialysis the preferred treatment of metabolic acidosis?
Severe oligo-anuric AKI + volume overload + pH <7.1 (hemodynamically unstable)
For whom is bicarbonate administration not preferred in cases of metabolic acidosis?
volume overload: causes large sodium load that can contribute to volume overload
2 ways to manage metabolic acidosis
Dialysis
Bicarbonate administrations
When can bicarb be given for metabolic acidosis?
not volume overloaded and: Diarrhea pH <7.1 awaiting dialysis Rhabdomyolysis → prevent further renal injury by myoglobin → Falling out of favor
Hyperkalemia presentation
Has very few symptoms, but is fatal
Impaired neuromuscular transmission and cardiac conduction abnormalities
Hyperkalemia treatment
Medical therapy + dialysis
→ Remove excess and drive extracellular K+ into cells
If a patient is asymptomatic, hypocalemic, and hyperphostphatemic
correct hyperphosphatemia
Why do Hypocalcemia and Hyperphosphatemia occur in AKI?
Reduced GFR→ increased phosphorus → decreased calcium
Common
When is the total serum concentration of ionized calcium inaccurate?
Low albumin
Signs of hypocalcemia
paresthesia, tetany (carpopedal spasm)
confusion
seizures
trousseau’s sign (carpal spasm after occlusion of brachial artery)
chvostek’s sign (tap facial nerve→ contraction)
QT prolongation
Treatment of symptomatic hypocalcemia and hyperphosphatemia
IV calcium
→ Severe hypocalcemia: given while awaiting dialysis regardless of risk of calcification
IV Calcium side effects
If severely hyperphosphatemic, IV calcium → calcium phosphate crystal deposition in vasculature/organs
Hyperphosphatemia >6 mg/dL treatment
dietary phosphate binders
If a hyperphosphatemic patient cannot tolerate oral intake
dialysis
Hyperphosphatemia >12 mg/dL treatment
dialysis
→ faster than binders
→ more effective in preventing injury to to crystal precipitation
Dietary phosphate binders if the patient is also hypocalcemic
Calcium acetate
Calcium carbonate
Dietary phosphate binders if the patient is not hypocalcemic
Aluminum hydroxide
Lanthanum carbonate
Severe uremia treatment
dialysis
Severe uremia symptoms
pericarditis
neuropathy
decline in mental status
When is severe uremia more common?
CKD
An episode of AKI
greater risk of CKD and ESRD
predictor poor prognosis for short term and long term mortality
serum creatinine increases by .3 mg/dL
If a patient gets AKI during their ICU stay
there is a 50% mortality rate
How many patients:
Have AKI on admission?
Develop AKI during hospitalization?
Develop AKI in the ICU?
1%
25%
60%
