AKI Flashcards
1
Q
ARF definition
A
SEVERE AKI - implies need for dialysis
2
Q
AKI Definition
A
ABRUPT decrease of kidney function
3
Q
Diagnosis of AKI
A
Based on serum Cr used to calculate GFR OR decrease in patient’s urine output
4
Q
Problem with using serum Cr for diagnosis
A
- In EARLY stages serum Cr may be low even though actual GFR is markedly reduced (not enough time)
- If patient is on dialysis there will be a false negative
5
Q
Best criteria for diagnosing AKI
A
KDIGO
6
Q
KDIGO diagnosis criteria
A
- Increase in serum Cr >0.3 mg/dL w/in 48 hours OR
- Increase in serum Cr >50% w/in 7 days OR
- Urine output <0.5 mL/kg/hour for > 6 hours
7
Q
KDIGO Stage 1
A
- Increase in serum Cr >0.3 mg/dL OR
- Increase in serum Cr 1.5 to 1.9 times baseline OR
- Urine output <0.5 for 6 to 12 hours
8
Q
KDIGO Stage 2
A
- Increase in serum Cr 2.0 to 2.9 times baseline OR
2. Urine output <0.5 for >12 hours
9
Q
KDIGO Stage 3
A
- Increase in serum Cr >4.0 mg/dL OR
- Increase in serum Cr 3.0 times baseline OR
- ANURIA for > 12 hours OR
- Initiation of renal replacement therapy
10
Q
Highest incidence of AKI
A
ICU - Develops in 60% of patients!
11
Q
Classifications of AKI
A
Prerenal, Intrinsic renal, postrenal
12
Q
Causes of prerenal AKI
A
Volume depletion Hypotension Edematous states Selective renal ischemia (bilateral renal artery stenosis) Drugs affecting GFR (NSAIDs, ACE-I)
13
Q
Causes of intrinsic renal AKI
A
Acute tubular necrosis (ATN) caused by:
- Renal ischemia
- Sepsis
- Nephrotoxins
14
Q
Types of nephrotoxins
A
Aminoglycosides IV CONTRAST* Heme pigments (rhabdo) Cisplatin HIV meds IVIG Mannitol
15
Q
Risk factors for ATN from IV contrast
A
Preexisting renal disease Volume depletion Repeated doses of contrast Comorbid conditions: DM, CHF Age
16
Q
Prevention of ATN by IV contrast
A
HYDRATION
Low osmolal agents at low doses
Avoid repetitive doses
Avoid nephrotoxic drugs for 48 hours after exposure
17
Q
Causes of postrenal AKI
A
Obstruction
18
Q
Most common cause of obstruction
A
Prostatic disease (hyperplasia or cancer) or metastatic cancer
19
Q
Reduction in GFR in patients without intrinsic renal disease requires…
A
BILATERAL obstruction (or unilateral in one functioning kidney)
20
Q
Nonoliguric
A
> 400 mL in 24 hours
21
Q
Oliguric
A
<400 mL but >100 mL in 24 hours
22
Q
Anuric
A
<100 mL in 24 hours
23
Q
Workup of AKI
A
UA
Serum metabolic panel
U/S, CT, MRI, or biopsy (as indicated)
24
Q
Core urine parameters in a UA
A
Heme Leukocyte esterase Nitrite Albumin pH Specific gravity Glucose
25
Pathognomonic cast of AKI
Muddy brown casts
26
Normal range for serum Cr
Male: 0.6 - 1.2 mg/dL
Female: 0.5 - 1.1 mg/dL
27
More accurate estimation of GFR
Modification of diet in renal disease (MDRD) - takes into account ethnicity and gender
28
Simplified measurement of GFR
Doubling of serum Cr is 1/2 GFR
29
Fractional excretion of sodium (FENa)
Percent of filtered sodium that is excreted in urine
30
FENa calculation
FENa = (Urine Na/Serum Na) / (Urine Cr/Serum Cr) x 100%
31
FENa <1%
Prerenal
32
FENa >2%
Intrinsic Renal
33
FENa between 1-2%
Either pre or intrinsic renal
34
When is FENa unreliable?
Pts on diuretics
| CHRONIC renal failure
35
Imaging for AKI
Renal U/S
36
When to image AKI
Underlying cause is unknown
| Assess for obstruction (postrenal)
37
Most common imaging finding with obstruction
Hydronephrosis
38
When to do a renal biopsy
No clear explanation of AKI AND
Disease is severe OR
Patient is declining FAST
39
Renal biopsy contraindications
Bleeding diathesis
Pyelonephritis
Renal tumor
Solitary native kidney
40
Mild AKI
Transient increase in serum Cr or fall in urine output without complications
41
Life-threatening complications of AKI
```
Volume imbalance
Metabolic acidosis (pH <7.4)
Hyperkalemia (>5.5 or rapidly increasing)
Hypocalcemia
Hyperphosphatemia
Uremia (urine in blood)
Altered mental status
```
42
Treating AKI with life threatening complications
Medical management of complications while waiting for HEMODIALYSIS (required for most patients)
43
First line management of AKI
Assess volume status and correct - correction may improve or even reverse AKI
44
Signs of volume depletion
Hx consistent with fluid loss (ie. diarrhea)
Hypotension
Tachycardia
Oliguria
45
What to do if signs of volume depletion
Administer IV fluids (crystalloid isotonic fluids preferred)
46
Fluid challenge helps identify...
PRERENAL failure. If patients don't respond to fluids, it is unlikely to be a prerenal cause
47
Treating with IV fluids (how much?)
Begin with 1-3 L and reassess patient status
48
Complication of fluid overload
Pulmonary edema >> Respiratory failure (monitor I&O)
49
Treating volume overload
Diuretics (typically furosemide) - Temporary
| Dialysis (most efficient method)
50
When administering diuretics
1. Should not be prolonged therapy
| 2. Monitor UOP
51
If UOP does not increase with diuretics you should...
Diuretics should be STOPPED and alternative therapy (ie. dialysis) started
52
Causes of metabolic acidosis in AKI
1. Excretion of acid and regeneration of bicarb is impaired with a low GFR
2. Many causes of AKI produce acid (sepsis, trauma)
53
What can worsen metabolic acidosis?
Diarrhea (net loss of bicarb)
54
Treating metabolic acidosis
Dialysis OR
| Bicarbonate administration
55
What treatment is preferred in a volume overloaded patient with metabolic acidosis?
Dialysis
56
When to use dialysis for metabolic acidosis
Severe oligo-anuric AKI who are volume OVERLOADED and have severe metabolic acidosis (pH <7.1)
57
Indication for treating acidosis with bicarb
1. Acidosis is related to diarrhea
2. No other reason for acute dialysis
3. pH <7.1 and awaiting dialysis
4. AKI due to RHABDOMYOLYSIS
58
S/Sx of Hyperkalemia
Very few until you DIE! May cause:
- Impaired neuromuscular function
- Arrhythmias
59
Treatment for hyperkalemia
Both medical therapy and dialysis
60
Main cause of hypocalcemia in AKI
Increase in serum phosphate from a reduced GFR
61
Treatment of hypocalcemia in an ASYMPTOMATIC patient
Correct the hyperphosphatemia
62
Accurate measurement of serum calcium
Ionized calcium
63
Treatment of hypocalcemia in a SYMPTOMATIC patient
IV calcium while waiting for DIALYSIS
64
Problem with IV calcium if hyperphosphatemic
Deposition of calcium phosphate into vasculature and organs
65
Symptoms of hypocalcemia
```
Paresthesias
Tetany
Confusion
Seizures
Trousseau's sign
Chvostek's sign
QT prolongation
```
66
Trousseau's sign
Carpal spasm after occlusion of the brachial artery with BP cuff for 3 min
67
Chvostek's sign
Contraction of the facial muscle in response to tapping the facial nerve anterior to the ear
68
Hyperphosphatemia value
>6 mg/dL
69
Treatment of hyperphosphatemia
Dietary (oral) phosphate binders or dialysis
70
Phosphate binders used if calcium is LOW
Calcium acetate or calcium carbonate
71
Phosphate binders used if calcium is HIGH
Aluminum hydroxide or lanthanum carbonate
72
When to dialyze patients with hyperphosphatemia
>12 mg/dL or patient cannot tolerate oral intake
73
Uremia is most common in...
CKD (not AKI)
74
When to treat uremia
Only if it is SEVERE
75
S/Sx of severe uremia
Pericarditis
Neuropathy
Unexplained decline in mental status
76
Treatment of severe uremia
Dialysis
77
AKI prognosis depends on
Cause of AKI
| Presence/absence of pre-existing renal disease
78
AKI prognosis
Most patients recover renal function, but remain with some renal dysfunction
79
How do you know if renal function has recovered
UOP and Cr normalize
80
Patient's who recover from AKI are at a high risk of...
CKD and ESRD
81
AKI during hospitalization is associated with...
High in-hospital and long-term mortality
