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Clin Med II Exam 3 > AKI > Flashcards

AKI Flashcards

1
Q

ARF definition

A

SEVERE AKI - implies need for dialysis

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2
Q

AKI Definition

A

ABRUPT decrease of kidney function

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3
Q

Diagnosis of AKI

A

Based on serum Cr used to calculate GFR OR decrease in patient’s urine output

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4
Q

Problem with using serum Cr for diagnosis

A
  1. In EARLY stages serum Cr may be low even though actual GFR is markedly reduced (not enough time)
  2. If patient is on dialysis there will be a false negative
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5
Q

Best criteria for diagnosing AKI

A

KDIGO

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6
Q

KDIGO diagnosis criteria

A
  1. Increase in serum Cr >0.3 mg/dL w/in 48 hours OR
  2. Increase in serum Cr >50% w/in 7 days OR
  3. Urine output <0.5 mL/kg/hour for > 6 hours
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7
Q

KDIGO Stage 1

A
  1. Increase in serum Cr >0.3 mg/dL OR
  2. Increase in serum Cr 1.5 to 1.9 times baseline OR
  3. Urine output <0.5 for 6 to 12 hours
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8
Q

KDIGO Stage 2

A
  1. Increase in serum Cr 2.0 to 2.9 times baseline OR

2. Urine output <0.5 for >12 hours

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9
Q

KDIGO Stage 3

A
  1. Increase in serum Cr >4.0 mg/dL OR
  2. Increase in serum Cr 3.0 times baseline OR
  3. ANURIA for > 12 hours OR
  4. Initiation of renal replacement therapy
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10
Q

Highest incidence of AKI

A

ICU - Develops in 60% of patients!

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11
Q

Classifications of AKI

A

Prerenal, Intrinsic renal, postrenal

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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)
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13
Q

Causes of intrinsic renal AKI

A

Acute tubular necrosis (ATN) caused by:

  • Renal ischemia
  • Sepsis
  • Nephrotoxins
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14
Q

Types of nephrotoxins

A 
Aminoglycosides
IV CONTRAST*
Heme pigments (rhabdo)
Cisplatin
HIV meds
IVIG
Mannitol
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15
Q

Risk factors for ATN from IV contrast

A 
Preexisting renal disease
Volume depletion
Repeated doses of contrast
Comorbid conditions: DM, CHF
Age
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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

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17
Q

Causes of postrenal AKI

A

Obstruction

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18
Q

Most common cause of obstruction

A

Prostatic disease (hyperplasia or cancer) or metastatic cancer

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19
Q

Reduction in GFR in patients without intrinsic renal disease requires…

A

BILATERAL obstruction (or unilateral in one functioning kidney)

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20
Q

Nonoliguric

A

> 400 mL in 24 hours

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21
Q

Oliguric

A

<400 mL but >100 mL in 24 hours

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22
Q

Anuric

A

<100 mL in 24 hours

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23
Q

Workup of AKI

A

UA
Serum metabolic panel
U/S, CT, MRI, or biopsy (as indicated)

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24
Q

Core urine parameters in a UA

A 
Heme
Leukocyte esterase
Nitrite
Albumin
pH
Specific gravity
Glucose
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25
Q

Pathognomonic cast of AKI

A

Muddy brown casts

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26
Q

Normal range for serum Cr

A

Male: 0.6 - 1.2 mg/dL
Female: 0.5 - 1.1 mg/dL

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27
Q

More accurate estimation of GFR

A

Modification of diet in renal disease (MDRD) - takes into account ethnicity and gender

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28
Q

Simplified measurement of GFR

A

Doubling of serum Cr is 1/2 GFR

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29
Q

Fractional excretion of sodium (FENa)

A

Percent of filtered sodium that is excreted in urine

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30
Q

FENa calculation

A

FENa = (Urine Na/Serum Na) / (Urine Cr/Serum Cr) x 100%

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31
Q

FENa <1%

A

Prerenal

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32
Q

FENa >2%

A

Intrinsic Renal

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33
Q

FENa between 1-2%

A

Either pre or intrinsic renal

34
Q

When is FENa unreliable?

A

Pts on diuretics

CHRONIC renal failure

35
Q

Imaging for AKI

36
Q

When to image AKI

A

Underlying cause is unknown

Assess for obstruction (postrenal)

37
Q

Most common imaging finding with obstruction

A

Hydronephrosis

38
Q

When to do a renal biopsy

A

No clear explanation of AKI AND
Disease is severe OR
Patient is declining FAST

39
Q

Renal biopsy contraindications

A

Bleeding diathesis
Pyelonephritis
Renal tumor
Solitary native kidney

40
Q

Mild AKI

A

Transient increase in serum Cr or fall in urine output without complications

41
Q

Life-threatening complications of AKI

A 
Volume imbalance
Metabolic acidosis (pH <7.4)
Hyperkalemia (>5.5 or rapidly increasing)
Hypocalcemia
Hyperphosphatemia
Uremia (urine in blood)
Altered mental status
42
Q

Treating AKI with life threatening complications

A

Medical management of complications while waiting for HEMODIALYSIS (required for most patients)

43
Q

First line management of AKI

A

Assess volume status and correct - correction may improve or even reverse AKI

44
Q

Signs of volume depletion

A

Hx consistent with fluid loss (ie. diarrhea)
Hypotension
Tachycardia
Oliguria

45
Q

What to do if signs of volume depletion

A

Administer IV fluids (crystalloid isotonic fluids preferred)

46
Q

Fluid challenge helps identify…

A

PRERENAL failure. If patients don’t respond to fluids, it is unlikely to be a prerenal cause

47
Q

Treating with IV fluids (how much?)

A

Begin with 1-3 L and reassess patient status

48
Q

Complication of fluid overload

A

Pulmonary edema&raquo_space; Respiratory failure (monitor I&O)

49
Q

Treating volume overload

A

Diuretics (typically furosemide) - Temporary

Dialysis (most efficient method)

50
Q

When administering diuretics

A
  1. Should not be prolonged therapy

2. Monitor UOP

51
Q

If UOP does not increase with diuretics you should…

A

Diuretics should be STOPPED and alternative therapy (ie. dialysis) started

52
Q

Causes of metabolic acidosis in AKI

A
  1. Excretion of acid and regeneration of bicarb is impaired with a low GFR
  2. Many causes of AKI produce acid (sepsis, trauma)
53
Q

What can worsen metabolic acidosis?

A

Diarrhea (net loss of bicarb)

54
Q

Treating metabolic acidosis

A

Dialysis OR

Bicarbonate administration

55
Q

What treatment is preferred in a volume overloaded patient with metabolic acidosis?

56
Q

When to use dialysis for metabolic acidosis

A

Severe oligo-anuric AKI who are volume OVERLOADED and have severe metabolic acidosis (pH <7.1)

57
Q

Indication for treating acidosis with bicarb

A
  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
Q

S/Sx of Hyperkalemia

A

Very few until you DIE! May cause:

  • Impaired neuromuscular function
  • Arrhythmias
59
Q

Treatment for hyperkalemia

A

Both medical therapy and dialysis

60
Q

Main cause of hypocalcemia in AKI

A

Increase in serum phosphate from a reduced GFR

61
Q

Treatment of hypocalcemia in an ASYMPTOMATIC patient

A

Correct the hyperphosphatemia

62
Q

Accurate measurement of serum calcium

A

Ionized calcium

63
Q

Treatment of hypocalcemia in a SYMPTOMATIC patient

A

IV calcium while waiting for DIALYSIS

64
Q

Problem with IV calcium if hyperphosphatemic

A

Deposition of calcium phosphate into vasculature and organs

65
Q

Symptoms of hypocalcemia

A 
Paresthesias
Tetany
Confusion
Seizures
Trousseau's sign
Chvostek's sign
QT prolongation
66
Q

Trousseau’s sign

A

Carpal spasm after occlusion of the brachial artery with BP cuff for 3 min

67
Q

Chvostek’s sign

A

Contraction of the facial muscle in response to tapping the facial nerve anterior to the ear

68
Q

Hyperphosphatemia value

69
Q

Treatment of hyperphosphatemia

A

Dietary (oral) phosphate binders or dialysis

70
Q

Phosphate binders used if calcium is LOW

A

Calcium acetate or calcium carbonate

71
Q

Phosphate binders used if calcium is HIGH

A

Aluminum hydroxide or lanthanum carbonate

72
Q

When to dialyze patients with hyperphosphatemia

A

> 12 mg/dL or patient cannot tolerate oral intake

73
Q

Uremia is most common in…

A

CKD (not AKI)

74
Q

When to treat uremia

A

Only if it is SEVERE

75
Q

S/Sx of severe uremia

A

Pericarditis
Neuropathy
Unexplained decline in mental status

76
Q

Treatment of severe uremia

77
Q

AKI prognosis depends on

A

Cause of AKI

Presence/absence of pre-existing renal disease

78
Q

AKI prognosis

A

Most patients recover renal function, but remain with some renal dysfunction

79
Q

How do you know if renal function has recovered

A

UOP and Cr normalize

80
Q

Patient’s who recover from AKI are at a high risk of…

A

CKD and ESRD

81
Q

AKI during hospitalization is associated with…

A

High in-hospital and long-term mortality

Clin Med II Exam 3 (2 decks)

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