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RUSVM SAM II > Acute Kidney Injury (Rolph) > Flashcards

Acute Kidney Injury (Rolph) Flashcards

1
Q

Define acute kidney injury and its causes.

A

Encompasses mild damage, that does not cause azotemia, to severe damage associated with complete anuria

  • Causes can be: pre-renal, renal, or post-renal
  • Term infers reversibility
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2
Q

Define acute renal failure.

A

Decreased GFR leading to the retention of nitrogenous wastes

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3
Q

What is seen with acute kidney injury?

A
  • Abrupt and severe decline in glomerular filtration rate
  • No time for compensatory adaptation
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4
Q

How is renal insufficiency classified?

A
  • Pre-renal
    • Can go to primary intrinsic
  • Primary Intrinsic
  • Post-renal
    • Can go to primary intrinsic
  • (Decompensated CRF: acute or chronic)
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5
Q

Where are some nephrotoxicy etiologies or acute kidney injury?

A
  • Ethylene glycol
  • Heavy metals
  • Solvents
  • Therapeutic agents (aminoglysodies, NSAIDs, etc.)
  • Tiger lilies (any flower from bulb is possibly nephrotoxic)
  • Grapes (depends on patient byt may not take much)
  • Tulips
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6
Q

What are some ischemic etiologies for acute kidney injury?

A
  • Hypotension
  • Hypovolemia
  • Sepsis
  • Pancreatitis
  • DIC
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7
Q

What’s the progression of acute kidney injury?

A
  1. Initiation
  2. Extension
  3. Maintenance
  4. Recovery
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8
Q

What is the initiation phase of acute kidney injury?

A
  • Without clinical signs
  • Definable by decrease in urine output or increase in creatinine
  • Intervention required
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9
Q

What constitutes the extension stage of acute kidney injury?

A
  • Continued hypoxia and inflammation
  • Proximal tubule and loop of Henle (cortical) suspectible to toxic and ischemic damage (90% of blood flow)
  • Compromised Na:K pumps (leads to cell swelling, death)
  • Increased cytosolic calcium
  • Loss of brush border or apical and basal cell surfaces
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10
Q

What is the maintenance stage of acute kidney injury?

A
  • 1-3 weeks duration
  • Urine output increased or decreased
  • Urine = ultrafiltrate
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11
Q

What is the recovery phase of acute kidney injury?

A
  • Demonstrates polyuria
  • Extreme Na loss (ascending limb of Henle and AQP-2 loss)
  • Takes weeks-months to recover
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12
Q

What contributes to tubular necrosis?

A
  • Intra-renal vasoconstriction
  • Tubular dysfunction
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13
Q

Describe intra-renal vasoconstriction and tubular necrosis.

A

Imbalance between vasoconstrictors (endothelin) and vasodilators (NO)

  • Endothelial injury
  • Decreased O2
  • ATP → AMP (ATP can’t be formed, leads to energy deficit)
  • Mitochondrial damage
  • Oxidant injury
  • Na/K pump stops working (cellular swelling)
  • Intracellular acidosis
  • Intracellular hypercalcemia
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14
Q

Describe tubular dysfunction in relation to tubular necrosis.

A
  • Tubular obstruction from crystals or detached RTE cells
  • Cytoskeletal injury w/ a loss of polarity
  • Loss of tight junctions between cells
  • Cell necrosis
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15
Q

Discuss lily toxicity.

A
  • All parts of the lily are toxic
  • Can lead to a disproportionate increase in creatinine
  • May take up to 72 hrs to develop
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16
Q

Discuss ethylene glycol toxicity and its metabolism.

A
  • Doses as low as 1.4 mL/kg toxic
  • Toxic products of the metabolism of ethylene glycol cause metabolic acidosis and renal tubular damage
  • EG metabolized by enzyme alcohol dehydrogenase (AD) to glycoaldehyde
    • Further metabolized to acidic products and oxalate
  • Formation of calcium oxalate crystals occurs resulting in hypocalcemia and crystalluria
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17
Q

What are the clinical signs of ethylene glycol toxicity?

A
  • <12 hrs post intoxication: GI (vomiting), neurological (ataxia, depression, ‘drunken’ appearance)
  • 12-24 hrs after ingestion: further depression observed along w/ anorexia, tachycardia, start of ARF
  • >24 hrs: clinical signs reflect ARF and include oliguria or anuria nad vomiting
    • If cat hyperkalemic, bradycardia may be noted
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18
Q

What are the clinical signs of ethylene glycol toxicity?

A
  • Lethargy
  • Anorexia
  • Vomiting
  • Dehydration
  • Uremic ulceration
  • Halitosis
  • Tongue tip necrosis
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19
Q

What is seen on bloodwork for ethylene glycol?

A

Sudden increase in

  • Urea
  • Creatinine
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20
Q

Should a renal biopsy be done with ethylene glycol toxicity?

A

Possible

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21
Q

What should be done to further investigate ethylene glycol toxicity?

A
  • Identify any pre- or post-renal element
  • Look for underlying cause
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22
Q

How should the underlying cause be investigated with ethylene glycol toxicity?

A
  • Withdraw any potentially nephrotoxic meds
  • Adminster antidote
  • Decrease further absoprtion of toxic substances
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23
Q

What’s the antidote for ethylene glycol?

A

4-methylpyrazole/fomepizole or ethanol

  • Give w/n 8 hours of ingestion
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24
Q

What’s the antidote for NSAIDs?

A

Misoprostal (PGE-analog)

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25
Q

How is acute kidney injury graded?

A
  • Grades I-V
  • Grade depends on blood creatinine levels
26
Q

Describe AKI grade I blood creatinine levels and clinical description.

A
  • Blood creatinine: <1.5 mg/dL
  • Non-azotemic AKI
    • Documented AKI: (historical, clinical, laboratory, or imaging evidence of AKI, clinical oliguria/anurua, volume responsiveness)
    • Progressive non-azotemic increase in blood creatinine (≥0.3 mg/dL w/n 48 hours)
    • Measured oliguria (<1 mL/kg/hr) or anuria over 6 hours
27
Q

Describe AKI grade II blood creatinine and clinical description.

A
  • Blood creatinine: 1.7-2.5 mg/dL
  • Mild AKI
    • Documented AKI and static or progressive azotemia
    • Progressive azotemic increase in blood creatinine; ≥ 0.3 mg/dL w/n 48 hrs
    • Measured oliguria (<1 mL/kg/hr) or anuria over 6 hrs
28
Q

Describe AKI grades III-V blood creatinine and clinical descriptions.

A
  • Grade III: 2.6-5.0 mg/dL
  • Grade IV: 5.1-10.0 mg/dL
  • Grade V: >10.0 mg/dL
  • Moderate to severe AKI:
    • Documented AKI and increased severeities of azotemia and functional renal failure
29
Q

What’s important about the volume responsiveness and grade I AKI grade?

A

Volume responsiveness is

  • An increase in urine production to >1 mL/kg/hr over 6 hours
  • And/or decrease in serum creatinine to baseline over 48 hours
30
Q

What are the AKI grading substages?

A

Each grade of AKI is further subgraded as:

  1. Non-oliguric (NO) or oligo-anuric (O)
  2. Requiring renal repalcement therapy (RRT)
31
Q

What are the goals for the first 4-8 hours of fluid therapy?

A
  • Replace deficit
  • Provide maintenance requirements
  • Cover ongoing losses
  • Monitor closely to avoid overhydration
32
Q

What should be considered with fluid therapy and how much fluid should be administered?

A
  • Fluid requirements
  • Insensible fluid loss (22 mL/kg/day) + sensible fluids losses → ongoing fluid losses (estimate vomiting, diarrhea, etc.) + urinary losses (usually around 44 mL/kg/day)
  • Adult maintenance around 60 mL/kg/day (in ARF, urinary losses vary)
33
Q

What should fluid therapy be adjusted for?

A

Adjust based on BW, urine output, respiratory rate, subcutaneous edema

34
Q

What are the options for fluid choices and fluid therapy?

A
  • 0.9% NaCl demonstrated to decrease renal blood flow in people
  • Balanced crystalloid solution
  • 0.45% NaCl and 2.5% dextrose if hypernatremic
  • Monitor for hypokelamic once polyuric
35
Q

What are patients with acute kidney injury initially like fluid-wise?

A
  • Often hyperkalemic initially
  • Often acidemic
36
Q

What needs to be monitored regarding acute kidney injury and how are they monitored?

A
  • Urine output (catheterization, weight litter tray in cats)
  • Electrolytes (potassium, sodium)
  • Cardiac rhythm
  • Blood pressure
  • Acid-base status
37
Q

What is oliguria?

A

<0.5-1 mL/kg/hr

38
Q

How is urine output restored with acute kidney injury?

A
  • Indwelling catheter and closed-collection system
  • Measurement of central venous pressure
39
Q

What’s the fluid challenge with restoring urine output and acute kidney injury?

A
  • 3-5% body weight
    • Corrects for unidentified dehydration
  • Monitor closely for over-hydration
40
Q

How does furosemide help with restoring urine output in acute kindey injury?

A
  • IV injection q6-8hrs or CRI
  • Incrementally increase dose hourly (3 doses)
  • Exacerbates aminoglycoside toxicity
  • May be combined w/ mannitol or dopamine
41
Q

How does mannitol help with restoring urine output in acute kindey injury?

A

10-20% solution

  • Slow IV (up to 2 doses)
  • Effect seen w/n 1 hr
  • May cause severe overhydration
  • Repeat bolus q4-6hrs or CRI of 5-10% solution
42
Q

What’s the maximum daily dose of mannitol for restoring urine output?

A

2 g/kg

43
Q

What’s the dopamaine infusion treatment regarding restoring urine output?

A
  • Low dose, dilute in 5% dextrose or saline
  • Monitor ECG
  • Possible synergistic effect w/ furosemide
44
Q

How is the dopamine infusion in cats?

A

Not effective

  • No renal DOPA receptors
45
Q

What is hemodialysis also known as?

A

Extracorporeal renal replacement therapy (ERRT)/Dialysis

46
Q

How does hemodialysis work?

A
  • CTT, IRD (TID)
  • Uses principle of diffusion and convection
  • Artificial porous membrane w/ artificial hydrostatic and solute concentrations to prevent solute loss
  • Dedicated centers for continuous and intermittent therapies (dialysis)
47
Q

What’s required in small patients and hemodyalysis?

A

Requires blood transfusion in smaller patients

48
Q

When is peritoneal dialysis indicated?

A
  • Non-responsive oliguria
  • Intoxification
  • Over-hydration
49
Q

What are the problems with peritoneal dialysis?

A
  • Labor intensive
  • Hypoalbuminemia
  • Peritonitis
50
Q

How can you treat moderate to severe hyperkalemia?

A
  • Glucose 5-10% CRI or 20-50% IV
    • Give slowly into large vein
    • Stimulates insulin release
  • Glucose + soluble insulin
    • Monitor for hypoglycemia
    • Stimulates cellular uptake of glucose and potassium
51
Q

How is severe life threatening hyperkalemia treated?

A

Calcium gluconate 10%

  • Slow over 10-20 minutes
  • DOES NOT lower potassium
  • Immediate myocardial production
52
Q

How is asymptomatic hyperkalemia treated?

A
  • Potassium free fluid therapy
  • Restore urine output
53
Q

What are the problems with acid-base in acute kidney injury?

A
  • Many normal metabolic processes w/n the body generate H+ ions, which must be excreted in the urine if acid-base balance is to be maintained
  • Damaged kidneys can lose ability to excrete H+ and resorb HCO3-
54
Q

What are the clinical effects of acid-base?

A
  • Progressive renal injury
  • Increased protein catabolism
55
Q

When should acidosis be treated with acute kidney injury?

A

ONLY if acidosis marked (less than pH 7.1)

  • Treated by administration of an alkalinising agent, e.g. sodium bicarbonate
56
Q

How do you calculate treating an acidosis and what can it lead to?

A

Base deficit x BW x 0.3 = HCO3- administration IV

  • Give 1/4 IV and remainder as a CRI (in dextrose saline or 0.45% NaCl) over 2-6 hrs
  • Care: can lead to severe hypernatremia
57
Q

When is treating an acidosis contraindicated?

A
  • When CO2 elevated
  • Could lead to paradoxical CNS acidosis
58
Q

How is calcium involved with acute kidney injury?

A

May be bound by underlying disease process

59
Q

What happens with hypocalcemia and when/how should it be treated?

A
  • If iCa significantly decreased: myocardial contractility impaired
  • If < 0.9 mmol/L: consider supplementation w/ calcium gluconate
60
Q
A

RUSVM SAM II (4 decks)

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