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
2
Q
Define acute renal failure.
A
Decreased GFR leading to the retention of nitrogenous wastes
3
Q
What is seen with acute kidney injury?
A
- Abrupt and severe decline in glomerular filtration rate
- No time for compensatory adaptation
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)
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
6
Q
What are some ischemic etiologies for acute kidney injury?
A
- Hypotension
- Hypovolemia
- Sepsis
- Pancreatitis
- DIC
7
Q
What’s the progression of acute kidney injury?
A
- Initiation
- Extension
- Maintenance
- Recovery
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
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
10
Q
What is the maintenance stage of acute kidney injury?
A
- 1-3 weeks duration
- Urine output increased or decreased
- Urine = ultrafiltrate
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
12
Q
What contributes to tubular necrosis?
A
- Intra-renal vasoconstriction
- Tubular dysfunction
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
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
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
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
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
18
Q
What are the clinical signs of ethylene glycol toxicity?
A
- Lethargy
- Anorexia
- Vomiting
- Dehydration
- Uremic ulceration
- Halitosis
- Tongue tip necrosis
19
Q
What is seen on bloodwork for ethylene glycol?
A
Sudden increase in
- Urea
- Creatinine
20
Q
Should a renal biopsy be done with ethylene glycol toxicity?
A
Possible
21
Q
What should be done to further investigate ethylene glycol toxicity?
A
- Identify any pre- or post-renal element
- Look for underlying cause
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
23
Q
What’s the antidote for ethylene glycol?
A
4-methylpyrazole/fomepizole or ethanol
- Give w/n 8 hours of ingestion
24
Q
What’s the antidote for NSAIDs?
A
Misoprostal (PGE-analog)
25
How is acute kidney injury graded?
* Grades I-V
* Grade depends on blood creatinine levels
26
Describe AKI grade I blood creatinine levels and clinical description.
* 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
Describe AKI grade II blood creatinine and clinical description.
* 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
Describe AKI grades III-V blood creatinine and clinical descriptions.
* 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
What's important about the volume responsiveness and grade I AKI grade?
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
What are the AKI grading substages?
Each grade of AKI is further subgraded as:
1. Non-oliguric (NO) or oligo-anuric (O)
2. Requiring renal repalcement therapy (RRT)
31
What are the goals for the first 4-8 hours of fluid therapy?
* Replace deficit
* Provide maintenance requirements
* Cover ongoing losses
* Monitor closely to avoid overhydration
32
What should be considered with fluid therapy and how much fluid should be administered?
* 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
What should fluid therapy be adjusted for?
Adjust based on BW, urine output, respiratory rate, subcutaneous edema
34
What are the options for fluid choices and fluid therapy?
* 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
What are patients with acute kidney injury initially like fluid-wise?
* Often hyperkalemic initially
* Often acidemic
36
What needs to be monitored regarding acute kidney injury and how are they monitored?
* Urine output (catheterization, weight litter tray in cats)
* Electrolytes (potassium, sodium)
* Cardiac rhythm
* Blood pressure
* Acid-base status
37
What is oliguria?
\<0.5-1 mL/kg/hr
38
How is urine output restored with acute kidney injury?
* Indwelling catheter and closed-collection system
* Measurement of central venous pressure
39
What's the fluid challenge with restoring urine output and acute kidney injury?
* 3-5% body weight
* Corrects for unidentified dehydration
* Monitor closely for over-hydration
40
How does furosemide help with restoring urine output in acute kindey injury?
* IV injection q6-8hrs or CRI
* Incrementally increase dose hourly (3 doses)
* Exacerbates aminoglycoside toxicity
* May be combined w/ mannitol or dopamine
41
How does mannitol help with restoring urine output in acute kindey injury?
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
What's the maximum daily dose of mannitol for restoring urine output?
2 g/kg
43
What's the dopamaine infusion treatment regarding restoring urine output?
* Low dose, dilute in 5% dextrose or saline
* Monitor ECG
* Possible synergistic effect w/ furosemide
44
How is the dopamine infusion in cats?
Not effective
* No renal DOPA receptors
45
What is hemodialysis also known as?
Extracorporeal renal replacement therapy (ERRT)/Dialysis
46
How does hemodialysis work?
* 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
What's required in small patients and hemodyalysis?
Requires blood transfusion in smaller patients
48
When is peritoneal dialysis indicated?
* Non-responsive oliguria
* Intoxification
* Over-hydration
49
What are the problems with peritoneal dialysis?
* Labor intensive
* Hypoalbuminemia
* Peritonitis
50
How can you treat moderate to severe hyperkalemia?
* 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
How is severe life threatening hyperkalemia treated?
Calcium gluconate 10%
* Slow over 10-20 minutes
* DOES NOT lower potassium
* Immediate myocardial production
52
How is asymptomatic hyperkalemia treated?
* Potassium free fluid therapy
* Restore urine output
53
What are the problems with acid-base in acute kidney injury?
* 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
What are the clinical effects of acid-base?
* Progressive renal injury
* Increased protein catabolism
55
When should acidosis be treated with acute kidney injury?
ONLY if acidosis marked (less than pH 7.1)
* Treated by administration of an alkalinising agent, e.g. sodium bicarbonate
56
How do you calculate treating an acidosis and what can it lead to?
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
When is treating an acidosis contraindicated?
* When CO2 elevated
* Could lead to paradoxical CNS acidosis
58
How is calcium involved with acute kidney injury?
May be bound by underlying disease process
59
What happens with hypocalcemia and when/how should it be treated?
* If iCa significantly decreased: myocardial contractility impaired
* If \< 0.9 mmol/L: consider supplementation w/ calcium gluconate
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