AKI in Small Animal Medicine Flashcards

(80 cards)

1
Q

kidneys have a high risk of

A

ischaemic & nephrotoxic insult

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2
Q

kidneys receive 25% of

A

cardiac output

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3
Q

Kidney jobs

A
  • filter to excrete urine
  • change composition of urine to excrete things they need to
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4
Q

kidneys are at a high risk for impaired fxn if

A

blood volume changes (hypovolaemia, hypotension, anaemia)
or anything that changes perfusion b/c of blood the kidneys must receive

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5
Q

if a toxin is ingested, it travels through

A

the kidney quickly

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6
Q

kidneys have high…

A

metabolic demands & nutrient requirements

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7
Q

Nephrotoxins can potentially accumulate in the…

A

tubules of the kidneys

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8
Q

Classic definition of AKI

A

serum creatinine above upper ref range

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9
Q

AKI is a complex…

A

dynamic metabolic disorder

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10
Q

AKI has a rapid decline in

A

renal fxn

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11
Q

AKI has retention of

A

uraemic waste (azotaemia)

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12
Q

AKI has a deranged…

A

fluid status (dehydration/fluid retention)

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13
Q

AKI has electrolyte…

A

imbalances & acid-base disorders

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14
Q

AKI is noted as what changes to creatinine?

A

Creatinine elevation >26.4 micromol/L OR >25% w/i 48 hrs

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15
Q

Grade 1 AKI (non-azotaemic AKI)

A
  • documented AKI (hx, clinical, lab, imaging evidence, clin anuria/oliguria, vol responsiveness) &/or
  • progressive non-azotaemic increase in blood creatinine w/i 48 hrs
  • measured oliguria or anuria over 6 hr
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16
Q

Grade II AKI (mild AKI)

A
  • documented AKI & static or progressive azotaemia
  • progressive azotaemia: increase blood creatinine w/i 48 hrs or vol responsiveness
  • measured oliguria or anuria over 6 hrs
    (values higher than Grade I)
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17
Q

Grade III-V AKI (mod to severe AKI)

A

Documented AKI & increasing severities of azotaemia & functional renal failure

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18
Q

What is the continuum in AKI?

A

event –> decreased kidney fxn –> progression up to stage 4, some sequelae or not

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19
Q

Phase I of AKI

A
  • no clin signs (non-azotaemic)
  • intrinsic injury/dysfxn
  • rapid haemodynamic, filtration, tubulointerstitial or outflow injury = accumulation of metabolic toxins, dysregulation of acid-base, electrolytes & ECF balance
  • Duration depends on nature of primary insult
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20
Q

Phase 2 AKI

A
  • cell death, cytokines, WBC –> repeats –> remodeling of tissue, cells dead replaced by fibrin; start of structural damage
  • tubules 1st site for remodelling/changes -> cases in urine formed by proteins or tubular cells
  • continued hypoxia & inflammation –> propagation of renal damages
  • cortical structures: 90% renal blood flow + high metabolism - predisposed to damages
  • intervention may not be successful
  • PU/PD, increase thirst due to Na loss
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21
Q

Phase 3 AKI

A
  • critical amt of damages has occurred - last few days to 1-3 wks
  • remodelling continues, cannot cope, fall into full kidney failure or Phase 4
  • urine output increases or decreases
  • loss of tubular fxn
  • oliguria, prod’n of urine abnormal, not full kidney filtration
  • if you restore blood flow, remove toxins, etc. can return to recovery phase & regain fxn
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22
Q

Phase 4 AKI

A
  • depends on how early & how well txt occurs (3 mos after AKI can regen tubules)
  • increased urinary output
  • vol depletion can lead to progression of kidney dz
  • vol depletion can lead to progression of kidney dz
    regeneration & repair of renal tissue can take mos & may not regain full fxn (CKD)
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23
Q

AKI results in abnormalities in..

A

CNS, immune, resp, haemostatic, GIT signs, dehydration from PU/PD in early stages

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24
Q

AKI impairs coag systems/aggregations to be

A

normal…

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25
Mild AKI = important
clinical consequences increased morbidity & increased increased mortality
26
AKI is a broad clinical
syndrome
27
unspecific clin signs of AKI
* acute onset <1 wk * lethargy -> depression/weakness -> comatose * inappetence -> anorexia * nausea -> V * D * PU -> oliguria -> anuria * PD * seizures * dyspnoea
28
Physical exam of AKI could show
* dehydration * good BCS * uraemic halitosis * oral ulceration * renomegaly, renal pain (abd pain?) * tachycardia or bradycardia * systemic hypertension -> retinal detachment, blindness, etc * bruising * melaena/D * bladder palpation - v. important
29
What do you look for in AKI patients in a bladder palpation?
* empty bladder? last voided? * anuria? * rupture? trauma? * distended? turgid? painful? pattern prior to presentation? * stranguria * pollakiuria * incontinence
30
Aetiologies of pre-renal AKI
Haemodynamic -> hypovolaemic -> hypotension -> arterial occlusion or stenosis of renal a. -> decreased afferent a. pressure (NSAIDs, ACEi)
31
aetiologies of renal AKI
* ischaemia (shock, decreased CO, vessel occlusion) * nephrotoxin (eth glycol, lilies, grapes/raisins, etc) * infectious (pyelonephritis, leptospirosis, etc) * immune-mediated * systemic inflammation * hypertension * neoplasia
32
Aetiologies of post-renal AKI
* UT rupture - uroabdomen * UT obstruction
33
What would you look for on haematology of AKI?
Anaemia Thrombocytopaenia Other
34
What do you look for on biochemistry profile & electrolytes for AKI?
* azotaemia * hyperkalaemia * metabolic acidosis * other changes related to underlying cause, Ca lvls
35
What do you look for on a U/A & culture for AKI?
* isosthenuria or low USG * proteinuria? * glucosuria?
36
When do you do abdominal rads for AKI?
* always - quick & inexpensive --> for stones/obstruction of UT * always incl entire UT
37
Why would you do Abd U/S for AKI?
* complements for anatomical anomaly or radiolucent stones * staging for underlying cause
38
Other diagnostic techniques for AKI
* CT * retrograde urinary contrast study
39
Why would you look at BP in AKI?
* hypertension is common (esp in dogs) * intra-renal hypertension leds to systemic hypertension
40
How does decreased renal blood flow cause systemic hypertension?
* decreased renal blood flow --> decreased GFR --> intra-renal release of renin --> activation of RAAS --> systemic hypertension
41
Target organ damages from hypertension include...
* retinal haemorrhage * retinal detachment * intracranial haemorrhage
42
What other diagnostic tests might be important in AKI?
* Urine culture * lepto! * tickborne dz * FIP, FeLV, FIV
43
what is the gold standard for testing for lepto? when is it used?
Culture difficult & not routinely available b/c does not grow well
44
what is the most available way of testing for lepto
MAT (antibody) vs PCR (presence of organism DNA/RNA)
45
When testing for lepto, what is important to remember about how it sheds in blood & urine?
* bacteraemia in blood for ~5 d * Bacteruria intermittent for ~10d
46
when could you do a lepto SNAP?
in the 1st wk of infection
47
What is important to know about MAT titre
* can be neg in acute phase * Vx'd may have elevated post-Vx titres * highest MAT titre can vary overtime * ideal = paired samples 2 wks apart - 4x increase in titre * Vx'd dog = convalescence titres rec'd
48
SNAP lepto tests for...
IgM, IgG
49
SNAPs that come back negative but P is clinical, then requires...
MAT
50
if you are taking samples for testing for lepto, it is important to remember...
to take samples prior at antibiotic admin
51
Clinical suspicion of acute lepto
PCR + confirmed in blood
52
Acute or chronic lepto
PCR + urine (some of these are renal carriers)
53
UPC use in AKI
Nephrotic syndrome -> acute loss of renal fxn glomerulonephritis
54
Other testing that could be used in AKI & what you might find
* cytology for lymphoma * Bx: immune-mediated dz * antinuclear antibodies - lupus
55
Goal of txt of AKI
* prevention of progression from sublethal/lethal injury -> normal as possible * prevention of additional renal injury
56
sequelae of AKI
* fibrosis * loss of renal fxn -> CKD
57
fluid overload in AKI has
neg side effects oedema cats = 1st impaired/impacted is the lungs -> see tachypnoea/dyspnoea as 1st signs
58
in AKI it is important to halt all...
potentially nephrotoxic drugs
59
how do you assess perfusion to start working on a fluid plan? How do you treat?
* hypovolaemia -> give crystalloids to effect, transfusion PRN * severe hypotension -> vasopressors, norepi (best) * dehydration w/ careful correction
60
How do you assess hydration?
skin tent, sunken eyes, mm PU: urine prod'n > 2 ml/kg/h Oliguria? anuria?
61
How do you assess ongoing losses?
Measure: GI (V/D), Urinary Use: indwelling u-cath; p's wt trends; collecting urine while walking P; weigh beds/litter boxes; fluid intake & output monitoring
62
when doing fluid therapy what should you monitor?
* fluid balance * fluid choice
63
What fluids do you use in AKI
crystalloids
64
how do you calculate the fluid rate for AKI
maintenance + ongoing losses + insensible loss +- dehydration correction
65
in AKI txt, ensure there is...
euvolaemia
66
For oliguria, when giving fluids, what must you take into account?
Ins & outs + DD (dialysis or diuretics) these go into sensible losses <1 ml/kg/hr
67
For anuria, when giving fluids, what must you take into account?
insensible losses ONLY + DD (dialysis or diuretics)
68
For overhydrated animals, when giving fluids, what must you take into account?
no fluid & DD
69
Use of diuretics can worsen...
AKI
70
Diuretics may help convert...
oligoanuric P to non-oliguria
71
Furosemide
* inhibits the Na-K-Cl cotransporter in the Loop of Henle * increases tubular flow w/o increasing GFR * w/ less Na reabsorption, the Na-K-ATPase activity is reduced; less O2 consumption by cell; may protect cell from death
72
Bolus amount of Furosemide & signs expected?
2-6 mg/kg IV should see UO Increase in 30 mins if it is going to respond
73
if there is a response to bolus of furosemide, then you should treat w/...
CRI furosemide 0.66-1 mg/kg/h
74
Mannitol
* osmotic diuretic leading to vol expansion * increased tubular flow - good if suspect tubular obstruction * increases renal blood flow & GFR * free radicle scavenger * stims prostaglandin prod'n in kidney (vasodilation)
75
Mannitol bolus
0.5 g/kg IV over 20 mins
76
Clinical signs of hyperkalaemia
* bradycardia * small QRS complexes * prolonged P-QRS intervals * small wide to absent P waves * tall-tented T waves
77
if ECG changes are present w/ hyperkalaemia then you must...
treat
78
how do you treat hyperkalaemia
* Ca gluconate - to protect myocardium * glucose - to increase endogenous insulin release * insulin/glucose protocol
79
How might you treat the underlying cause of AKI?
* antibiotics or adapted antimicrobial therapies * Sx - cystotomy, SQ ureteral bypass, Sx repair of UT after med mgmt w/ U-cath if uroabd
80
Supportive care to help renal fxn restoration may include...
dialysis if supportive care failed to restore adeq. UO