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Urinary > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

What is azotemia?

A

incr in urea +/- incr in creatinine in the blood

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2
Q

what are the cx signs of azotemia?(and what would you call this collection of cx signs)

A

lethargy/nausea/vom/inappetance/oral ulcers

uraemia

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3
Q

what causes pre-renal azotemia?

A

reduction in renal blood flow (or incr protein catabolism/GI haemorrhage)

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4
Q

why does this reduction in blood flow lead to azotemia?

A

reduced blood to kidney = filters less blood = cant get rid of waste

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5
Q

what sort of conditions can result in pre-renal azotemia?

A

hypovolaemia/severely dehydrated/CHF (any that causes poor renal perfusion)
OR anything that causes incr urea e.g. high protein meal/GI haem

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6
Q

how would you ID a pre-renal azotemia?

A

azotemia on bloods + concentrated urine > 1.030D/1.035 C

as kidneys are doing everything to preserve water

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7
Q

what causes renal azotemia?

A

fewer functional nephrons! due to underlying kidney dz.

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8
Q

how can you ID renal azo? (dilute/conc urine)

A

Azotemia on bloods + dilute urine <1.030D/1.035C (cant concentrate urine) (nephrons concentrate urine so if have lost them then cant do it!)

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9
Q

what can cause post renal azotemia?

A

after the kidneys - something is stopping the waste being excreted.
2 mechanisms -> obstruction/blockage.

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10
Q

how can you ID a urethral blockage?

A

obvious - animal is trying to urinate but nothing coming out

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11
Q

how to ID a uretal blockage?

A

challenging - can be silent if unilateral. Abdo scan - see urine accumulating in renal pelvis, proximal ureter will become expanded.

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12
Q

how can you ID from certain tests, a ruptured bladder?

A

leak into abdo - waste products are reabsorbed into the body - ever escalating levels of urea etc in circulation.
Dx - imaging. Free abdo fluid + take sample

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13
Q

what do you expect to see from the abdo fluid sample of a ruptured bladder?

A

creatinine in fluid will be 2 x more than in serum (overtime equilibrium though)

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14
Q

what is the normal level of creatinine in the blood?

A

less than 1.4mg/dl

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15
Q

define acute kidney injury vs chronic

A 
acute = sudden organ damage
chronic = gradual, deteriorating day to day, compensating, scarring
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16
Q

why are kidneys highly susceptible to toxic/ischaemic injury?

A

as they egt 20% of CO

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17
Q

what is anuria

A

no urine production

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18
Q

what is oliguria?

A

less urine production

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19
Q

why do you see anuria/oliguria in severe AKI?

A

damage to nephrons (cells lining nephron swollen + can slough into tubules -> non-functional +/ obstruct tubules)

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20
Q

what changes on bloods/biochem will you see in AKI?

A
  • azotemia - incr urea/cr
  • acid-base disturbances
  • electrolytes -> hyperkalaemia
  • fluid balance problems
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21
Q

why is hyperkalaemia a problem?

A

can cause heart problems e.g. cardiac arrest. As the kidneys are the main source of excretion for potassium

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22
Q

how would a AKI case present?

A 
- uraemic (lethargic/inappetant/
nausea/vom/D)
- +/- dehydrated/hypovol
- temperature changes (up/down)
- +/- renomegaly (symmetry?)
- +/- renal/referred abdo pain
- concurent signs of other affected organs
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23
Q

what concurrent problems/other dz could be present in AKI case?

A

hypocalcaemia can cause seizures/tremors
leptospirosis - can cause AKi and you will see icterus/petechial haemorrhages
possible to see cutaneous lesions (CRGV)

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24
Q

what are the main causes of AKI?

A
  • toxins/drugs (furesemide/NSAIDs)

- vascular - ischaemic (hypoperfusion due to any reason)

25
Q

what are 3 other causes of AKI?

A
  • Infectious i.e. lepto/pyelenephritis/CRGV
  • Metabolic (vit D products cause elevated CA:P product)
  • uncorrected pre/post renal
26
Q

how can NSAIDs cause AKI?

A

inhibit PGs which are responsible for regulating renal blood flow (NSAID inhibit cox which in turn inhibits PG synthesis)

27
Q

(what is CRGV? + what does it cause?)

A

cutaneous renal glomerular vasculopathy AKA alabama rot

- causes AKI + skin lesions.

28
Q

where are the lesions typically seen in CRGV?

A

well demarcated and seen in distal legs + mouth

29
Q

What is your main DDx for AKI/what should you rule out if you suspect AKI in a dog?

A

Addisons disease (-> lack of cortisol, present the same)

30
Q

What test would you perform if you suspect AKI?

A
  • haematology
  • Biochemistry
  • urinalysis
  • imaging (to rule out pre/post renal causes)
    Others (metabolic acidosis often seen. Changes due to underlying causes may be seen)
31
Q

What would results would you expect from haematology/biochem?

A

Azotaemia
hyperphosphataemic
variable potassium

32
Q

what would you expect to see on urinalysis?

A
  • dilute urine (<1.030D/1.035C)
  • +/- proteinuria/ glucosuria (damage to PCT)
  • Sediment exam = casts/crystals
  • cytology -> inflam cells/bacteriuria
    (bacteria culture and sensitivity should be done + fungal if travelled recently)
33
Q

How can imaging be useful in AKI?

A

Mainly used to exclude post renal causes (may see renal pelvis dilation (>7mm)/free fluid if rupture).
US/xray- renal size, symmetry? (xray also see uroliths)

34
Q

what other diagnostic tests might you consider?

A

Testing for lepto (serology/PCR)
tests for toxins e.g. ethylene glycol.
(renal cytology FNA - rarely indicated only if suspect renal lymphoma, but this is a more chronic presentation)

35
Q

what are the 2 main things you should do to manage AKI?

A

Remove underlying cause (stop drugs/decontamination if ingested - gastric decontamination/adsorption - activated charcoal)

Supportive management

36
Q

what supportive management would you do for AKI?

A

Manage fluid balance/electrolytes/uraemic toxins using fluid therapy

Manage clincial consequences

37
Q

what % dehydration would

  • dry MM/CRT>2-3sec/+/-signs of shock, marked skin tent, sunken eyes.
  • incompatible with life
  • tacky MM, loss in skin elasticity
  • dry MM, mild incr CRT, loss skin elasticity, +/- sunken eyes.
  • not detectable clinically
A 
1 = >10-12%
2 = >15%
3 = 5-6%
4 = 6-8%
5 = <5%
38
Q

how would you assess for hypovolaemia?

A

intravascular assessment -> HR/BP/pulse quality/CRT

39
Q

how quickly would you treat hypovolaemia? dehydration?

A 
Hypo = bolus
dehydration = continuous flow over 6 hours
40
Q

what are the risks involved if a patient in an/oliguria + you give fluids?

A

progressive azotemia/metabolic derangements/ life threatening incr potassium. Volume overload -> worse outcome (drown them fluid in cavities)

41
Q

what are the risks involved if pt is polyuria and give fluids?

A

dehydration/hypovol/potassium wasting - hypoK

but can excrete toxins

42
Q

what is the normal urine output for D/C?

A

1-2ml/kg/hr

43
Q

what is the maintenance rate for IVFT? and why wouldnt you use it in AKI cases?

A

2ml/kg/hr - becuase you need to match the ins/outs

44
Q

what is the main complication with AKI?

A

hyperkalaemia

45
Q

how could you dx hyperkalaemia in AKI?

A

If they have an AKI and have bradycardia (due to reduced pacemaker activity => VF -> CA)

46
Q

what are the typical signs/pattern on ECG for hyperkalaemia?

A

wide QRS/flattened P/Spiked T

47
Q

How would you manage hyperkalaemia? (any cause)

A
  • restore renal perfusion
  • give calcium gluconate (stabilises cardiomyocyte membranes - calcium incr the threshold so less likely to spontaneously discharge, 30mins)
  • redistribute potassium - intracellularly -> admin glucose = endogenous insulin release = moves glucose/pot/phos into cells (can give neutral insulin if needed)
48
Q

what parameters would you monitor on a pt with aKi?

A
  • Fluid blaance - hydration/BW/ins + outs
  • renal perfusion -> systemic BP (maintain SBP >80 at least)
  • electrolytes -> supplement as necessary
  • azotemia
49
Q

if a pt had AKI + it was caused by ethylene glycol, what would be the treatment/management?

A

ethanol within 8hrs

50
Q

AKI - cuased by leptospirosis, Rx/management?

A

clavulanate amoxicillin IV

doxycycline 2 weeks later to clear spires from renal tubules

51
Q

AKI - pylenephritis, Rx/management?

A

clavulanate amoxicillin -> pending C+S

52
Q

NSAID induced AKI, Rx/management?

A

misoprostol

53
Q

what drugs could you use to Rx the nausea?

A

maropitant

metaclopramide (reduce by 50% as renally metabolised)

54
Q

how would you manage any GI haemorrhage?

A

Omeprazole - reduces gastric acidity(reduce by 50%

Sucralfate - coats ulcers

55
Q

4 other considerations in the AKI pt?

A
  • nutrition (oral/assisted)
  • manage any hypertension with amlodipine (NOT ACEi which are normally first line, ACEi result in efferent arteriolar dilation -> decr GFR)
  • azotemia may not normalise pre-discharge (can take up to 3 months)
  • 3 month monitoring
56
Q

what if the pt is still anuric?

A

double check - fluid vol/obstruction/rupture

consider trial diuretic -> e.g. furesemide)

57
Q

what are 3 indications for renal replacement or euthanasia?

A

persistent anuria (few days)
+/- volume overload
+/- unmanageable hyperkalaemia
(ERRT dialysis - may be used for some toxins/peritoneal dialysis doesnt really work)

58
Q

what is the prognosis for AKI?

A

severity of azotemia does NOT determine prognosis.

- around half survive, around half have CKD

Urinary (2 decks)

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