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URI 2 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is included in an acute kidney injury?

A
  • No uniform definition in the veterinary literature
  • Abrupt reduction in kidney function
  • Alterations in
  • GFR
  • Urine production
  • Tubular function
  • Inability to maintain fluid, electrolyte and acid base balance
  • May lead to azotaemia and acute renal failure
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2
Q

Define acute kidney injury

A

“The term “acute kidney injury” (AKI) has been adopted in human medicine to reflect the broad spectrum of acute diseases of the kidney and to reinforce the concept that AKI encompasses a continuum of functional and parenchymal damage from its least to its most severe manifestations.

Kidney injury may be imperceptible clinically at early stages and culminate with the requirement for renal replacement therapy (RRT, various forms of dialysis or renal transplantation) with the onset of overt failure of kidney function or death.”

In the early stages of AKI you wont be aware they are at risk of struggling

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3
Q

What can be done about an acute kidney injury?

A

Emphasises the need for early recognition and treatment to prevent progression to acute renal failure

“Prevention is far better than cure” in KI

Recognise early and treat promptly!

Often about supporting kidneys and allowing nature to do a good job!

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4
Q

What is auto regulation?

A
  • Ability to maintain renal blood flow and GFR within a narrow range irrespective of fluctuations in systemic blood pressure
  • Important safety mechanism for the kidneys
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5
Q

How much of the renal cortex receives the renal blood flow?

A

90%

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6
Q

How much of the renal blood flow goes to the medulla?

A

10%

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7
Q

What is the initiation phase? How long does it last?

A
  • Exposure to renal insult
  • Duration: hours to days
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8
Q

What pathophysiology is involved in the initiation phase? (3)

A

•GFR reduces due to

Reduced renal blood flow

tubule obstruction

  • Fluid back leak
  • Hypoxia & cell swelling
  • Any cell swelling compromises the blood flow
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9
Q

Which phase of acute kidney injury is clinically silent?

A

Initiation phase

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10
Q

What is phase two of the acute kidney injury?

A

Extension phase

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11
Q

What is the pathophysiology of the extension phase?

A
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12
Q

What are the clinical signs of the extension phase?

A

Non specific clinical signs include lethargy, inappetance & abdominal pain

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13
Q

What are the 2 categories under the extension phase? What is the pathphysiology of these?

A
  • Severe injury (spiraling out of control)
  • More necrosis
  • Further localised inflammation & damage
  • Milder injury
  • Controlled apoptosis
  • Less effect as reversible problem
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14
Q

What is the third phase of acute kidney injury?

A

Maintenance

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15
Q

What is the duration of the maintenance?

A

1-2 weeks (longer phase)

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16
Q

What is the pathophysiology of the maintainance phase in AKI?

A

•Constriction of afferent arterioles worsens ischemia delivering to glomerulus which then worsens what is going on

Reduced GFR

●This is a problem!

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17
Q

What is the fourth phase of AKI?

A

Recovery

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18
Q

What is the duration of the recovery phase?

A

Weeks to months

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19
Q

What is the pathophysiology of the recovary phase of AKI?

A
  • Renal tubules
  • Repair and heal?
  • Scar and fibrose?
  • GFR
  • Full recovery?
  • They remain vulnerable!
  • Permanent drop?
  • Kidneys remain vulnerable
  • If they receive another insult then they may not be so lucky
  • We particularly want to look after them!
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20
Q

What is a significant marker for the recvoery phase?

A

Polyuria

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21
Q

What are the clinical signs of AKI? (9)

A
  • Anorexia
  • Vomiting
  • Lethargy
  • Diarrhoea
  • Polydipsia/polyuria
  • Oliguria = anuria
  • Ataxia
  • Dyspnoea
  • Seizures
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22
Q

What are the physical exam findings of AKI? (8)

A
  • Dehydration
  • Tachycardia
  • Bradycardia
  • Hyperkalemia! (Which is a problem with AKI)
  • Renomegaly or asymmetry
  • Palpate for size
  • Renal pain
  • Pyrexia
  • Halitosis +/- oral ulcers
  • Evidence of platelet dysfunction?
  • rare but can occur
  • Uremic or azotemia environment causing dysfunction can cause ecchymosis.
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23
Q

How can you explain the physical findings of AKI?

A

Dehydration can be mild to severe, tachycardia due to pain or hypovolaemia, bradycardia due to hyperkalaemia, renal pain due to swelling and inflammation, pyrexia due to pyelonephritis

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24
Q

What clinical pathology can we measure?

A

PCV and total solids

Creatinine

  • Electrolytes
  • potassium
  • calcium
  • Haematology
  • Anaemia – have they got an underlying perfusion issue which has cause AKI?
  • Biochemistry
  • Hyper or hypokalaemia
  • Hypocalcaemia in ethylene glycol toxicity can exacerbate hyperkalaemic cardiovascular effects
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25
Q

What is seen on urinalysis with AKI?

A
  • Sg 1.007-1.015 (or higher?)
  • Protein
  • Glucose
  • Rule out diabetes with a blood sugar
  • Haematuria
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26
Q

What do we look for sediment analysis/cytology?

A
  • Pyuria
  • Bacteriuria
  • Casts
  • Crystalluria (rarely significant)
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27
Q

Is there such a thing as a “normal” urine SG?

A

No such thing as a normal – about having an appropriate SG for the situation

28
Q

What is the diagnostic plan for AKI?

A
  • Are the history and clinical signs appropriate?
  • Can you identify any possible underlying cause or access to toxins?
  • Can you identify any predisposing problems?
  • Is there any evidence of pre renal azotaemia?
  • Is your patient dehydrated/hypovolaemic?
  • Do your physical exam findings support AKI?
  • Can you rule out post renal azotaemia?
  • Urethral obstruction
  • Ureteric obstruction
  • Ureteric obstruction in one ureter will only cause azotaemia if there is already a problem in the other kidney. Azotaemia requires 75% loss of functional nephrons.
  • Are blood and urine tests consistent with AKI?
  • Give iv fluids as soon as you have your samples
  • Would diagnostic imaging be helpful to rule in or rule out (want to find out if urine cannot leave – post renal)
  • Urinary tract rupture?
  • Ureteric calculi?
  • Urolithiasis?
  • Evidence of pyelonephritis?
  • Are there tests to rule in or rule out specific diseases?
  • Any evidence of haemolytic anaemia à haemoglobinuriaà AKI
  • PCR testing for leptospirosis?
  • any evidence of jaundice/hepatic involvement?
  • Don’t want to miss lepto! Treatable and can do well.
  • May also be jaundiced
29
Q

What diagnostic imaging can we do for AKI?

A

Radiography:

  • Assess renal size (and number!)
  • Radiopaque uroliths
  • Contrast studies
  • IVU?
  • retrograde study?

Ultrasound

  • Uroliths?
  • ureteric dilation/obstruction?
  • Renal pelvic dilation?
  • pyelonephritis?
  • volume overload?
30
Q

What is the prognosis of AKI?

A
  • Overall mortality rate reported to be 50% in a referral population
  • Worst affected?
  • Best treatment?
  • Late treatment?
  • Committed owners? Huge budget and would go all out…
  • Improved prognosis if a treatable underlying cause is found and treatment is rapid
31
Q

What is the survival of lepto?

A

83%

32
Q

What is the prognosis of ethylene glycol in dogs?

A

Grave

33
Q

What are negative prognositc indicators for AKI in dogs? (5)

A
  • Creatinine >885umol/l
  • Anaemia: PCV <33%
  • Proteinuria
  • Hypocalcaemia
  • Concurrent disease
  • Pancreatitis?
  • Sepsis
34
Q

What are negative prognostic indicator in cat with AKI?

A
  • hypoalbuminaemia
  • hyperkalaemia
35
Q

What is the prognosis in cats with ethylene glycol?

A
  • Ethylene glycol prognosis poor, especially
  • > 12 hours post ingestion
  • once azotaemia is documented
36
Q

How do you approach managing AKI?

A
  • “Treat the treatable”
  • pre renal?
  • correct dehydration!
  • post renal?
  • relieve any obstruction!
  • “Test for the testable”
  • IMHA
  • Lepto
  • Support the kidneys
  • Anything else which may be adversely affecting it
  • STOP before you give NSAIDs before a renal or dehydrated patient
37
Q

What can we do to help volume overload?

A

Use diuretics e.g. furosemide to help the patient excrete volume overload

But this is relying on the fact kidneys can excrete

38
Q

“administer iv fluids at as high a rate as the patient can tolerate without adverse signs” was the old approach to fluid therapy. What is the new approach? Why is this?

A

“just enough but not too much”

Misconceptions regarding the role of fluid therapy in improving GFR are still common

39
Q

How can we match the ins and outs of fluid therapy with AKI?

A
  • Correct the fluid deficit over 4-12 hrs
  • Monitor urine output
  • How can we do this?
  • Using a urine catheter. Means we have less problems with a urine leakage in a sick patient.
  • Where possible and where it can be done with strict hygiene- think about placing a urine catheter to monitor urine output. BUT be aware of the significant risk of creating a hospital acquired infection. Think of all the ways you could try to reduce the risk.
  • Potential for a nasty infection which can be AB resistant
  • Recalculate fluid requirements > 4 x a day
  • Monitor:
  • Body weight
  • Respiratory rate and effort
40
Q

What is oliguria define as?

A

•urine output < 0.5mls/kg/hour

41
Q

What is the use of furosemide in AKI?

A
  • no effect on GFR or RBF
  • ­ Increased urine output helps manage the patient
  • 0.5-1mg/kg bolus (repeat)
  • CRI 1mg/kg/hr
42
Q

Is there any use of mannitol in AKI?

A
  • avoid if (avoiding in so many situations by the time you want to use it, it is probably pointless)
  • oliguric + fluid overload
  • anuric + fluid overload
  • actions
  • volume expander
  • osmotic diuretic
  • natriuretic
  • 0.5-1g/kg over 15-20 mins q 4-6 hrs
  • CRI 1-2mg/kg/minute
43
Q

How is dopamine used in AKI?

A
  • No longer recommended because
  • potential for significant adverse effects
  • no evidence to say the drug is beneficial
44
Q

How can we manage hyperkalaemia in cats? (4)

A
  • Think about an ECG monitor
  • What would you expect to see?
  • Manage oliguria/anuria
  • Fluid therapy to restore renal perfusion and GFR (if dehydrated/hypovolaemic)
  • Relieve any urethral obstruction
  • If anuria persists – not good!!!
  • How it works – try to get to urinate to allow the kidneys to excrete K+
  • Protect the heart
  • Calcium gluconate slow iv
  • Increase K+ uptake by cells – drive intracellularly
  • Glucose 1-2mls/kg (50% soln) diluted and given iv
  • Might encourage release of endogenous insulin
  • +/- Soluble insulin CRI?
45
Q

How can you manage acidosis?

A
  • Correct dehydration and let the kidneys manage the acidosis if you can
  • If pH <7.1
  • sodium bicarbonate
  • 1-5 mEq/kg in 0.9% saline
  • calculate deficit and give as CRI
  • Monitoring is crucial ie don’t give bicarbonate if you can’t measure serum bicarbonate
46
Q

What are the signs of fluid overload?

A
  • Weight gain (unexpected as not peed out)
  • Tachypnoea/dyspnea
  • Fluid goes to lung!
  • Pulmonary crackles
  • Fluid goes to lung! Want to pick up subtle changes.
  • Nasal discharge
  • Peripheral oedema
  • Chemosis
  • Ascites
  • Jugular venous distension
47
Q

What are the indications for renal replacement therapy? (4)

A
  • Persistent oliguria or anuria (6-12 hrs)
  • Anuria longer than 6 hours is too long!
  • As soon as there is no urine produced need to be PTS or sent straight to renal replacement unit
  • Life threatening electrolyte or acid-base imbalance
  • Exposure to dialysable toxins
  • Ethylene glycol coming straight in. Can go straight to referral!
  • Fluid overload
  • Don’t just keep going with higher fluid rates.
48
Q

What are the options for renal replacement therapy? (3)

A
  • Peritoneal dialysis
  • Continuous renal replacement therapy (CRRT)
  • Intermittent haemodialysis
  • Renal transplant
  • the RCVS does not currently support the use of living source donors for renal transplantation
49
Q

What do we do alongside managing nutrition?

A
  • Manage nausea
  • Maropitant
  • CRI metoclopramide
  • Analgesia?
  • Opioid not nsaid
  • Address uraemic gastritis
  • Catabolic state will worsen
  • Hyperphosphataemia
  • Hyperkalaemia
  • Blood urea
  • Enteral feeding

Naso-oesophageal

50
Q

When does fluid therapy stop

A
  • “plateau phase”
  • Well hydrated patient
  • Stable renal parameters over 24 h
  • Might not be normal! But as long as they are stable.
  • Taper fluids and review
  • Physical exam
  • Renal parameters
51
Q

Name some causes of AKI.

A
  • Poor renal perfusion
  • Hypovolaemic shock
  • Severe trauma
  • E.g. RTA and hamorrhage
  • Anaesthesia & surgery
  • Hypotension
  • Idiopathic drug reaction
  • Septic pyometre
  • Severe hypothermia
  • Heat stroke
  • Severe dehydration
  • Severe hypoxia
  • Near drowning
  • Pneumonia
  • GA related
  • Nephrotoxins – make sure you can name some!
  • Cardiovascular
  • Decreased Cardiac output= poor perfusion
  • Chf
  • Dysrhythmia
  • Tamponade
  • Hypertension
  • Thrombosis
  • Coagulopathy
  • Urinary tract obstruction
  • Urethral
  • Ureteric
52
Q

Ureteric obstruction for 14 days allows how much of GFR to return after 6 months?

A

70%

53
Q

What are the guidelines for intervention for ureteric obstruction?

A
  • static for 48-72hrs?
  • worsening azotaemia or electrolytes?
54
Q

What do you look for if you suspect urinary tract rupture? (3)

A
  • Signs of trauma?
  • Calculi?
  • Peritoneal or retroperitoneal effusion?
55
Q

What are the creatinine and potassium levels in urinary tract rupture?

A

Creatinine and K+ in effusion would be

>2 x serum levels

56
Q

What are the common causes of AKI in cats? (4)

A
  • Pyelonephritis
  • Ethylene glycol
  • Lily toxicity
  • Ureteric obstruction
57
Q

What is this?

A

Calcium dihydrate crystals…monohydrate crystals are often only seen in the very early stages of ethylene glycol toxicity

58
Q

What are the common causes of AKI in dogs? (4)

A
  • Leptospirosis
  • Grapes/raisins
  • Ischaemic events
  • Pancreatitis
  • DIC
  • Sepsis
  • Hypovolaemia
  • Liver failure
  • Hypotensive shock
  • Alabama rot
59
Q

What is alabama rot?

A

Cutaneous & renal glomerular vasculopathy in dogs

60
Q

What are the signs of alabama rot and prognosis? What is seen on histopathology?

A
  • Becoming more common!
  • Initial presentation:
  • Distal extremity skin lesion(s)
  • Systemic signs ~ 4 days later
  • Progressive/non responsive AKI
  • Anaemia
  • Thrombocytopenia
  • ­ Increased Bilirubin
  • Prognosis grim/hopeless…At the moment
  • Consider the RVC for CRRT? (continued renal replacement therapy)
  • We currently do not know the underlying cause and therefore treatment
  • Histopath:
  • Renal thrombotic microangiogopathy
61
Q

How can we manage risk factors for AKI?

A
  • Fluid therapy for GA
  • Drug choices
  • think before giving NSAIDs
  • In critical patients monitor
  • Blood pressure
  • Avoid hypotension <70mmhg
  • Creatinine
  • Is it increasing even if it’s “normal”?
  • Urine output
  • Urinalysis
62
Q

What do we need to consider about the geriatric dental?

A
  • Consider pre GA bloods and urinalysis?
  • Fluid therapy but beware of fluid overload
  • underlying heart disease?
  • Blood pressure monitoring
  • Careful choice of drugs for rapid recovery
  • Avoid hypothermia
63
Q

What does hypercalcaemia cause in the kidneys?

A
  • PU = PD = dehydration = prerenal effects & risk of AKI
  • calcification of the renal tubules = exacerbates damage
64
Q

What can we do if we suspect high calcium effects on the kidneys?

A
  • Diagnose the cause of hypercalcaemia
  • Manage the hypercalcaemia
  • Protect the kidneys
65
Q

What are the 5 risk factors for AKI you want to avoid in ICU?

A
  • Sepsis
  • Septic pyo
  • Rupture GI FB
  • Major surgery
  • Low cardiac output
  • Hypovolaemia
  • Bleeding bitch spay
  • Rupture splenic mass
  • Medications

URI 2 (44 decks)

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