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Y4 SA - urinary & endocrine disease > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

What does acute on chronic mean?

A
  • an acute injury suffered in addition to pre-existing chronic renal disease
    – the injury may or may not be related to the cause of pre- existing disease
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2
Q

3 categories of AKI

A
  • Haemodynamic i.e. volume responsive (pre-renal azotaemia)
  • Intrinsic Renal i.e. actual damage to the kidneys
  • Postrenal i.e. urethral obstruction
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3
Q

What contributes to haemodynamic AKI?

A
  • Anything that affects renal blood flow locally or systemic hypotension will contribute to this
  • common causes being hypovolaemia, anaesthesia, use of NSAIDS (prostaglandin inhibition)
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4
Q

What does haemodynamic AKI cause and why?

A
  • produces a pre-renal azotaemia due to reduced clearance that is rapidly resolved by correcting the underlying cause (often fluid therapy to restore renal perfusion)
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5
Q

What happens if you don’t correct haemodynamic AKI?

A

– progression to intrinsic renal damage occurs
– ischaemia and hypoxia

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6
Q

Most common causes of intrinsic renal damage

A
  • ischaemic/hypoxic or toxic in nature
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7
Q

Ischaemic causes of intrinsic renal AKI

A
  • Hypovolaemia, distributive, obstructive, cardiogenic shock*
  • Deep / prolonged anaesthesia*
  • Thrombosis / DIC
  • Hyperviscosity / polycythaemia
  • NSAIDs*
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8
Q

Causes of primary renal disease

A
  • Infectious
    – UTI (e.coli / gram negative most common) – pyelonephritis
    – Lepto
  • Immune mediated e.g. glomerulonephritis, SLE
  • Neoplasia e.g. lymphoma
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9
Q

Secondary disease that causes intrinsic renal AKI

A
  • Infectious e.g. FIP, Leishmania
  • Malignant hypertension
  • Hepatorenal syndrome in cirrhosis (rare)
  • Sepsis – endothelial glycocalyx damage, vascular leak, microcirculatory disruption*
    –- S-AKI*
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10
Q

Nephrotoxins that cause intrinsic renal AKI

A
  • NSAIDs*
  • Ethylene Glycol*
  • Lillies (cats)*
  • Vitamin D toxicity
  • Aminoglycoside antibiotics
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11
Q

Causes of post-renal AKI

A

Urinary obstruction
- Ureteral obstruction
– Ureterolithiasis is becoming more common in cats
– Iatrogenic post spey
- Urethral obstruction (blocked bladder)*
- Prolonged obstruction will lead to intrinsic renal damage

Urinary leakage
- Ureteral, bladder or proximal urethra damage leading to uroabdomen
- Distal urethra leading to tissue leakage
- If a UTI is present, septic peritonitis can develop

Resolves with treatment of the underlying problem

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12
Q

The 4 phases of intrinsic AKI

A

Phase 1 – Asymptomatic phase of the initial insult, towards the end of this phase Azotaemia begins to develop and urine output drops.

Phase 2 – hypoxia and inflammatory responses propagate renal damage, particularly proximal tubule and loop of Henle (highly metabolic cells).

Phase 3 – can last up to three weeks, urine output may be increased or decreased.

Phase 4 – recovery phase, can last weeks to months. During this period, sodium may be lost and severe polyuria – this can result in hypovolaemia, causing recurrent damage through hypoxia.

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13
Q

Diagnosis - history

A
  • Presence of a predisposing factor e.g. anaesthesia, toxin exposure
  • <1w history – anorexia, vomiting, PUPD, lethargy, diarrhoea.
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14
Q

Diagnosis - Clinical exam

A
  • Signs associated with fluid loss
    – dehydration/hypovolaemia.
  • Signs associated with concurrent illness e.g. sepsis

Specific signs:
- Renal pain +/- palpable enlargement
- Uremic halitosis and oral ulceration
- Jaundice - Lepto

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15
Q

Diagnosis - biochem

A
  • in phase 1 these changes may be subtle
  • Azotaemia
  • Hyperphosphataemia (relatively marked)
  • Hyperkalaemia – to a possibly dangerous level
  • Hypokalaemia possible
  • Hypocalcaemia
  • Elevated hepatic parameters in Lepto
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16
Q

Diagnosis - urinalysis

A
  • in phase 1 these changes may be subtle
  • Inappropriate USG
  • Proteinuria
  • Glucosuria
  • Get a sample for culture and sensitivity
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17
Q

Diagnosis - US: POCUS

A
  • Kidneys may appear normal or enlarged
    – Dogs – 5.5 - 9.1x Aortic Diameter
    – Cats – 3 – 4.3cm in length
  • Peri-renal free fluid may be seen with Lepto in dogs, or lymphoma in cats
  • Hydronephrosis – obstruction or pyelonephritis
  • Allows for FNA (may allow rapid diagnosis of lymphoma on cytology) or Biopsy (risk of bleeding)
18
Q

Diagnosis - Radiography/CT

A
  • Identification of obstructions
  • Intravenous contrast studies elucidate better
19
Q

Problems caused by leptospirosis

A
  • Renal damage (99.6%)
  • Hepatic damage (26%)
  • Dyspnoea – Leptospira pulmonary haemorrhage syndrome (LPHS)
    (76.7%)
  • DIC (18.2%)
20
Q

Leptospirosis - diagnosis

A
  • Findings can include
    thrombocytopaenia, anaemia, electrolyte disturbances.
  • Imaging may reveal interstitial/alveolar patterns, hepatomegaly, splenomegaly, abdominal free fluid, mild lymphadenomegaly.
  • SNAP Lepto antibody test (needs antibodies to have been generated,
    so early false negatives)
  • External lab – PCR or MAT (microscopic agglutination test)
21
Q

Is lepto zoonotic?

A
  • yes
  • so any dog with a possible AKI should be tested
22
Q

Fluid therapy

A

The goal is to maintain volume status and renal perfusion, but avoid volume overload – close monitoring is key, and regular alterations in fluid rates to maintain normal volume status in the face of either polyuria, oliguria or anuria.

Monitoring – ins/outs and body weight

Match the losses – this means in severe polyuria you may need high fluid rates, but if losses are less, titrate down to avoid volume overload as damaged kidneys can’t get rid of it– don’t go over the target weight and reassess your target weight daily.

23
Q

Oliguria definition

A

= <1ml/kg/hr in the hydrated and perfused patient

24
Q

Anuria definition

A

= little to no urine in the hydrated and perfused patient

25
Q

Treatment – Oliguria/Anuria

A
  • Loop diuretics e.g. furosemide
  • Osmotic diuresis :mannitol
  • Dopamine
  • Fenoldopam
  • Ca2+ channel antagonists: diltiazem
  • Renal Replacement Therapy: Dialysis
26
Q

Use of loop diuretics e.g. furosemide for tx of oliguria/anuria

A
  • no good evidence for improved outcomes in AKI, however may be justified to prevent fluid overload and allow increased volumes of e.g. nutrition (tube feeding)
  • Furosemide is nephrotoxic in the poorly hydrated patient.
27
Q

Use of osmotic diuresis e.g. mannitol for tx of oliguria/anuria

A
  • no good evidence for improved outcomes despite many theoretical benefits
  • may also cause AKI itself.
28
Q

Use of dopamine for tx of oliguria/anuria

A
  • increases afferent renal blood flow, but not GFR
  • no evidence for improving outcomes
29
Q

Use of Fenoldopam for tx of oliguria/anuria

A
  • increases urine output
  • no evidence for improved outcomes yet.
30
Q

Use of Ca2+ channel antagonists (diltiazem) for tx of oliguria/anuria

A
  • afferent renal vasodilation
  • some non-significant findings supporting improved resolution of azotaemia and urine output
  • other study showing no significant increase in GFR or UO.
31
Q

Indications for dialysis for tx of oliguria/anuria

A
  • Indicated for the non-responsive patient to fluid therapy or acute poisoning e.g. lilly/ethylene glycol toxicity in cats.
32
Q

Types of dialysis

A
  • Peritoneal dialysis: the first opinion option
  • Haemodialysis: the referral option
33
Q

Peritoneal dialysis (procedure, complications, outcome)

A
  • Peritoneal catheter is placed
  • Dialysate solution (glucose containing) is infused, left anywhere from 20 minutes to a few hours, to allow for diffusion, then drained.
  • Repeated as needed
  • Complications are moderate, including causing a septic abdomen.
  • Moderately improved outcomes.
34
Q

Haemodialysis

A
  • Requires dialysis machine and specific training
  • Improved outcomes
35
Q

Suspected urinary tract infection tx

A
  • Amoxy-Clav is a good first line choice for e.coli
  • Doxycycline for Lepto.
36
Q

Complications of AKI

A
  • Suspected urinary tract infection
  • Metabolic acidosis
  • Tachyarrythmias
  • Hyperkalaemia
  • Hypertension
  • Nutrition (catabolic disease)
37
Q

Metabolic acidosis tx

A
  • Hartmann’s (Careful if considering sodium bicarbonate, could worsen hypernatraemia if present, and if lung function is impaired can paradoxically cause CNS acidosis)
38
Q

Tachyarrythmias tx

A
  • ECG for VTACH and consider lidocaine
39
Q

Hyperkalaemia tx

A
  • Glucose, insulin, bicarbonate or beta agonist
40
Q

Hypertension tx

A
  • not uncommon and further damages the kidneys
    – amlodipine
  • Avoid ACE inhibitors which reduce afferent renal blood flow
41
Q

Prognosis without dialysis

A
  • Obstructive (cats) – 91%
  • Infectious – 82%
  • Metabolic/haemodynamic – 66%
  • Other – 50%
  • Toxin – 43-69%
42
Q

Prognosis

A

Realistically – in the non-obstructive, non-infectious case, there is a 50/50 chance for a good outcome

Y4 SA - urinary & endocrine disease (17 decks)

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