SA AKI

Question 1

Classifications for acute kidney injuries?

Answer 1

Vascular.
Traumatic.
Toxic.
Inflammatory (sterile, infectious).

Question 2

Normal renal filtration.

Answer 2

Glomerulus - a tuft of capillaries interposed between 2 arteries.
- afferent artery in, efferent artery out.
- filtrate pushed out of the capillaries and into nephron, and travels down to be modified and ultimately create urine.
Substances are conserved or excreted e.g. electrolytes, waste products, water.
Allows maintenance of homeostasis and excretion of products we do not want present.

Question 3

1. What is azotaemia?
2. What is uraemia?

Answer 3

1. Increased urea +/- increased creatinine in the blood.
   Can be pre-renal, renal or post-renal.
2. Clinical syndrome arising from azotaemia.
   Inappetent, nauseous, encephalopathic.
   *nephron dysfunction.
   - azotaemia at ~75% nephron loss.

Question 4

Pre-renal azotaemia.

Answer 4

Reduction in renal blood flow.
Increased protein catabolism.
GI haemorrhage.
Kidneys will be doing everything they can to conserve water:
- azotaemia with concentrated urine (>1.030 dog, >1.035 cat).

Question 5

Renal azotaemia.

Answer 5

Fewer functional nephrons.
Kidneys unable to conserve water:
- azotaemia with dilute urine (<1.030 dog, <1.035 cat).

Question 6

Post-renal azotaemia.

Answer 6

Urinary tract obstruction so back-pressure:
- urethral.
- ureteric – bilateral.
Urinary tract rupture so urine leakage so reabsorption of waste products:
- typically uroabdomen.
– less commonly retroperitoneal or into hindlimb tissues.
- usually traumatic.
Identify with Hx, imaging +/- effusion analysis.
- confirm uroabdomen: fluid creatinine > serum creatinine.
Evidence of either urinary obstruction (clinically or on imaging)
OR
Urinary tract rupture (on imaging).

Question 7

Acute vs chronic organ insults.

Answer 7

Acute injury = sudden organ damage and associated dysfunction. Clinical signs usually severe.
- Outcome could be fatal, could get complete recovery, or could get partial recovery and development of chronic disease.

Chronic injury = gradual/ongoing organ damage/dysfunction.
Compensatory mechanisms.
No signs shown until a long way down the line.

Question 8

1. Why are kidneys so susceptible to changes in cardiac output and why are they also susceptible to toxic injury?
2. Typical signs of severe AKI?
   - less common signs?

Answer 8

1. weigh 0.5% of bodyweight but receive 20% of the CO.
   Susceptible to toxic injury as receive such a large volume of blood.
2. Anuria/oliguria.
   - Less common – polyuria (~10% patients) – Px better.

Question 9

Physiological consequences of AKI?

Answer 9

Failure to excrete nitrogenous waste products:
- azotaemia = increased serum urea, creatinine.
- increase phosphate.
Acid-base disturbances.
Electrolyte disturbances:
- hyperkalaemia (with anuria/oliguria).
- various with polyuria.
Fluid balance disturbances.

Question 10

Clinical presentation of an AKI?

Answer 10

Uraemia - lethargy, inappetence, nausea, vomiting, diarrhoea.
+/- dehydration / hypovolaemia.
Increased or decreased temperature.
+/- renomegaly.
- symmetry?
+/- renal/abdominal pain.
+/- concurrent signs due to other affected organ systems;
- hypocalcaemia; tremors/seizures (ethylene glycol).
- Icterus, petechiae (leptospirosis).
- Cutaneous lesions (CRGV).

Question 11

Aetiologies of AKI?

Answer 11

Toxic, toxins, drugs.
Ischaemic.
- hypoperfusion.
Infectious:
- Leptospirosis.
- Pyelonephritis.
- CRGV (Cutaneous and renal glomerular vasculopathy).
Metabolic.
- elevated Ca : P product.
Uncorrected pre/post renal.

Question 12

Diagnosis of AKI?

Answer 12

Acute azotaemia, with exclusion of pre-renal and post-renal causes.
- non-azotemic AKI possible.
Often hyperphosphataemic.
Potassium variable.
- increased if anuric/oliguric.
- decreased if polyuric.
Metabolic acidosis.
+/- changes related to underlying cause.

Question 13

Specific urinalysis findings for AKI?

Answer 13

Submaximally concentrated urine.
- USG <1.030 dog, <1.035 cat.
- +/- proteinuria/glucosuria.
Sediment examination:
- casts.
- crystals.
Cytological examination.
- inflammatory cells/baceriuria?
Bacterial C&S (ideally cystocentesis sample).
- pyelonephritis.

Question 14

Imaging findings in AKI.

Answer 14

Useful for exclusion of post-renal causes.
- ureteric obstruction – pelvic dilation.
- urinary tract rupture – free fluid.
Ultrasonography:
- renal size normal to renomegaly.
- pyelonephritis may cause pyelectasia.
- +/- hyperechoic cortices, peri-nephric fluid.
Radiographs:
- +/- renomegaly.
- +/- radio-opaque uroliths.

Question 15

Other diagnostics for AKI?

Answer 15

Renal cytology (FNA).
- rarely indicated, use if suspect renal lymphoma.
- thrombocytopathia?
Specific testing for infectious disease:
- leptospirosis.
– serology.
– PCR (blood first 5-7d of illness, urine thereafter).
Specific tests for toxins; ethylene glycol.

Question 16

AKI management?

Answer 16

Remove underlying cause:
- stop known nephrotoxic drugs.
- if recent ingestion of substance, gastric decontamination / absorption.
Supportive management, pending renal recovery:
- manage fluid balance, electrolytes, uraemic toxins.
- manage clinical consequences (e.g. nausea, pain).
Specific treatment (where available).

Question 17

Initial fluid therapy for AKI?

Answer 17

Crystalloids (Hartmann’s).
Correct any hypovolaemia (pre-renal component) within 1-2hrs.
- 10ml/kg dog, 5ml/kg cat, over 10-15 mins.
– reassess/repeat as necessary to restore euvolaemia.
Once euvolaemic:
- correct any dehydration (pre-renal component).
– replace over 6hrs.
– if clinically euhydrated but hx of recent fluid losses (e.g. v+/d+/PUPD), assume 5% dehydrated.
– consider potential contraindications e.g. overhydration, clinically significant cardiac disease.

Question 18

1. Outcome for patient with normal renal function?
2. What if patient anuric/oliguric?
3. What if patient is polyuric.

Answer 18

1. Establish normal urine output following restoration of euvolaemia and euhydration.
2. Risk progressive azotaemia, metabolic derangements, life threatening hyperkalaemia.
   Risk overload and worse outcome.
3. Risk dehydration, hypovolaemia, potassium wasting, hypokalaemia.
   Easier to manage these patients so better prognosis because can excrete uraemic toxins.

Question 19

Determining anuria/oliguria vs polyuria?

Answer 19

Measure ‘ins’ and ‘outs’.
- closed urinary catheter system.
- failing this, weigh urine (1ml = 1g).
- ‘normal’ UOP (for dog/cat on fluids) = 1-2ml/kg/hr.

Question 20

Ongoing fluid therapy for AKI?

Answer 20

Hartmann’s usually most appropriate.
2ml/kg/hr ‘maintenance’ obsolete in patients with high or low UOP.
Match ‘ins’ with ‘outs’.
Outs:
- measured UOP
- insensible losses (e.g. respiratory, normal faecal losses) = 1ml/kg/hr.
– NB panting.
- v+/d+ (guestimate hourly rate).
Measure and evaluate bodyweight.
Re-evaluate every 1-4hrs.

Question 21

Hyperkalaemia as a consequence of AKI?

Answer 21

Reduced pacemaker activity, may be bradycardic which may ultimately lead to v-fib and cardiac arrest.
On ECG - wide QRS, spiked T and lose P wave.
If see bradycardia, pop on ECG and ideally measure potassium levels.

Question 22

Hyperkalaemia management.

Answer 22

Restore renal perfusion.
Ca Gluconate (10%) IV.
- DOES NOT ADDRESS HYPERKALAEMIA.
- Stabilises cardiomyocyte membranes.
Redistribute potassium
- intracellularly.
– glucose –> 2.5-5% infusion, in Hartmann’s.
– +/- exogenous insulin (neutral).
–> requires regular BG monitoring.
- +/- sodium bicarbonate – rarely indicated –> requires acid-base monitoring.

Question 23

Monitoring AKIs.

Answer 23

Fluid balance:
- hydration, bodyweight.
- ins/outs – post-AKI polyuria may be profound.
Renal perfusion (systemic BP).
- normotension = SBP 120-140mmHg.
- must maintain SBP >80mmHg (ideally higher).
- avoid hypertension.
Electrolytes (supplement as necessary).
Azotaemia - want it to be trending down.

Question 24

AKI specific antidotes and therapies…
1. NSAID induced?
2. Pyelonephritis?
3. Leptospirosis.
4. Ethylene glycol.

Answer 24

1. Misoprostol.
2. ABX - clavulanate poten, amoxicillin = reasonable choice pending culture.
3. Calvulanate poten. amoxicillin IV (pending results / if too sick for oral doxycycline).
   Doxycycline (2w, orally) to eliminate carrier state.
4. Ethanol (or 4-methylpyrazole) within 8hrs of ingestion.

Question 25

Adjunctive management for AKI?

Answer 25

Consider dose reductions for renally metabolised drugs.
Manage nausea:
- maropitant.
- metaclopramide (reduce 50%).
Manage GI haemorrhage (may cause nausea):
- omeprazole.
- sucralfate.
Analgesia (opioids) if required.

Question 26

Other considerations in AKI patients.

Answer 26

Nutrition - oral vs assisted.
- if feeding liquid food incorporate into fluid ‘ins’ calculation.
Manage hypertension (amlodipine).
Azotaemia may/may not normalise pre-discharge.
Monitoring/management of residual CKD.
- 3m post-injury.

Question 27

What if anuria persists in a patient?

Answer 27

Double-check:
- euvolaemic, euhydrated.
- no post-renal disease (obstruction/rupture).
Consider trial diuretic:
- no evidence that improves outcome.
- frusemide; 2mg/kg; single dose, expect response in 20-60 mins.
– may repeat.
Still anuric; indication for renal replacement (dialysis); Px guarded.

Question 28

Renal replacement (dialysis).

Answer 28

Persistent anuria.
+/- volume overload.
+/- unmanageable hyperkalaemia.
Peritoneal dialysis - practically frustration and rarely utilised.
Extracorporeal renal replacement therapy.
- need to be >2.5kg bodyweight.
- limited availability.
50% success rate.

Question 29

Prognosis of AKI?

Answer 29

Severity of azotaemia not associated with outcome.
Survival: 34-59% (dogs) and 27-42% (cats).
- polyuria better.
- obstructions/infections/ischaemia better.
- toxins worse (<40%).
– esp. anuric ethylene glycol.
- 40-60% dialysed patients survive.
Approx. half survivors have CKD.
All survivors should be considered as CKD IRIS stage 1 (minimum).