13 | The complete guide to managing acute kidney injury in dogs and cats

PodcastRenal
Written By Laura Jones

Unlike CKD, AKI is a potentially reversible loss of renal function.

 

These patients usually present as an emergency, and require intensive treatment and nursing care. 

These guys benefit a lot from advanced monitoring, intensive nursing, and many advanced nursing skills - but before we talk about that, we need to look at what AKI is, how it occurs, and what impact it has on our patients.

What is acute kidney injury?

Acute kidney injury is an often severe, life-threatening emergency requiring intensive treatment and nursing care. It is defined as an abrupt and sustained decrease in kidney function, leading to an abnormal glomerular filtration rate, decrease in renal tubular function, and a drop in urine output.

Cases can vary and range from mild injury without azotaemia or many clinical signs, to patients with sudden and severe disease where marked renal injury is present (leading to acute renal failure). 

Unlike CKD, resolution of kidney injury, treatment of the underlying cause, or adaptation of the kidney can reverse the signs, hence the term ‘kidney injury’ rather than kidney disease/failure. Prompt recognition and aggressive management, alongside careful monitoring, is vital to successfully treat AKI.

In addition to azotaemia, AKI patients often present with:

  • Marked dehydration and/or hypovolaemia.

  • Marked acid-base abnormalities (metabolic acidosis)

  • Marked electrolyte abnormalities (classically hyperkalaemia)


Treatment is aimed at managing the underlying cause, correcting fluid, acid-base and electrolyte derangements and providing supportive care.
  

How does AKI occur?

AKI occurs in 4 stages - first we have initiation, then extension, then maintenance, and then finally, recovery (if the patient is seen in time and recovery is possible)

Initiation is the stage where the insult to renal function is actively taking place. In this stage, the patient may show clinical signs, but they do not always. Biochemistry is usually normal at this point.

Next is extension. Here, the damage to the kidney has occurred, and the patient will have obvious clinical signs and biochemical abnormalities.

Then we have maintenance. Here, the kidneys have reached their maximum damage level, and we begin to see some regeneration of renal function.

And lastly we have recovery. In this stage, we will see improvement in the patient’s clinical signs/examination findings, GFR and renal tubular function, and biochemistry. 

By the time of presentation, most patients are in the extension or maintenance stage. This means that, in these cases, the renal damage has already occurred - so treatment is aimed at allowing the kidneys to repair and renal function to recover, whilst minimising complications associated with reduced renal function (such as fluid overload).

What causes AKI?

There are many causes of AKI, which can broadly be categorised into pre-renal, intrinsic renal or post-renal causes, based on where in the body the ‘injury’ is originating from.

Pre-renal azotaemia

Pre-renal azotaemia is defined as a decreased GFR secondary to hypoperfusion in a structurally normal kidney. It can be caused by any disease resulting in insufficient perfusion (delivery of blood and oxygen) to the kidneys, such as hypovolemia, hypotension, cardiac failure, SIRS or sepsis.

It can also be hospital-acquired (e.g., due to prolonged hypotension under GA) and, if left untreated, can lead to intrinsic renal AKI (as the renal hypoperfusion causes injury to the nephrons).

Intrinsic renal azotaemia

Intrinsic renal azotaemia occurs due to injury to the nephrons causing dysfunction. There are a variety of causes, including toxin ingestion, internal toxic damage, and infection. Things like leptospirosis, pyelonephritis, grape/raisin, lily, and ethylene glycol toxicity are common causes of intrinsic renal AKI.

Post-renal azotaemia

Post-renal azotaemia occurs where urine cannot leave the body, or if the flow is redirected. It is a common cause of AKI especially in cats, and can be caused by urinary tract obstruction, or bladder rupture. 

Like pre-renal azotaemia, post-renal azotaemia can lead to intrinsic renal AKI if it is not resolved promptly.

What signs do we see in an AKI patient?

Clinical signs of acute kidney injury are varied, and include:

  • Polyuria and polydipsia

  • Lethargy

  • Depressed mentation

  • Hyporexia or anorexia

  • Vomiting

  • Oliguria or anuria in cases of urinary tract obstruction or severe loss of renal function

  • Stranguria in cases of urinary tract obstruction

  • Bradycardia or bradyarrhythmias in cases of hyperkalaemia

  • Neurological signs in cases of toxin ingestion


And how is it diagnosed?

Several diagnostic tests are performed in patients with AKI, including biochemistry, haematology, venous blood gas analysis, urine analysis and diagnostic imaging.

Biochemistry typically reveals acute, severe azotaemia with marked increases in BUN and creatinine. Phosphate levels are also increased, and hypo- or hypercalcaemia may be seen. Hyperkalaemia is also common as the kidneys lose their ability to excrete potassium - and where severe hyperkalaemia is present, it’s a potentially life-threatening emergency, since it results in bradycardia and cardiac arrhythmias.

On blood gas analysis, a metabolic acidosis is seen with decreases in pH, base excess, and bicarbonate.

Haematology is often unremarkable in AKI patients, but changes associated with specific underlying causes may be seen, for example haemoconcentration where patients are hypovolaemic/dehydrated, or evidence of inflammation or infection in cases of SIRS or sepsis.

Urine analysis is used to assess the patient’s concentrating ability, alongside determining whether abnormal cells, crystals or infection is present, which could help identify an underlying cause of the patient’s AKI.

Finally, diagnostic imaging such as abdominal ultrasound or contrast radiography, may also be performed in AKI patients. Ultrasound can be used to identify stones, strictures or masses causing post-renal AKI, and detects free fluid. Radiographic studies can also be enhanced with contrast to identify post-renal abnormalities.

So how do we treat and nurse patients with AKI?

The treatment options for AKI patients will vary depending on the underlying cause of the disease.

  • Patients with pre-renal AKI need to have their renal perfusion restored, and any underlying diseases - such as sepsis, SIRS or cardiac failure - managed.

  • Patients with intrinsic renal AKI require supportive care, alongside administering antidotes to any specific toxins and treatment of infectious diseases/infection

  • Patients with post-renal AKI need to have that urinary flow restored - so we’ll be relieving any urinary tract obstructions, and repairing a ruptured or herniated bladder surgically.

Alongside, supportive treatment including analgesia, appropriate IV fluid therapy, and anti-emetics is provided as necessary - regardless of the type of AKI the patient has.

First up, let’s look at fluids

Fluid therapy is a vital treatment for AKI.  It restores hydration and perfusion status in dehydrated and hypovolaemic patients, corrects acid/base disturbances and can correct electrolyte imbalances as well as reduce azotaemia and hyperkalaemia. 

However, fluid therapy needs to be administered carefully to AKI patients, since these patients often have a reduced ability to form urine - leading to oliguria or anuria.
Where this is present, continuing to administer fluid therapy at high rates will quickly lead to fluid overload.

If the patient becomes fluid intolerant during treatment, we need to change our approach. This is focused on trying to get the kidneys to form urine again, rather than continuing to administer potentially high rates of fluid therapy. Options for this include administering diuretics - which are a bit of a ‘hail mary’ in terms of increasing urine production, and are generally used more to manage fluid overload - and dialysis. 

What is dialysis?

Dialysis is the process of externally removing toxins and accumulated waste products from the bloodstream when the kidneys stop functioning. There are two methods of performing dialysis in veterinary patients - haemodialysis and peritoneal dialysis:

Haemodialysis is the most effective method, but requires specialist kit and for this reason, it is not performed outside of large ICU facilities. 

Peritoneal dialysis is a more accessible but less effective method of dialysis. It is very nursing intensive, like haemodialysis, and patients require 1:1 intensive nursing care and treatment.

Let’s talk about potassium…

Patients with AKI are frequently hyperkalaemic. Where hyperkalaemia is present, this requires prompt correction to prevent life-threatening consequences. Because potassium exists in high concentrations inside our muscle cells - and the heart is a muscle - we can see cardiac issues with hyperkalaemia, including bradycardia, and bradyarrhythmias which can be fatal in severe cases.

We manage hyperkalaemia by administering calcium gluconate, glucose, or a combination of glucose and insulin.

Calcium gluconate protects the heart from the effects of hyperkalaemia but does not actually lower the potassium level itself.

Glucose reduces blood potassium levels by stimulating the body to release insulin, driving potassium from the bloodstream into cells.

Neutral insulin reduces blood potassium levels by driving it into cells. As hypoglycaemia can result, glucose is typically given at the same time.

And what about our nursing considerations?

There’s a lot to think about when it comes to nursing AKI patients, including:

  • Monitoring renal function

  • Urinary catheter management

  • Nutrition

  • Monitoring fluid balance

  • Vascular access

  • General monitoring, repeat examinations and general nursing care.

So as you can see, there is a lot to think about when caring for AKI patients! Though they are often very intensive and challenging to nurse, there are so many skills we can use in their day-to-day nursing care. From placing urinary catheters to placing and managing central venous catheters, calculating and forming nutritional plans and placing naso-oesophageal tubes… all the way to managing patients on dialysis, there are so many opportunities for us to get hands-on with these patients.

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on instagram (@vetinternalmedicinenursing) so I can give you a shout out, and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
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