A renal emergency! Acute kidney injury in cats and dogs
Acute kidney injury is an often severe, life-threatening emergency requiring intensive treatment and nursing care. It is a rapid and significant loss of renal function, leading to the accumulation of nitrogenous waste products, fluid imbalance and electrolyte disturbances (classically, hyperkalaemia). 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.
Pathophysiology
Several factors can cause AKI, including toxin ingestion, infectious disease, urinary tract obstruction, and following the administration of certain medications.
These causes can broadly be categorised into pre-renal, intrinsic renal or post-renal causes since different causes result in injury to different areas of the urinary tract.
Pre-Renal Causes
Pre-renal azotaemia occurs when there is reduced blood flow to the kidney. This can be caused by severe hypotension, shock, and general anaesthesia (any cause of significant, sustained hypotension).
Intrinsic Renal Causes
Renal azotaemia results from injury to any part of the kidney itself. Causes of renal azotaemia include toxins, medications and/or infection (e.g. leptospirosis, pyelonephritis).
Post-Renal Causes
Post-renal azotaemia occurs due to urinary tract obstruction. In these cases the obstruction puts pressure on the kidneys, reducing glomerular filtration and causing azotaemia.
Obstructions can be present in the lower urinary tract (urethra) or upper tract (ureters), or both, and can be caused by stones, crystalline sludge, or neoplasia.
Clinical Signs
Clinical signs of acute kidney injury are varied, and include:
Polyuria
Polydipsia
Lethargy
Depressed mentation
Hyporexia
Anorexia
Vomiting
Oliguria (urine output <0.5ml/kg/hour) (in cases of urinary tract obstruction or severe loss of renal function)
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)
Triage and Stabilisation
AKI patients typically present as an emergency, and the veterinary nurse is heavily involved in their triage and immediate stabilisation.
On their presentation to the clinic, the veterinary nurse should undertake an immediate triage assessment, to identify and correct any life-threatening changes to the cardiovascular, respiratory and central nervous systems, which typically includes:
Assessment of heart rate and rhythm
Assessment of pulse quality and rate
Assessment of respiratory rate, effort and pattern
Assessment of the patient’s neurological status
+/- Measurement of blood pressure
+/- ECG assessment
Securing intravenous access
Running initial bloods (such as venous blood gas, electrolytes, PCV and total solids measurement, alongside renal parameters)
Administration of crystalloid fluid boluses
Administration of analgesia
Administration of medications to reduce potassium level (where appropriate)
Applying warming devices to a hypothermic patient
Following initial stabilisation, further diagnostics are obtained and appropriate treatment and nursing care are initiated based on the results.
Diagnostics
A variety of diagnostic tests are performed on renal patients. The exact tests performed, and the results we see will vary depending on whether the patient has chronic kidney disease or acute kidney injury. Common tests in the AKI patient include:
Biochemistry
Biochemistry often reveals marked azotaemia (increased BUN and creatinine level) alongside electrolyte abnormalities, depending on the underlying cause for the AKI:
Hyperkalaemia is common in AKI patients, due to the inability to eliminate potassium in the urine. Marked increases can be seen.
Hyperphosphataemia is also common in AKI patients, as it is in chronic kidney disease.
Hypocalcaemia is common alongside hyperphosphataemia, due to the inverse relationship between calcium and phosphate (note that this is different to CKD patients who are often hypercalcaemic). In addition, some toxins such as ethylene glycol cause the binding of calcium, decreasing the volume available in the bloodstream. There are some specific exceptions to this, such as patients with vitamin D toxicity, where they have hypercalcaemia - which leads to a secondary AKI.
Blood Gas Analysis
If available, venous blood gas analysis is recommended to examine the patient’s acid-base balance:
pH will be low (<7.4) if acidosis is present.
Base Excess may be low if the acidosis is metabolic.
Bicarbonate (HCO3-) may be low if the acidosis is metabolic.
Urine Analysis
Urine analysis is commonly performed to determine the presence of stones, crystals or infection which could identify an underlying cause for the AKI. Depending on the suspected cause, this should include a full assessment including chemistry strip, specific gravity, sediment examination, urine protein:creatinine ratio and culture and sensitivity testing.
In addition to the tests mentioned above, monitoring urine output is vital in the AKI patient - since this is used to indicate renal function and guides further treatments such as administration of diuretics or dialysis therapies.
Diagnostic Imaging
Much like patients with chronic kidney disease, a variety of diagnostic imaging modalities are used in patients with AKI. These include abdominal ultrasound, which allows us to:
Assess the size of the kidneys and detect enlargement
Assess the shape of the kidneys
Determine whether pylectasia (renal pelvic dilation) is present
Detect stones or masses obstructing the upper or urinary tract
Collected guided FNAs and cystocentesis samples
Abdominal radiography is also commonly performed in patients with urinary tract stones, with or without contrast enhancement.
Treatment
AKI patients require a variety of treatments depending on the underlying cause of their disease. These include:
IV fluid therapy
Drugs to reduce/manage hyperkalaemia
Supportive medications
Antibiotics (e.g. to treat pyelonephritis)
Relief of urinary tract obstructions
Specific treatments for toxins (e.g. alcohol treatment for ethylene glycol toxicity)
Additional treatments such as diuretics and dialysis
Intravenous Fluid Therapy
Fluid therapy support is a vital part of treating AKI. The administration of intravenous fluids 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, we need to be particularly careful about the volumes of fluid we administer, since these patients often have a reduced ability to form urine - leading to oliguria (urine output <0.5ml/kg/hr) or anuria.
Where anuria or oliguria is present, continuing to administer fluid therapy at high rates will quickly lead to fluid overload. So in AKI cases, what we actually want to do is measure the patient’s fluid output, and ensure we are adjusting our fluid rates to match (or very slightly exceed) this.
Fluid rates should be calculated and administered based on a careful assessment of the patient’s hydration and perfusion status and reassessed regularly throughout hospitalisation.
What happens if my patient’s urine output drops and they develop 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. We achieve this firstly by administering diuretics such as mannitol or furosemide and measuring the patient’s response (seeing if their urine output increases).
If this doesn’t work, we’re left with the option of renal replacement therapies, aka. performing dialysis.
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 not performed outside of very specialist settings. A large dialysis catheter is placed into the jugular vein and connected to an extracorporeal circuit, containing a specialised filter and dialysate fluid. The filter and dialysate fluid is able to draw waste products and toxins from the bloodstream into the dialysate/filter, leaving the ‘clean’ blood to be returned to the patient.
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. With peritoneal dialysis, a peritoneal catheter is surgically placed into the abdomen, through which dialysate is infused via a closed system. The fluid sits in the abdomen for a specified ‘dwell time’ before it is drained into a collection bag. During this dwell time, solutes and waste products cross the capillary walls and peritoneal membrane, entering the dialysate which is then removed.
Managing Hyperkalaemia
Patients with AKI are frequently hyperkalaemic and require correction of this to prevent life-threatening consequences. Potassium levels may be managed or reduced by administering:
Calcium gluconate, which protects the heart from the effects of hyperkalaemia but does not actually lower the potassium level itself.
Glucose, which reduces blood potassium levels by stimulating the body to release insulin, driving potassium from the bloodstream into cells.
Neutral insulin, which reduces blood potassium levels by driving it into cells. As hypoglycaemia can result, glucose is typically given at the same time.
Supportive Treatments
In addition to managing specific causes of AKI, we also need to manage their clinical signs and minimise the effects these have on the patient’s wellbeing. We can do this through:
Administering antiemetics (e.g. maropitant and ondansetron) to manage nausea or vomiting.
Administering prokinetics (e.g. metoclopramide) to patients with regurgitation or ileus.
Administering antacids (e.g. omeprazole) to patients with uraemia and GI ulceration/haemorrhage.
Administering analgesia (not NSAIDs due to their effects on the kidneys) to painful patients.
Nursing Care
Our considerations for nursing the AKI patient are vast - there is a huge amount to think about when looking after these guys! Areas to incorporate into your nursing plan include:
Monitoring renal function
Repeat assessments and examinations
Urinary catheter management
Nutrition
Monitoring fluid balance
Vascular access
Monitoring cardiovascular function
Renal Function
Monitoring renal function is a vital part of nursing the AKI patient. In addition to performing regular bloods to check renal parameters, an easy way to do this is by measuring urine output. This is best achieved by placing an indwelling urinary catheter, but if this isn’t possible, then it can be performed by weighing bedding and litter trays before and after use and catching any urine passed outside in a jug or bowl.
Repeat Assessments/Examinations
Regular clinical examinations are required in these often severely ill patients. This should include a full clinical examination with thoracic auscultation, pain assessment and (where appropriate) abdominal palpation, in addition to a TPR/MM/CRT assessment. Bodyweight should also be checked every 6-12 hours in these patients since most acute weight changes are associated with changes in fluid balance.
These assessments should also include carefully monitoring fluid balance, checking for signs of volume overload (such as weight gain, oedema, chemosis, tachypnoea or crackles) and monitoring for signs of nausea.
Where hyperkalaemia is present, heart rate and rhythm should be regularly checked, and the patient placed on a continuous ECG if possible.
Nutrition
AKI patients are frequently anorexic and nutritional support forms a large part of their nursing care.
Patients should be weighed regularly and their resting energy requirement calculated each day (based on their current or admitted weight). Percentage of RER consumed each day should be recorded, and enteral feeding support is given where less than 85% of RER is consumed for 3+ days.
Naso-oesophageal tubes can be beneficial in these patients and are quick and simple to place, can be placed conscious, and can be placed by nurses.
The best food we can give to an AKI patient is the one they will eat - rather than focusing specifically on a particular diet type.
Vascular Access
Vascular access is another important consideration when nursing the AKI patient. In addition to requiring regular blood sampling to check electrolyte, BUN and creatinine levels and acid-base balance, these patients also need multiple IV fluids, constant rate infusions and IV medications.
In most cases, a single peripheral IV catheter will not be sufficient, so further options such as central venous catheter placement or peripherally-inserted central catheter (PICC) placement will be required.
So as you can see, AKI patients present us with a lot of challenges - they are often critically ill, requiring intensive 1:1 nursing care. Though this makes them challenging to nurse, the rewards that come with this are huge, and there’s nothing quite like seeing one of these guys get discharged from the clinic after spending days doing dialysis on them!
To accompany this post, I’m sending out a fluids in and out monitoring sheet to all of our medicine midweek check-in members this - so make sure you’re signed up to our check-in list to get your copy!
It’ll also be available in our resources library - simply head to the downloads page to sign up, then jump into the resource library to download yours.
References
Ettinger, S., Feldman, C., and Cole E. Textbook of Veterinary Internal Medicine. 8th ed. Missouri: Elsevier, 2016.
Merrill L. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell, 2012.
Nelson, R W. and Couto, C G. Small Animal Internal Medicine. 5th ed. Missouri: Elsevier Mosby, 2014.
