U4 O3 - Urogenital Emergencies Flashcards
What is Acute Kidney Injury (AKI) – previously
acute renal failure?
A sudden and potentially reversible reduction in the
kidney function- with a sudden marked decrease in
glomerular filtration. From a severity perspective, IRIS
(2016) proposed a grading scheme (I- V) with grade V
having the poorest prognosis
What is Anuria** ?
Complete suppression of urine formation (depending on the source consulted this could be considered < 0.08 ml/kg/hr; < 0.5 mL/kg/hr)
What is azotaemia?
An abnormally high blood level of urea, creatinine and
other nitrogen containing compounds in the blood stream.
Can be pre-renal, renal or post-renal.
Azotaemia is not apparent until > 75% of the kidneys are non-functioning (Foster and Humm, 2018)
This does NOT always equal renal failure
What percentage of the kidney are not functioning if a patient is azotaemic?
Azotaemia is not apparent until > 75% of the kidneys are non-functioning
what is oliguria?
Reduced volume of urine production (depending on the source consulted this figure can vary but is generally
considered < 1.0 ml/kg/hr).
N.B. The actual volume of urine output that is considered oliguric depends on individual patient factors as well as the source consulted. Many sources state that oliguria is < 1.0 ml/kg/hr (IRIS, 2016). However, Foster and Humm (2018) state that oliguria is urine output < 2ml/kg/hr Matthews (2007) and Smarick (2009) define oliguria as being urine production of <0.27 ml/kg/hr. Both sources, however state that
normal urine output would be expected to be above 1ml/kg/hr for most patients.
What is pollakiuria?
Passing frequent small amounts of urine
What is polydipsia?
Increased drinking
What is polyuria?
Increased volume of urine production (> 2ml/kg/hr)
What is the glomerular filtration rate?
Total filtration rate of both kidneys
What is Pyelectasia?
Dilatation of the renal pelvis
What is renal replacement therapy?
The three types of dialysis that could be used for patients in renal failure (peritoneal dialysis, haemodialysis and continuous RRT. Suitable for patients with a reasonable chance of regaining renal function
What are the several variables when determining if a patient is oliguric?
However, it is situational there are several variables e.g. a neonate has poor concentrating power so urine output of ~ 2ml/kg/hr is more likely. Depending on therate of fluids being delivered and the reason for it, a patient receiving intravenous fluid therapy (IVFT), could, however, be considered relatively oliguric if the urine output was 1-2 ml/kg/hr- it should be higher if the patient is receiving adequate IVFT and the
kidneys are functioning correctly.
What are the varying degrees of severity of acute kidney injury?
There can be varying degrees of severity of acute kidney injury (AKI) depending on how many nephrons are damaged.
In its mildest form only a few nephrons will be damaged and there may be no obvious signs of a problem; however, if many nephrons are suddenly damaged and unable to function, the kidneys could acutely fail to function
What 4 recognised clinical phases are there with an acute kidney injury?
AKI has four recognised clinical phases-
the induction phase
where there is an initial nephrotoxic or ischaemic episode;
extension phase
if the induction phase is not recognised/ managed or the kidney damage is severe and there is ongoing inflammation, it progresses to the extension phase where further kidney damage occurs. Depending on the severity of the kidney injury and loss of function, the patient may not survive this or the next stage.
Maintenance phase
However, the next stage is the maintenance phase where following significant kidney damage, clinical signs e.g. oliguria and azotaemia become apparent. If the patient survives, this stage may last from days to weeks depending on the underlying cause.
Recovery phase
The final stage is the recovery phase where the damaged kidney tissues repair and regenerate.
Describe the induction phase with an acute kidney injury?
the induction phase where there is an initial nephrotoxic or ischaemic episode;
Describe the extension phase with an acute kidney injury?
if the induction phase is not recognised/ managed or the kidney damage is severe and there is ongoing inflammation, it progresses to the extension phase where further kidney damage occurs. Depending on the severity of the kidney injury and loss of function, the patient may not survive this or the next stage
Describe the maintenance phase with an acute kidney injury?
the next stage is the maintenance phase where following significant kidney damage, clinical signs e.g. oliguria and azotaemia become apparent. If the patient survives, this stage may last from days to weeks depending on the underlying cause.
Describe the maintenance phase with an acute kidney injury?
The final stage is the recovery phase where the damaged kidney tissues repair and regenerate.
What kidney functions are affected in acute kidney injury?
Acute kidney injury is a potentially very serious syndrome caused by the acute failure of haemodynamic, filtering and excretory functions of the kidneys
What can be the three causes of acute kidney injury?
The cause of AKI can be pre-renal, renal or post-renal in origin.
If severe enough, AKI leads to a build-up of what?
If severe enough, AKI leads to a build-up of toxins (azotaemia), altered acid- base balance and electrolyte
imbalance as filtration via the kidneys is compromised. It is essential to identify as soon as possible whether the patient has acute versus chronic renal failure - however ‘acute on chronic’ can occur.
How can pre-renal, renal or post-renal in a patient with acute kidney injury be significant at affecting the management and treatment of the patient?
Whether azotaemia is pre-renal, renal or post-renal is also very significant as this will affect the management and treatment of the patient i.e. a patient with pre-renal
azotaemia may have hypovolaemia or dehydration and will require intravenous fluid therapy; a patient with urinary tract obstruction will require the obstruction to be removed. On clinical examination, a patient with pre-renal azotaemia, will usually have a small bladder as less urine is being produced; if post-renal, the bladder may be large and distended if a urethral obstruction is present. N.B. great care is required when
assessing. However, if the bladder has ruptured e.g. RTA and the patient has a uroabdomen, then the bladder may not be palpable or will be very small. The results of other diagnostics can help to identify whether the cause of the azotaemia is prerenal, renal or post-renal (e.g. urethral obstruction/ rupture).
What will a urinalysis likely reveal on a patient with an acute kidney injury?
If pre-renal the SG is usually high (although not always depending on the underlying cause); if there is a
renal insult, there may be blood, protein and /or glucose on dipstick urinalysis and there may be abnormalities on examination of the urine sediment – e.g. bacteria, red blood cells, white blood cells, casts etc.
What will a ultrasound likely reveal on a patient with an acute kidney injury?
Diagnostic imaging e.g. ultrasound may demonstrate enlarged kidneys and abnormal renal architecture if there is kidney disease/ injury e.g. nephritis. In a patient, with a ruptured bladder, free fluid may be
apparent on point of care ultrasound (POCUS) examination; plain radiography may demonstrate radiopaque urethral calculi or an iodine positive contrast cystogram may confirm bladder rupture
What is an indicator of renal function?
Azotaemia is an abnormally high level of nitrogenous compounds (urea, creatinine and other nitrogen containing compounds) in the blood stream. As these products should normally be excreted by the kidneys, they can be used as an indicator of renal function.
What is pre-renal azotaemia and what is it usually caused by?
Pre-renal azotaemia refers to azotaemia that has developed because of a problem before (i.e. pre-) the kidney. It is usually caused by decreased kidney perfusion i.e. blood loss or ischaemia. The kidneys cannot perform their role if they do not have blood delivered to them
What will a specific gravity and a dipstick usually reveal on a patient with pre renal azotaemia?
Depending on what the underlying cause is, a patient with pre-renal azotaemia, will usually have a decreased volume of concentrated urine (hypersthenuric) with a high specific gravity. Dipstick examination is usually unremarkable.
A patient with prerenal azotaemia will show clinical signs of marked dehydration and/or hypovolaemia and will typically have concentrated urine (high S.G.) unlike renal causes of azotaemia.
What percentage of cardiac output does the kidney require t be adequately perfused - what can affect this?
The kidney requires 20% of the cardiac output to be adequately perfused so when hypovolaemia and hypoperfusion occur the kidney is commonly compromised.
What happens to the kidneys with pre renal azotaemia and what is it typically caused by?
Pre-renal azotaemia occurs when there is inadequate glomerular filtration rate (GFR) secondary to inadequate perfusion of the kidneys. The kidney requires 20% of the cardiac output to be adequately perfused so when hypovolaemia and hypoperfusion occur the kidney is commonly compromised. This is typically caused by hypovolaemia and may be a result of severe dehydration or blood loss. Inadequate perfusion to the kidneys may also result from septic or cardiogenic shock
What are the clinical signs for pre renal azotaemia?
Clinical signs
Patients will likely have clinical signs related to the underlying condition rather than signs of kidney disease / azotaemia. Signs of hypovolaemia, shock and/or marked dehydration will be present
What will biochemistry usually reveal on a patient with pre renal azotaemia?
A patient with pre-renal azotaemia will usually have increased blood urea nitrogen (BUN), creatinine and SG. N.B. A patient with decreased renal perfusion, leading to pre-renal azotaemia, could initially have elevated blood urea nitrogen (BUN) with a normal creatinine. The elevation in BUN is typically mild-moderate but not severe. The discrepancy in creatinine to BUN as compared to renal or post-renal causes of azotaemia is secondary to the increased solubility of BUN. Other differentials for elevated BUN with normal creatinine include GI haemorrhage and renal disease in cachectic patients
What might electrolytes reveal on a patient with pre renal azotaemia?
The patient may also have hyperkalaemia
What is the treatment for pre renal azotaemia and what does the patients prognosis depend on ?
Correction of the impaired perfusion and/or hydration with intravenous fluid therapy and management of the underlying cause, should lead to a rapid resolution of
azotaemia, acidosis ( anaerobic respiration and hydrogen ion retention) and electrolyte abnormalities (possibly potassium, sodium, chloride, phosphate and calcium). If the patient has clinical signs of hyperkalaemia, however, e.g. bradycardia and ECG
dysrhythmia, the specific treatment may be required Provided renal perfusion has not been impaired for too long- the prognosis for the kidneys is good as glomerular filtration is restored. Ischaemic renal damage could, however, arise secondary to longer duration decreased perfusion. The patient’s
general prognosis, however, will largely be dependent on the underlying cause of the hypoperfusion.
What does azotaemia of renal origin mean?
Renal Azotaemia
Azotaemia of renal origin means the kidneys have been damaged or are malfunctioning. As previously discussed, acute kidney injury is a sudden, serious
reduction in kidney function secondary to some insult e.g. infection, poisoning. Consequently, if the kidneys are damaged, there is decreased excretion of urea and creatinine and loss of urine concentrating ability. It is important to differentiate acute kidney injury from chronic renal failure, despite several clinical similarities, as the treatment and prognosis is different for the two conditions
What physiological processes occur with renal azotaemia?
Renal azotaemia occurs when there is impaired glomerular filtration rate (GFR) secondary to intrinsic renal damage i.e. damage to the kidney tissue. Acute kidney injury can occur for several reasons (see below) – N.B. a patient with chronic renal failure could also deteriorate acutely and develop acute kidney injury- ‘acute on chronic’ renal failure.
What are the causes of renal azotaemia caused by an acute kidney injury?
Causes of AKI include
1. Ischaemia (e.g. hypovolaemia, prolonged hypoperfusion during an anaesthetic
or renal thrombosis)
2. Infection (e.g. Leptospira spp., Leishmania, pyelonephritis)
3. Drug induced toxicity (e.g. aminoglycosides, NSAIDs)
4. Intoxication (e.g. ethylene glycol poisoning, grapes/raisin toxicity, lilies in cats)
5. Immune mediated disease (e.g. glomerulonephritis)
6. Systemic disease (e.g. hypercalcaemia)
7. Trauma/crush injury
8. Neoplasia
9. Cutaneous and renal glomerular vasculopathy
What are the clinical signs of an acute kidney injury?
Clinical signs
These can be vague and may be non-specific especially if AKI. They can include
1. hypovolaemia
2. dehydration
3. lethargy/depression/ collapse
4. oliguria/anuria
5. previous polyuria/polydipsia (if ‘acute on chronic’)
6. seizures
7. ataxia
8. diarrhoea
9. vomiting
10. hypothermia or pyrexia (depending on cause and stage)
11. uraemic halitosis
12. enlarged painful kidneys on abdominal palpation
13. small, irregular kidneys if chronic renal failure
14. bradycardia (if hyperkalaemia is present)
Why is it important to consider leptospirosis in a patient with an acute kidney injury with no explanation for it?
It is important to be aware of the possibility of leptospirosis as a cause of AKI in dogs
care must be when handling patients, equipment or any excretions, especially urine due to the zoonotic potential. If there is any suspicion of leptospirosis, barrier nursing should be implemented. Whilst, an increase in cases of leptospirosis has not been reported specifically, with an increasing number of clients choosing not to vaccinate beyond an initial primary course, for various reasons, and the fact that leptospirosis may be underdiagnosed due to non-specific signs, it is important to consider it in patients with no explanation for AKI
What might haematology reveal on a patient with an acute kidney injury?
Haematology may show an elevated white cell count in cases of bacterial infection e.g. pyelonephritis or interstitial nephritis. The animal may be anaemic, depending on the degree of chronicity- this may help in discriminating between renal and post-renal
causes of azotaemia. Since erythropoietin is produced in the kidney, patients with chronic renal disease usually have non-regenerative anaemia. Thrombocytopaenia may be present alongside immune- mediated glomerulonephritis.
What might biochemistry reveal on a patient with an acute kidney injury?
Biochemistry tends to show an elevation in both BUN and creatinine that may be mild, moderate or marked depending on the severity of the reduction in GFR. If it can be measured, SDMA is likely to be increased as well. Phosphate excretion will also be decreased so many cases will have hyperphosphataemia.
Hypocalcaemia may develop with AKI secondary to ethylene glycol intoxication, or advanced or chronic renal disease. Hypercalcaemia may be seen in a patient with AKI- as discussed in Unit 4 Outcome 2 hypercalcaemia can cause AKI e.g. vitamin D
toxicosis or neoplastic disease, such as lymphoma.
What might electrolytes reveal on a patient with an acute kidney injury?
As the GFR declines further, potassium levels will also start to rise due to decreased excretion - hyperkalaemia is often associated with serious, acute renal disease. N.B. In chronic or polyuric renal disease, potassium is often decreased due to increased losses and inappetence- in these patients a subclinical ongoing global hypokalaemia is common.
What might blood gas analysis reveal on a patient with an acute kidney injury?
Patients may also develop a metabolic acidosis due to the accumulation of hydrogen ions, phosphates and sulphates in the blood stream- these would normally be excreted in the urine. In addition, if they are hypovolaemic, anaerobic respiration will lead to
lactic acidosis.
What might urinalysis reveal on a patient with an acute kidney injury?
Urinalysis samples should be collected by cystocentesis, where possible, to avoid lower urinary tract contamination. In AKI of renal origin or CRF, the urine SG generally ranges from 1.008-1.012- this isosthenuric urine is consistent with a lack of urine
concentrating ability i.e. decreased functioning nephrons. Azotaemia in the presence of decreased S.G. is suggestive of renal disease- patients with pre-renal azotaemia usually have increased urine S.G.
There is often moderate proteinuria +/- haematuria- microscopy may demonstratetubular casts, red blood cells, white blood cells, and bacteria depending on the causal agent. In cases of ethylene glycol poisoning, calcium oxalate crystals may be present
from 3- 6 hours post ingestion however these can also be an incidental finding. A sample should also be taken for microbial culture and sensitivity as bacteria can
proliferate in dilute urine
What might radiography and ultrasound reveal on a patient with an acute kidney injury?
Radiography and ultrasound may show misshapen, small or enlarged renal shadows. There may be altered opacity e.g. mineralisation in the case of EG toxicity.
Ultrasound will reveal more about the internal architecture of the kidneys. It may also reveal renal dysplasia, abnormal cortico-medullary architecture and pyelectasia. In cases of ethylene glycol poisoning, ultrasound examination shows increased echogenicity of the cortex, secondary to calcium oxalate crystal deposition.
What might an ECG reveal on a patient with an acute kidney injury?
ECG changes may be seen secondary to hyperkalaemia- typically bradycardia with
peaked T waves, loss of P waves, wide QRS complexes and prolonged PR interval.
What might a renal biopsy reveal on a patient with an acute kidney injury?
Renal biopsy will provide a definitive diagnosis but is obviously invasive. It carries
a risk of haemorrhage and further reduction of renal function. In addition, patients with
AKI, in particular, are normally critical ill and a GA may be detrimental at this stage.
What are the goals of treating patients with an acute kidney injury?
The goals of treating patients with acute kidney injury are
1. restore normovolaemia
2. induce diuresis to correct azotaemia, electrolyte abnormalities and acid-base
abnormalities
3. correct dehydration
4. reverse oliguria/anuria
5. +/- correct life-threating electrolyte abnormalities
6. +/- correct life-threatening acid-base abnormalities
What are the considerations when administering intravenous fluid therapy to a patient with an acute kidney injury?
Intravenous fluid therapy (IVFT) is necessary to restore normovolaemia, correct dehydration and induce diuresis. This may also help to address acid/base and electrolyte issues – it is possible, however, they may need additional treatment. It is vital that when nursing and monitoring a patient with a reduced urine output, that the patient is closely watched when fluid therapy is administered. If the glomerular filtration rate is decreased and urine output is reduced, there is a significant risk of volume overload. Careful and regular patient re-evaluation should be carried out.
When might antibiosis be warranted in a patient with an acute kidney injury?
Specific therapy should be tailored to the underlying aetiology. In the absence of a specific diagnosis (as is often the case) broad spectrum antibiosis may be warranted if diagnostics e.g. urinalysis or haematology suggest potential pyelonephritis or leptospirosis. N.B. it is important to remember that leptospirosis is zoonotic
What is the treatment for ethylene glycol toxicity nd when is it beneficial to the patient?
If it is known that ethylene glycol has been
ingested then fomepizole or ethanol (alcohol), as a 20% ethanol solution, can be administered. Fomepizole is a competitive inhibitor of alcohol dehydrogenase, the enzyme responsible for converting ethylene glycol to the toxic metabolites glycolic and oxalic acid and is considered to be safer than ethanol. Ethanol also inhibits the alcohol dehydrogenase. However, these
treatments would only be of use PRIOR to the onset of renal failure – they should ideally be administered as soon as possible after ingestion of EG. They are unlikely to be of benefit once the animal has become azotaemic.
What fluids and drugs may be given to a patient with hypercalcaemia to induce calciuresis?
Where hypercalcaemia is present, administration of 0.9% sodium chloride solution encourages renal excretion of calcium as discussed in Unit 4 Outcome 2. Furosemide may be administered alongside this once the patient is haemodynamically stable to
induce calciuresis.
What is a normal urine output?
Normal urine output is ~ 2.0 ml/kg/hr. in the normovolaemic, well-hydrated patient. This figure can be affected by various parameters- many sources state
normal urine output is 1-2 ml/kg/hr
What urine output would be considered oliguric and anuric?
Oliguria is anything less than this- as stated previously, many sources state that oliguria is < 1.0 ml/kg/hr and anuria is < 0.5ml/kg/hr. However, Foster and Humm (2018) state that oliguria is urine output < 2ml/kg/hr. Pachtinger (2013) defines oliguria as being a urine output of less than 0.5 ml/kg/hr and anuria as no urine output. Again, the most important thing
to appreciate is that it is dependent on the patient circumstances and monitoring trends is crucial.
A hypovolaemic and dehydrated patient that presents as an emergency with acute kidney injury, urine output will be low until … ?
It is important to remember that if an animal is hypovolaemic and dehydrated, when it is presented as an emergency with acute kidney injury, that urine output will be low until normovolaemia and hydration have been restored. A patient cannot be considered truly oliguric or anuric if it is hypovolaemic or dehydrated.
How do you accurately assess urine output?
To accurately assess urine output in the oliguric/anuric patient, placement of a urinary catheter,
connected to a closed collection system, is required. Urinary catheterisation is not likely to be required in a polyuric patient however urine output should still be monitored.
It is also important to assess the nature of the urine especially in a patient with intrinsic renal injury/ disease.
What is the best way of restoring normovolaemia in a patient with an acute kidney injury?
As discussed previously, decreased renal perfusion leads to decreased urine production and excretion of nitrogenous waste products- prerenal azotaemia.
Increasing renal perfusion by correcting hypovolaemia +/- dehydration is always the priority for restoring urine output in this situation. Relatively aggressive IVFT is indicated in this situation- this is most safely achieved with multiple, incremental boluses of isotonic crystalloid solutions and very close patient monitoring for signs of fluid overload/ hypoperfusion
What type of fluid is usually preferred when correcting normovolaemia in a patient with an acute kidney injury?
A balanced solution, such as lactated ringers, is usually preferred to normal 0.9% saline, since it contains a lower concentration of sodium
(which the kidneys are unable to handle appropriately at this point) and will buffer the
metabolic acidosis. As previously discussed, the potassium levels in this solution are
low so not an issue in a patient with hyperkalaemia.
What is a normal bolus rate for a patient in shock?
Boluses of ~ 10-30 ml/kg should be given over 20-30 minutes (10-20 ml/kg in a cat) to correct any underlying shock.
What monitoring does a patient receiving IVFT with an acute kidney require?
Monitoring blood pressure is important in assessing the effectiveness of IVFT aiming for a MAP of ~ 80 -120mmHg (or systolic ~100 -140mmHg). Whilst the patient is hypotensive, it requires ongoing boluses of IVFT. Once it is normovolaemic, the rate of IVFT can be decreased to deliver maintenance fluid requirement, replace the fluid deficit and any ongoing losses. The patient’s perfusion parameters, heart rate, mucous
membrane colour, CRT and pulse quality etc. and hydration status should be monitored closely. A comparison should be made of the fluids in vs the fluids out.
Large volumes of maintenance fluids are NOT indicated in patients with normal ongoing losses and can lead to increasing risk of renal oedema and fluid overload.
Assessment of volaemic status is important.
It is hoped that once normovolaemia is restored that urine output will increase. If not, diuretics may be indicated at this stage
why will some patients with acute kidney injury be hypertensive?
Occasionally patients with acute kidney injury will be hypertensive because of sodium, chloride and water retention secondary to activation of the renin angiotensin aldosterone (RAAS) system
Why should intravenous fluid therapy be administered with care in patients with an acute kidney injury?
IVFT should be administered with care to oliguric/ anuric normovolaemic patients with AKI due to the risk of volume overload.
Why is it common for anuric patients to be volume overloaded? How do you assess for overhydration and what can be done if this occur? How does overhydration affect the patient?
Volume overload is associated with poor prognosis in human studies. IVFT in oliguric/ anuric normovolaemic patients should manage insensible losses and any fluid deficit. Unfortunately, without careful monitoring and planning, it is extremely common for anuric patients to become significantly over-hydrated. This is caused by continuing to give multiple fluid boluses where there is no urine output. Fluid administration is often continued because the patient’s mucous membranes remain tacky- this can, however, be a finding associated with azotaemia called xerostomia. The axillary region is the easiest place to assess overhydration in the dog- it develops a gelatinous feel when the dog becomes overhydrated. Stopping IVFT once the dog has significant peripheral oedema or abdominal effusion is too late. By this stage, all cells will be swollen, surrounded by more interstitial fluid and at an increased distance from the nearest capillary so deprived of oxygen and nutrients. If an animal has peripheral oedema, it follows that the rest of the organs will be oedematous too. GI oedema is likely to cause nausea/vomiting and decreased intestinal motility. Hepatic, renal and cardiac tissues are also unlikely to be functioning normally if affected by oedema. Rather than volume overloading the anuric/ oliguric, normovolaemic patient, early therapy with diuretics
may be indicated. Sometimes agents such as mannitol are used- see below
Arterial blood pressure monitoring is very important in determining the volume of fluids required- if the blood pressure is within the normal range then large volumes of IVFT are not required. Measuring central venous pressure (CVP) can also be used to assess venous volume but this is a relatively late change i.e. the CVP increases once the right side of the heart cannot cope with the venous volume.
What central venous pressure will cause oedema?
If a central line/ jugular catheter is placed, central venous pressure could be measured.
In hypovolaemic, anuric patients, incremental fluids boluses should be given so that
CVP is no more than 8-12cmH2O. Anything above this figure will cause oedema (see
above) and will not increase the GFR so is counterproductive
What is a normal central venous pressure?
the CVP for a normovolaemic patient is usually quoted as 0-5 cmH2O - there are, however, many
variables
What central venous pressure would indicate bolus fluid therapy?
In a hypovolaemic patient a higher CVP (8-12 cmH2O) would be acceptable whilst trying to restore normovolaemia and increase urine output
(Reems and Aumann, 2012). Early goal directed therapy aims to achieve haemodynamic stability in critical patients and the recommended CVP for patients
receiving bolus IVFT as stated above is < 8-12 cm H2O
What is mannitol and what physical effects does it have in the body with acute kidney injury?
Mannitol is an osmotic diuretic that can increase tubular flow rate and promote diuresis. Because of its hypertonicity, if mannitol enters the glomerular filtrate it draws fluid into the lumen of the nephrons/ kidney tubules- this both increases urine output and ‘flushes’ cellular debris through into the renal pelvis. A theoretical problem with mannitol is that it requires some glomerular filtration to be occurring to exert its effect – i.e. it must get into the tubular lumen which can be problematic in the AKI patient.
What is the initial dose of mannitol? and what time length should it be given over?
The initial dose is 0.25- 0.5 g/kg IV infusion administered over 5-10 minutes (BSAVA, 2020). If there is a favourable response then it can be repeated as intermittent lower dose boluses or as a constant rate infusion (CRI)
What is mannitol contraindicated in patients with acute kidney injury?
Because of its tonicity, however, the administration of mannitol should not be repeated if the animal is completely anuric.
Mannitol is contraindicated in a dehydrated or hypervolaemic/ volume overloaded patient. N.B. Mannitol is not currently recommended for anuric AKI in human patients due to the risk of volume overload and kidney damage
What is furosemide and what effect does it have in the body with acute kidney injury?
Furosemide is a loop diuretic that works at the loop of Henle- it inhibits the sodium, potassium and chloride ion transporter in the ascending limb of the loop of Henle (BSAVA, 2020). This results in loss of sodium (natriuresis), loss of chloride, loss of potassium (kaliuresis), loss of calcium (calciuresis) and a secondary diuresis (loss of water). Incremental doses can be administered to the oliguric/anuric patient.
What is furosemide contraindicated in patients with acute kidney injury?
As with mannitol, to have an effect, however, furosemide needs to be filtered to reach the loop
of Henle which relies on there being some glomerular filtration. However, when discussing treatment options for sepsis induced AKI, Keir and Kellum (2015) state that furosemide is not helpful; and Foster and Humm (2018)advise that when used in patients with AKI, it was ineffective and potentially harmful. Despite this, it will
sometimes promote polyuria in oliguric veterinary patients. If it is going to be successful, urine output is usually apparent within one hour of an IV initial bolus. If
successful, further boluses can be administered or it can be continued as a CRI.
What is dopamine and what use can it have in patients with acute kidney injury?
Dopamine is a complex drug that is a precursor of noradrenaline (BSAVA, 2020) - it has effects on alpha-1 and beta-1 adrenergic receptors. It also effects dopamine receptors and can theoretically increase GFR by dilatation of afferent renal arterioles (and probably through an increase in cardiac output). It has been used people and patients with AKI but is not currently recommended due to reported lack of efficacy in
multiple human studies and potential toxic effects. Previously, dopamine was used in people with sepsis to prevent renal failure but a landmark study failed to demonstrate this benefit (Abay et al., 2007). In fact, Keir and Kellum (2015) consider dopamine, hydroxyethyl starches (HES) and supraphysiological concentrations of chloride to be harmful to patients with AKI due to sepsis.
Foster and Humm (2018) state that dopamine is also not recommended in veterinary patients due to a lack of evidence-based benefit and risk of side-effects.
As there is insufficient of a “best” protocol for treating a veterinary patient with AKI, the priorities are careful fluid therapy intervention and restoring perfusion, whilst correcting acid-base and electrolyte abnormalities alongside ‘forcing’ diuresis, in some cases.. WSAVA (2015) state that further research and clinical trials are needed to develop evidence-based recommendations for treating AKI in dogs
What treatments can be used for the management of hyperkalaemia?
If required, there are various treatments for hyperkalaemia. Calcium gluconate,
dextrose and insulin can all be used in the management of hyperkalaemia.
How can calcium gluconate help to treat hyperkalaemia and what use does it have in a patient with an acute kidney injury?
Treatment with 10% calcium gluconate does NOT actually decrease serum potassium levels- it does, however, restore the difference between resting and threshold potentials thus allowing normal cardiac conduction to occur and antagonising the
effect of hyperkalaemia on the heart (Odunayo, 2014). This therapy is rapid, although short-lived- it can be repeated but the patient should be monitored for arrhythmias
using ECG. It allows us some time to try and restore renal function and as such improve glomerular filtration.
How can intravenous dextrose and insulin help to treat hyperkalaemia and what use does it have in a patient with an acute kidney injury?
Intravenous dextrose and regular insulin will directly
reduce serum potassium levels by promoting intracellular translocation of potassium.
The patient must have dextrose added to its isotonic fluids to prevent hypoglycaemia- and to promote the further release of insulin. The patient’s blood glucose should be monitored closely
How can intravenous fluid therapy help to treat hyperkalaemia and what use does it have in a patient with an acute kidney injury?
Intravenous fluid therapy further reduces potassium via
dilution.
Why is sodium bicarbonate often not indicated in a patient with an acute kidney injury?
Sodium bicarbonate therapy may occasionally be necessary in severe cases of hyperkalaemia and metabolic acidosis, especially in a patient with acute kidney injury where it is not possible to restore urine output. However, due to the efficacy of appropriate fluid therapy, calcium gluconate and insulin/dextrose, sodium bicarbonate treatment is not often indicated for hyperkalaemia except in the case of anuric renal
failure (that is NOT of post-renal origin).
What are the serious potential side effects of sodium bicarbonate?
The serious potential side effects of sodium
bicarbonate, including metabolic alkalosis, paradoxical CNS acidosis and ionised hypocalcaemia (Odunayo, 2014), must be carefully before its use and it is essential to be able to monitor blood pH.
What are the 4 different types of renal replacement therapy?
peritoneal dialysis (PD) or extracorporeal therapy, intermittent haemodialysis (HD) and continuous renal replacement therapy (CRRT),
What is renal replacement therapy and what use does it have in patients with acute kidney injury?
If medical management of intrinsic renal failure is unsuccessful then renal replacement therapy (RRT) may be considered – peritoneal dialysis (PD) or extracorporeal therapy, intermittent haemodialysis (HD) and continuous renal replacement therapy (CRRT),
are potential options. Forster and Humm (2018) state that indications for RRT include volume overload and hyperkalaemia refractory to medical management, symptomatic uraemia and acidosis.
HA and CRRT are superior to PD but require referral – however, if required, this should be prompt as the morbidity and mortality is likely to increase with delay
What are the two different types of dialysis and when is it indicated?
Peritoneal dialysis and haemodialysis are options for a patient that remains anuric, despite volume expansion and/ or administration of diuretics to increase urine output.
As stated above, indications for dialysis include ongoing oliguria/anuria; severe clinical signs secondary to the azotaemia or volume overload e.g. congestive cardiac failure; or life-threatening electrolyte and/ or acid/base derangements.
What does extracorporeal mean?
Extracorporeal means occurring outside the body. Extracorporeal treatment (HD and CRRT) requires specialist equipment, training and facilities. It can only be delivered in a few institutions in the UK currently.
What is continuous renal replacement therapy?
Continuous Renal Replacement Therapy
The Royal Veterinary College (RVC) currently offer Continuous Renal Replacement Therapy or Prolonged Intermittent (PIRRT) Renal Replacement Therapy (RVC, 2017) in the UK. The blood is filtered through an extra-corporeal filter to remove toxins and returned to the patient. Depending on the inciting cause it may offer sufficient time for kidney function to recover.
As both HD and CRRT require referral, they are not discussed further here
How does peritoneal dialysis work and what conditions should it not be used in ?
Peritoneal dialysis does not require specialist facilities and equipment but it is very labour intensive and requires careful and close patient monitoring (BSAVA, 2014). It should not be performed in patients with hypoalbuminaemia, peritonitis or coagulopathy (BSAVA, 2014). An aseptic technique is absolutely essential and
ongoing one to one monitoring is needed for these patients as it is a procedure fraught
with potential complications.
Peritoneal dialysis uses the peritoneum as a membrane across which fluids and uremic solutes are exchanged
How do you perform peritoneal dialysis?
How to perform Peritoneal Dialysis
Preparation of equipment (BSAVA, 2014)-
• Dialysate - this can either be bought commercially (Baxters – Dianeal®) or can be made using lactated Ringers solution with added dextrose. For
patients that are normally hydrated, 1.5% dextrose is used. If the patient is oedematous (as is often the case if anuric) then 4.5% dextrose is used. The dialysate should be warm when instilled.
• Peritoneal dialysis catheter - there are various commercial peritoneal
dialysis catheters available for veterinary use.
• Urinary Catheter- prior to introducing the peritoneal dialysis catheter the bladder should be catheterised and drained to reduce the risk of accidental
perforation. It should also be maintained as an indwelling catheter, attached to a closed collection system, as this will allow accurate monitoring of urine
output and as such response to intervention
• +/- sedation; local anaesthetic
• Skin prep e.g. chlorhexidine
• Sterile gloves
• Sterile drape
• Monofilament suture material
• Means of infusing and collecting dialysate e.g. collection bag, extension tubing and 3-way tap
• Dressing material
What is the technique for a performing peritoneal dialysis?
The technique for peritoneal dialysis (PD) is as follows (BSAVA 2014):
1. The patient may require sedation- however, these patients are normally critically ill so it may be possible to complete with infiltration of local anaesthetic.
2. The ventral abdomen should be clipped and surgically prepared. Local anaesthetic may be infiltrated around the PD catheter insertion site.
3. The bladder should be catheterised and drained.
4. The PD catheter is surgically inserted into the peritoneal cavity and sutured in place, close to the dependant part of the abdomen. A dressing is applied The PD catheter should be connected to the introduction/collection system and a small amount of dialysate introduced. If this flow and drains freely,
then the remainder can be introduced.
5. ~ 20ml/kg of the dialysate is infused into the peritoneal cavity by raising the bag, attached to the dialysis tube, above the patient and allowing it to gravity
feed in. Throughout the procedure, and whilst the dialysate is ‘dwelling’, it is essential to monitor the patient for any sign of discomfort, distress or
breathing difficulties.
6. The amount of fluid administered should be recorded and the fluid left in the peritoneal cavity for 30-45 minutes (dwell time). During this period, gentle
movement can be helpful if the patient is able. To minimise the risk of developing difficulty in breathing, the patient should be placed in sternal recumbency with its head elevated
7. When it is time to drain the dialysate, place the dialysate collection bag below the level of the patient and allow the fluid to feed back into the bag by
gravity. Allow this to take place over a 15-20 minute period.
8. This process can be repeated every hour until clinical improvements are seen. Thereafter it can be gradually decreased to 2-4 hourly.
9. Strict asepsis should be adhered to always, as the development of septic peritonitis is a significant risk. There is also the risk of wound infection,
perforation of abdominal structures, overhydration and electrolyte abnormalities.
What monitoring and nursing considerations should be carried out on a patient after peritoneal dialysis?
Ongoing patient monitoring includes assessing demeanour; twice daily weighing; monitoring the wound site; regular assessment of TPR and hydration status. Increased urine output is a favourable sign so urine volume should be recorded.
Additionally, cytology should be performed daily on the dialysate to look for signs of infection e.g. presence of neutrophils and bacteria. PCV/TS/TP; urea and creatinine and serum electrolytes should be monitored regularly. If PD is successful, creatinine, urea and potassium levels should start to decline.
It is very important to ensure all the patient’s basic nursing requirements are met- it is essential to appreciate the patient’s needs and try to meet them. Patients with AKI undergoing PD may be depressed so appropriate tender, loving care and nursing
interventions are essential (Hall and Jolliffe, 2015). This is a time consuming and advanced intervention. The feasibility and ability of performing this procedure in
practice should be considered and discussed within the practice team before embarking on it. Ideally one nurse will be dedicated to that patient throughout.
Why may a patient with azotaemia need gastrointestinal protectants and medications?
Supportive therapy
Azotaemia can result in gastric ulceration. Treatment with proton pump inhibitors or H2 blockers may be administered. Anti-emetics may be necessary if there is persistent vomiting. See for discussion of ACVIM consensus statement:
Support for rational administration of gastrointestinal protectants to dogs and cats
Why may a patient with azotaemia need nutritional support?
Patients with AKI often feel nauseous and will be reluctant to eat or they may have oral ulceration which causes discomfort. If they are unwilling/ unable to eat, assisted tube feeding is a consideration to meet the daily RER requirements.
When does post renal azotaemia occur?
Post-renal azotaemia occurs when there is a mechanical disruption to the urinary tract,
distal to the kidney (hence post-renal)
What are the causes of post renal azotaemia?
Post-renal azotaemia occurs when there is a mechanical disruption to the urinary tract, distal to the kidney (hence post-renal). The aetiologies (causes) can be considered by anatomical location-
• Ureter
o Obstruction e.g. urolith(s), stricture, iatrogenic ligation, neoplasia
o Tear/avulsion e.g. trauma
• Bladder
o Rupture e.g. trauma, dehiscence of cystotomy wound, urethral obstruction, iatrogenic cystocentesis
o Tumour- transitional cell tumour can infiltrate into urethra and cause
progressive obstruction
• Urethra
o Obstruction e.g. uroliths, Feline Lower Urinary Tract Disease (FLUTD)/ Feline Idiopathic Cystitis (FIC), neoplasia
o Tear e.g. iatrogenic, trauma
What are the clinical signs of a patient with a urethral obstruction?
They may include pain and distress, secondary to distension of the bladder, if there is a urethral obstruction; or signs related to uroabdomen and
secondary chemical peritonitis if there is rupture of the distal ureter/bladder. Patients with urethral obstruction generally demonstrate frequent, unsuccessful attempts at urination. Patients with urethral obstruction will usually be dysuric, making repeated attempts to urinate and possibly passing small drops of blood-stained urine. The condition is painful. Complete urinary tract obstruction will lead to pressure associated renal damage and failure. The patient may be
hypovolaemic and dehydrated with a metabolic acidosis. In addition, the patient may have a serious arrhythmia secondary to hyperkalaemia e.g. bradycardia may be apparent.
What are the clinical signs of a bladder rupture?
Bladder rupture can follow trauma- the size of the perforation will dictate how rapidly the patient develops clinical signs and how severe these are. The bladder may have a small rupture with slow accumulation of urine in the abdomen over 24-48hrs; with a
large tear, there will a rapid development of uroabdomen and clinical signs may develop sooner. N.B. A patient could still have a palpable bladder and be passing urine even if there is a bladder rupture (depending on the size and location of the tear)
(Aldridge and O’Dwyer, 2013). Urine output, however, is likely to be decreased and there may be haematuria, proteinuria etc. Serial POCUS can be invaluable in
assessing increasing volumes of abdominal effusions.
What are the clinical signs of rupture of the proximal ureter?
If the proximal ureter is ruptured, urine will accumulate in the retroperitoneal space rather than the abdomen. Signs consistent with the underlying cause will be present. Additionally, clinical signs due to azotaemia and hyperkalaemia are also likely to be present (due to the failure of excretion). The patient is also likely to be hypovolaemic and dehydrated.
What can a point of care ultrasound reveal in a patient with post renal acute kidney injury?
POCUS will demonstrate free fluid in the case of bladder rupture- abdominocentesis
can confirm the presence and composition of free fluid. Analysis of this fluid should include PCV, TS/TP and cytology. In addition, a diagnosis of an uroabdomen is based upon paired (abdominal fluid and blood) potassium and creatinine concentrations.
What test is diagnostic for a uroperitoneum in dogs and cats?
A ratio of creatinine concentration in the effusion to serum creatinine above 2:1 is diagnostic for uroperitoneum in dogs and cats. A ratio of potassium concentration in the effusion to serum potassium above 1.4:1 in dogs; and 1.9:1 in cats is diagnostic
for uroperitoneum. Urea is highly soluble, so BUN alone cannot be used to diagnose uroabdomen. Ultrasound may also confirm ureteral obstruction, stricture, dilatation and hydronephrosis.
What may urinalysis in a patient with post renal acute kidney injury reveal?
Urinalysis- urine findings will depend on the underlying cause - the SG may be
increased or decreased. There may be crystalluria and haematuria.
What may radiography in a patient with post renal acute kidney injury reveal?
Diagnostic imaging will assist confirmation that the azotaemia is post-renal in some cases e.g. ruptured bladder or radiopaque uroliths. Radiopaque calculi may be visualised in the urethra +/- bladder of affected patients. Calculi may lodge in the ischial or penile urethra of male dogs. Positive contrast radiography may confirm bladder rupture. However, the patient will generally need emergency treatment before
it can be safely sedated or anaesthetised for radiography.
What treatment is a priority in an emergency situation when a patient presents with a urethral obstruction?
Treatment of life-threatening hyperkalaemia is the priority. As these patients are also commonly hypovolaemic +/- dehydrated, IVFT will be indicated. Although the bladder may be distended in a urethral obstruction, no more urine will be produced until kidney perfusion has been re-established. Therefore,
IVFT is a priority even if the bladder feels very distended in a ‘blocked’ patient.
Urinary diversion is required to allow for excretion +/- relieve pressure on the kidneys in the case of obstruction either by passing a urinary catheter or cystocentesis in a patient with an obstructed urethra.
What treatment is a priority in an emergency situation (before surgical repair) when a patient presents with a ruptured bladder or urethra?
For other causes of post-renal azotaemia, placement of a urinary catheter, a cystostomy tube or a peritoneal drain may be indicated. Surgical repair may be
required in some cases e.g. ureteral/bladder rupture. Where surgery is indicated, the patient will require to be stabilised as much as possible first e.g. treat hypovolaemia, hyperkalaemia and metabolic acidosis. N.B. In many cases, IVFT will address each of
these issues.
Why might a patient with chronic renal renal replacement often present as an emergency and what is an acute on chronic crisis?
Patients are sometimes presented as ‘emergencies’ with clinical signs of chronic renal failure (CRF). This may be a previously unrecognised and, as yet, undiagnosed case of CRF; or may be secondary to an ‘acute-on-chronic’ crisis, where a previously stable
animal with CRF has developed another condition (e.g. pyelonephritis) that has led to its clinical deterioration. Cats with CRF may be accidentally exposed to antifreeze and develop AKI due to ethylene glycol toxicity. As a result of their peculiar drinking habits
when polydipsic, they will often drink from unusual places e.g. the gutter- antifreeze from a leaking car radiator may be present. It is frequently not possible to identify the underlying cause of the chronic renal disease unless structural changes (e.g. polycystic kidney disease) can be identified with ultrasound.
Why is it important to differentiate between acute and chronic renal failure?
It is important to try to differentiate between acute and chronic renal failure since the prognosis is different for each. The long-term prognosis for patients with chronic renal failure is poor whereas there is a chance of full recovery following an acute kidney injury, if recognised early and managed appropriately.
What are the clinical signs associated with chronic renal failure?
The clinical signs associated with CRF include - 1. polyuria 2. polydipsia 3. weight loss 4. anorexia 5. vomiting 6. diarrhoea 7. seizures 8. uraemic breath 9. irregular small kidneys on palpation Some cats, especially, may present with complications of CRF e.g. fractured femur or rubber jaw secondary to renal secondary hyperparathyroidism; intraocular haemorrhage secondary to hypertension.
What may haematology in a patient with chronic renal failure reveal?
- Haematology often shows non-regenerative anaemia (due to lack of production of erythropoietin). In cats, in particular, this non-regenerative anaemia can be severe with a PCV of 12-15% not being uncommon.
What may biochemistry in a patient with chronic renal failure reveal?
Biochemistry tends to show increases in plasma creatinine, urea and phosphate.
Failing kidneys will often retain phosphate and excrete calcium leading to altered serum Ca: P ratio and causing secondary renal hyperparathyroidism (WikiVet, 2012).
Potassium is only likely to be elevated in oliguric/ anuric patients with an ‘acute on chronic’ crisis. Patients with polyuria will often have hypokalaemia especially if their
appetite is decreased. There is often a metabolic acidosis. SDMA, which is eliminated by the kidneys, is being used also as a biomarker for diagnosing and managing CRF
What may urinalysis in a patient with chronic renal failure reveal?
Urinalysis samples should be collected by cystocentesis, where possible, to avoid lower urinary tract contamination. In CRF, the urine SG is generally from 1.008 -1.012 in dogs, showing a lack of urine concentrating ability (isosthenuria)- in cats with CRF
the SG may be 1.008-1.020. The level of proteinuria can give an indication of the degree of renal failure and can be considered a prognostic indicator (Harley and
Langston, 2012). Best practice for quantifying proteinuria, is to compare urine protein (UP) to urine creatinine (UC) - this avoids confused results caused by varying urine protein levels depending on the urine output at a particular time of day.
The normal urine protein to urine creatinine ratio (UP: UC) for dogs is < 0.5; and cats < 0.4 (Grauer, 2015). Values over 1 are clinically significant
Urinary tract infections are common especially in female cats with CRF- E. coli is often the causative agent. Cytology, culture and sensitivity may be required.
UTIs will need appropriate management to prevent ascending infection- antibiotic choice should be based on culture and sensitivity. It is, of course essential to avoid nephrotoxic drugs.
What is the normal urine protein creatinine ratio in dogs and cats?
The normal urine protein to urine creatinine ratio (UP: UC) for dogs is < 0.5; and cats < 0.4 (Grauer, 2015). Values over 1 are clinically significant
What does the Feline Urine Protein: Creatinine Value indicate if it is <0.2?
<0.2 No proteinuria
What does the Feline Urine Protein: Creatinine Value indicate if it is 0.2-0.4?
Borderline proteinuria
What does the Feline Urine Protein: Creatinine Value indicate if it is >0.4?
Proteinuria
What may radiography in a patient with chronic renal failure reveal?
Radiography may show shrunken renal shadows as may ultrasonography. Contrast studies can be performed e.g. intravenous urography (IVU) can give an indication of kidney size, shape, position and, to some extent function. Whilst an IVU can be performed in a patient with azotaemia, it must not be performed if the patient is dehydrated due to the associated risks. Non-ionic, iodine-based contrast media would be preferred to ionic media. The procedure would require general anaesthesia which may cause worsening of renal GRF and should be considered carefully on a risk:
benefit assessment. This is not likely to be an emergency procedure. Kidneys are often
irregular in shape and lack normal corticomedullary differentiation on ultrasound examination.
What may a renal biopsy in a patient with chronic renal failure reveal?
Renal biopsy provides a definitive diagnosis- but is invasive, carries a risk of haemorrhage and, of course, further reduction of renal function
What may a blood pressure assessment in a patient with chronic renal failure reveal?
Blood pressure assessment is important in any patient with either AKI or CRF. Patients with CRF are commonly hypertensive- sustained systemic hypertension can
cause further damage to nephrons, both further complicating and worsening the renal disease
What does staging of chronic renal failure involve?
The International Renal Interest Society (IRIS) provides news and information on renal failure in dogs and cats. It guides on how staging of the CRF can be performed- this is important for deciding the most effective treatment and monitoring.
Staging involves assessment of serum creatinine levels, degree of proteinuria and blood pressure
A urine sample may be collected from a patient with chronic renal failure. Name the 2 parameters which would normally be assessed and explain why.
Specific gravity: provides information about the concentrating ability of the kidney
Culture: in case of infection
State 3 clinical signs of bladder rupture
Absence of urination or decreased volumes Swelling of the abdomen Haematuria Dullness and lethargy Hypothermia & other signs of shock Pain
A number of conditions (in male & female patients) mentioned in this outcome can lead to septic shock. Name 3 of these conditions
Metritis Pyometra Uterine torsion Prostatic abscess GIT rupture Others
List 3 main parameters which should be monitored when nursing a patient with acute kidney injury
Urine output
Hydration status
Perfusion parameters
Blood pressure
Mannitol is a diuretic that may be used in the treatment of acute kidney injury. State 2 ways in which it exerts its effects
Osmotic diuretic
Increases tubular flow rate and promote diuresis
