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
State 6 clinical signs associated with chronic renal failure
Polyuria Polydipsia Weight loss Anorexia Vomiting Diarrhoea Seizures Uraemic breath Irregular small kidneys on palpation UTI Anaemia
Pollakiuria means that the animal is producing
Select one:
a. no urine
b. small amounts of urine frequently
c. increased amounts of urine
d. dilute urine
The correct answer is: small amounts of urine frequently
A patient with chronic renal failure could present with which of the following
Select one:
a. metabolic alkalosis
b. respiratory alkalosis
c. respiratory acidosis
d. metabolic acidosis
The correct answer is: metabolic acidosis
Which of the following conditions could cause post-renal azotaemia?
Select one:
a. Hypovolaemia
b. Nephritis
c. Chronic kidney disease
d. Urethral blockage
The correct answer is: Urethral blockage
Why should potassium levels be monitored throughout fluid therapy, following the unblocking of a urethral obstruction?
Select one:
a. Because they can fall and rise throughout fluid therapy
b. Because they can fall
c. Because they can rise
d. Because they may not change at all
The correct answer is: Because they can fall
In male dogs, uroliths most commonly cause blockage of the urethra
Select one:
a. at the ureter
b. at the trigone
c. at the pelvis
d. proximal to the os penis
The correct answer is: proximal to the os penis
Which of the following uroliths is most likely to be present in a Dalmatian?
Select one:
a. Struvite
b. Oxalate
c. Uric acid
d. Cystine
The correct answer is: Uric acid
In a patient with bladder rupture, uroperitoneum is confirmed by testing the fluid drained from the abdomen for
Select one:
a. Urea & potassium
b. Creatinine & urea
c. Potassium & creatinine
d. All of the above
The correct answer is: Potassium & creatinine
An excretory urogram (IVU) could be used to identify which of the following?
Select one:
a. Damage to the ureters
b. Blockage of the urethra
c. Ruptured bladder
d. Damage to the urethra
The correct answer is: Damage to the ureters
Oliguria means that the animal is producing
Select one:
a. Increased amounts of urine
b. Reduced amounts of urine
c. Dilute urine
d. Minimal amount of urine
The correct answer is: Reduced amounts of urine
How soon after whelping is eclampsia most likely to develop?
Select one:
a. 4-5 weeks
b. 2-3 weeks
c. 1-2 weeks
d. 5-6 weeks
N.B. It can arise at any time time during the peri-parturient period depending on various factors
The correct answer is: 2-3 weeks
The main clinical sign of eclampsia is ….
Select one:
a. vomiting
b. diarrhoea
c. polyuria / polydipsia
d. muscle twitching/ spasm
The correct answer is: muscle twitching/ spasm
Which of the following should be closely monitored when administering IV calcium gluconate to a bitch with eclampsia?
Select one:
a. Body weight
b. Potassium levels
c. ECG
d. Urine output
The correct answer is: ECG
Which of the following is least likely to cause acute kidney injury?
Select one:
a. Hypercalcaemia
b. Parvovirus infection
c. Ethylene glycol poisoning
d. Aminoglycoside overdose
The correct answer is: Parvovirus infection
Which of the following statements about the treatment of a patient with acute kidney injury (AKI) is FALSE?
Select one:
a. Intravenous fluid therapy with an isotonic crystalloid is part of the treatment protocol
b. Calcium gluconate can help to counteract hyperkalaemia caused by AKI
c. Mannitol may be administered to promote diuresis in a patient with oliguric AKI
d. Intravenous fluid therapy with a hypotonic crystalloid is part of the treatment protocol
The correct answer is: Intravenous fluid therapy with a hypotonic crystalloid is part of the treatment protocol
Furosemide could be administered to a patient with acute kidney injury to
Select one:
a. Stimulate diuresis
b. Decrease GFR
c. Treat hypertension
d. Decrease cardiac output
The correct answer is: Stimulate diuresis
A patient with chronic renal failure could have non-regenerative anaemia.
Which hormone promotes haemopoeisis?
Select one:
a. Cortisol
b. Parathyroid hormone
c. Erythropoietin
d. Calcitonin
The correct answer is: Erythropoietin
What are the nursing considerations in regards to electrolytes for a patient with chronic renal failure?
Being a chronic condition, the patient will require life-long management which should be discussed carefully with the owner prior to discharge.
If the patient has hyperkalaemia, it should be managed as previously discussed although hyperkalaemia is less likely than hypokalaemia with CRF. Hypokalaemia
causes muscle weakness and potassium may require oral supplementation in these patients.
What are the nursing considerations in regards to urine production for a patient with chronic renal failure?
Patients with CRF usually produce copious volumes of dilute urine- anuria or oliguria is unlikely unless there is an acute crisis. Most patients are dehydrated because of the decreased concentrating ability of the kidneys; and many are severely hyperphosphataemic. Ready access to water is imperative and fluid therapy will be
required for dehydrated patients.
What are the nursing considerations in regards to nutritional management and gastrointestinal support for a patient with chronic renal failure?
Nutritional management is essential and aimed at slowing the progression of the condition, limiting signs associated with uraemia and ensuring the patient has as good a quality of life as possible (Codi, 2017). Appropriate consideration should be given to
dietary management: ‘Dietary management is the single most beneficial treatment for
cats with CKD’ Caney (2010).
Many patients are nauseous, inappetant or anorexic- assisted feeding may be required. Due to uraemic
gastritis and/or gastric ulceration, gastrointestinal ‘protectants’ such as ranitidine, PPIs and sucralfate; as well as anti-emetics such as metoclopramide are often required.
Depending on the stage of the CRF, the diet should have moderately restricted protein levels but the protein should have optimum biological activity; sodium levels should also be restricted to reduce the chance of fluid retention leading to hypertension. A
moist diet increases fluid intake. There are various prescription diets available.
What qualities should the ideal diet have for a patient with chronic renal failure?
Depending on the stage of the CRF, the diet should have moderately restricted protein levels but the protein should have optimum biological activity; sodium levels should also be restricted to reduce the chance of fluid retention leading to hypertension. A
moist diet increases fluid intake. There are various prescription diets available.
It is, however, crucial that the patient receives sufficient calories to meet its daily needs (RER). If it does not eat sufficient food to meet its daily needs, it will start to break down its own proteins e.g. muscle. As well as further contributing to loss of condition, this can cause further complications which impact on the kidneys (Wallace, 2001). As with most conditions, a change in diet whilst the patient is hospitalised may not be
appropriate as it could lead to food aversion. Feeding low phosphate diets and oral administration of phosphate binders (e.g. aluminium hydroxide, calcium carbonate) aid the management of hyperphosphataemia- there are several commercial products available for veterinary use.
How can red blood cell production be stimulated in a patient with non-regenerative anemia associated with chronic renal failure?
Clinical signs associated with non-regenerative anaemia can be a problem. The kidneys are the site for erythropoietin production-the hormone that regulates bone marrow maturation and release of red cells. In an emergency, whole or red blood cell transfusions; or haemoglobin replacers could be considered. Other options include androgenic steroids and human erythropoietin agonists
What organs are the site of erythropoietin production?
The kidneys are the site for erythropoietin production-the hormone that regulates bone marrow maturation and release of red cells
How can chronic renal failure affects blood pressure and what medications can be used in relation to this?
Hypertension is common in patients with chronic renal failure cases- it is managed medically using drugs such as amlodipine and benazepril alongside sodium restricted diet. IRIS (2015) provides guidance on the management of hypertension.
What are the most common forms of urinary tract disease?
Urinary bladder rupture/ rupture of the urinary tract
Urethral obstruction in male dogs and cats
What are the different types of feline lower urinary tract disease and what is the most serious form?
Feline lower urinary tract disease (FLUTD) or feline idiopathic cystitis (FIC) is a common condition in cats- it may be obstructive or non-obstructive. Obstructive is the most serious form of FLUTD- there may be a potentially fatal urethral obstructioncaused by a urethral plug or a urolith. Not all cats with FLUTD have a urethral
obstruction, however- urethral spasm is common and rarely there may be anatomical defects or neoplasia. As the clinical signs of obstructive and non-obstructive FLUTD are similar, any cat with suspicious clinical signs should be seen as soon as possible.
What different factors have been suggested as contributing to the development of
urethral obstruction in cats?
A number of factors have been suggested as contributing to the development of urethral obstruction in cats (International Cat Care, 2018) - these include diet (increased incidence with dried food); access to water; sex (more common in male cats due to narrow urethra); neutering; obesity; lifestyle (more risk if sedentary lifestyle); indoor or outdoor cat and level of exercise. Research has demonstrated the role of stress ‘in triggering and exacerbating’
The signalment and history are often suggestive e.g. overweight, male, house cat with recent ‘stress’.
What physiological effects does a urethral obstruction cause in a cats?
In the obstructive form, a mucoid plug or a urolith blocks the urethra at the narrowestpoint (penis) preventing the flow of urine. This leads to overfilling of the bladder- once the bladder has reached its maximal capacity the urinary pressure will increase up the
ureter to the level of the kidney. Due to this increased back pressure within the renal tubules, glomerular filtration ceases and nephrons become damaged. This leads to azotaemia, hyperkalaemia and metabolic acidosis. Bladder rupture is a serious, potential complication.
What are the clinical signs of a urethral obstruction in cats?
Clinical signs These can include 1. tenesmus 2. excessive grooming in the perineal area 3. haematuria 4. pollakiuria 5. anuria 6. pain, aggression, ANY changed behaviour 7. vocalisation 8. straining outside the litter tray or inappropriate attempts at urination (periuria) 9. anorexia 10. distress 11. hiding 12. collapse
Systemic signs are not often present until several hours (up to 24 hours) after the urethra actually becomes blocked. The longer the obstruction has been present, the worse the clinical signs will be. Outdoor cats, as an example, may not be seen for 12-24hrs at a time and more subtle, early signs can be missed.
Why should great care be taken when palpating a bladder in a cat with a potential urethral obstruction - why may a bladder not be palpable?
With a complete obstruction, the cat will have a distended and painful bladder. Great care should be taken during handling and abdominal palpation not to cause rupture of the distended bladder. Bladder rupture may have occurred in a cat with a history
suggestive of FLUTD whose bladder is not palpable- in which case it will have uroabdomen/uroperitoneum.
What associated complications can be seen with Urethral obstruction that has lead to to post-renal azotaemia?
Urethral obstruction can lead to post-renal azotaemia and associated complications-
• secondary (pressure induced) acute kidney injury with renal azotaemia
• hyperkalaemia
• hypocalcaemia
• hyperphosphataemia
• metabolic acidosis
What urgent diagnostics tests should be performed in a patient with urethral obstruction and why?
A clinical assessment of the cardiovascular and perfusion status should be performed; and a minimum database (MDB) should be obtained. Checking serum electrolytes and ECG tracings is essential due to the likelihood of hyperkalaemia. Ideally blood gas
analysis, biochemistry (creatinine and urea) and haematology should also be performed.
What should diagnostics should be limited to when a patient presents for a urethral obstruction and why?
Diagnostics should be limited at first to those required for diagnosis of the condition and treatment of the most life-threating abnormalities- hyperkalaemia, poor perfusion and metabolic acidosis. This should be performed before sedation/anaesthesia is anticipated even if obstruction is present. Stabilisation of these abnormalities is vital to improve the safety of sedation or anaesthesia.
What may haematology reveal on a patient with a urethral obstruction?
Haematology may be normal or may show an elevated leucocyte and neutrophil count. There may be haemoconcentration in the hypovolaemic/dehydrated patient.
What may biochemistry and blood gas analysis reveal on a patient with a urethral obstruction?
Biochemistry and blood gas analysis may confirm post-renal azotaemia, hyperkalaemia and metabolic acidosis.
What may an ECG reveal on a patient with a urethral obstruction?
ECG changes with hyperkalaemia will show a bradycardia with peaked T waves, loss
of P waves and wide QRS complexes and prolonged PR interval
What may an urinalysis reveal on a patient with a urethral obstruction?
Urinalysis will often reveal struvite or calcium oxalate crystals, red cells, leucocytes.
Urine is typically sterile in cats with feline lower urinary tract disease (FLUTD)-bacterial infection is rare
What may radiography and ultrasound reveal on a patient with a urethral obstruction?
Radiography and ultrasonography should NOT be performed prior to stabilisation of the patient. POCUS examination, however, may confirm the presence of a ruptured bladder with the presence of free fluid in the abdomen. Once the urethra has been
unblocked, full ultrasound examination and radiography (including double contrast studies) can be performed in an attempt to diagnose an underlying cause of the
condition. They can help to identify structural abnormalities and underlying causes e.g. cystoliths/uroliths, bladder wall inflammation and neoplasia etc.
What should the focus initially be on where there is suspicion of a urethral obstruction on emergency presentation?
Upon presentation, where there is suspicion of a urethral obstruction, the focus should initially be on the cardiovascular system. Ultimately, it is the hyperkalaemia that will kill the cat due to its effects on the heart. Hyperkalaemia can lead to atrial standstill
and fatal arrythmia occurring. The first priority should be to obtain venous access- the cephalic vein should typically be used. Care must be taken when handling the patientit may be aggressive due to discomfort, and fear and a distended bladder is at risk of being ruptured. Analgesia should be considered early in admission. When placing the intravenous catheter, it may be possible to obtain a small amount of blood for the MDBelectrolytes/blood gas and PCV and TP/TS. Further blood sampling can be performed
following initial stabilisation
What type of fluid should be used and fluid therapy should proceed on emergency presentation of a urethral obstruction?
Following placement of the intravenous catheter, intravenous fluids should be started to begin to correct the hypovolaemia and potential hyperkalaemia. Assuming that there are no complicating factors (e.g. heart disease), a bolus of 10-20 mL/kg of a
balanced isotonic electrolyte solution should be administered. Hypotonic fluids should NOT be given. Previous recommendations were to avoid any potassium-containing fluids (e.g. LRS) due to the hyperkalaemia- however, the buffering effect of a balanced solution is useful for managing the metabolic acidosis. The small amount of potassium
within the fluids is negligible considering the overall dilutional effect of the administered fluids on the serum potassium concentration. There was a study completed comparing serum potassium levels the use of LRS versus 0.9% saline alongside how rapidly the
acidosis associated resolves. There was no change in serum potassium levels when using LRS however the metabolic acidosis present resolved 12-24 hours sooner in those patients receiving LRS versus saline
Should you wait until a cat with a urethral obstruction is unblocked before starting intravenous fluid therapy?
A common misconception is to wait until the cat is unblocked before giving intravenous fluids. However, as most cats die from hyperkalaemia rather than the rarer complication of bladder rupture, the beneficial effects of fluids out-weigh the risks and should be instituted, especially as the urethra will be unblocked shortly afterwards in most cases anyway. N.B. spontaneous bladder rupture is rare in FLUTD but can arise,iatrogenically, if the bladder is squeezed or cystocentesis has been performed. There are however various reports of decompressive cystocentesis being used to manage urethral obstruction
How do you confirm hyperkalaemia in a cat with a urethral obstruction? What monitoring should be carried out?
Correction of hyperkalaemia
Determining what effect the likely hyperkalaemia is having on the heart should be a priority. Electrocardiography should be performed as soon as possible to identify any ECG abnormalities associated with hyperkalaemia (see above). The actual potassium
levels can be confirmed by blood sampling.
What are the treatment options for hyperkalaemia?
Treatment of hyperkalaemia is based on the following (as previously discussed) –
1. Dilution through administration of intravenous fluids
2. Restoration of GFR
a. Intravenous fluids to restore renal perfusion pressure
b. Unblocking
3. Calcium gluconate- this does not reduce the serum potassium concentration
but protects the heart from the effect of potassium.
4. Insulin and dextrose
5. Sodium bicarbonate**
How does intravenous fluid therapy help to treat hyperkalaemia and improve glomerular filtration rate?
Intravenous fluids will restore intravascular volume and correct dehydration. In addition, they will decrease the serum potassium concentration by dilution. Once the urinary obstruction has been relieved, GFR will be restored and the potassium will be rapidly normalised.
How does calcium gluconate help to treat hyperkalaemia in a patient with a urethral obstruction?
Calcium gluconate (10%) will rapidly oppose the effects of potassium on the cardiac myocytes and is the first-line therapy for hyperkalaemic patients to prevent potentially fatal arrhythmias. It increases the threshold potential (less negative) thus returning
the threshold/resting action potential difference to normal, without actually altering the potassium concentration. A calculated volume of 10% calcium gluconate is administered slowly intravenously, over approximately 10 minutes, whilst monitoring
the ECG. Too rapid an injection of calcium gluconate can lead to further cardiac arrhythmias and even cardiac arrest- thus close monitoring of the ECG is essential.
The effects of the calcium gluconate typically last approximately 10-15 minutes.
How does insulin and dextrose help to treat hyperkalaemia in a patient with a urethral obstruction?
If there are ECG abnormalities suggestive of hyperkalaemia, administration of exogenous regular (soluble) insulin and dextrose may also be required. Insulin causes intracellular translocation of the potassium resulting in a decreased serum potassium concentration
Dextrose is also administered to avoid hypoglycaemia- it also stimulates natural insulin release. Dextrose should be added to the maintenance fluids to create a 2.5-5% solution. The blood glucose levels concentration should be checked every 1-2 hours
as these patients can become hypoglycaemic. Intracellular translocation of potassium, secondary to this treatment, will last approximately 4-6 hours.
How does dextrose help to treat hyperkalaemia in a patient with a urethral obstruction?
Dextrose is also administered to avoid hypoglycaemia- it also stimulates natural insulin release. Dextrose should be added to the maintenance fluids to create a 2.5-5% solution. The blood glucose levels concentration should be checked every 1-2 hours
as these patients can become hypoglycaemic. Intracellular translocation of potassium, secondary to this treatment, will last approximately 4-6 hours
An injection of dextrose alone could be considered if there are no serious ECG signs of hyperkalaemia to induce an endogenous release of insulin. This is not often used,however, due to time it takes to promote the endogenous release. It is a consideration,
however, for those patients that have mild elevations in potassium that is not affecting the ECG.
Can sodium bicarbonate be used to help to treat hyperkalaemia in a patient with a urethral obstruction?
**Sodium bicarbonate was historically the first-line treatment for hyperkalaemia, but is now seldom used due to availability of better and safer treatment options; it can worsen the hypocalcaemia by further decreasing the ionised calcium concentration and cause
irreversible metabolic alkalosis.
How often should electrolytes be tested on a patient that has had a urethral obstruction and has been unblocked and why?
Once the blockage has been removed regular assessment of the serum electrolyte levels should be made (every 2-4 hours). Serum potassium is often high initially but may drop dramatically during fluid diuresis, and may, ultimately, even need to be
supplemented.
How often should urea, crea and glucose be tested on a patient that has had a urethral obstruction and has been unblocked and why?
urea and creatinine levels should be measured every 12-24 hours to ensure that they are decreasing as expected. If the hyperkalaemia was treated with
insulin and dextrose, then glucose levels will need to be monitored every hour.
What type of analgesia is appropriate for a patient with a urethral obstruction?
This is a very painful condition and it is important to provide appropriate analgesia as soon as possible. NSAIDs are not appropriate in the acute presentation due to the risk of further kidney damage. Opioids are preferred at this stage- they may be incorporated into the sedation/anaesthetic regime as part of the premedication used.
A coccygeal local block may be used to promote relaxation and reduce spasm.
What equipment is needed for urethral catheterisation?
Urethral catheterisation should be performed where possible to remove the obstruction/ enable urine outflow. It is essential that an aseptic technique is used.
The equipment needed is listed
1. Sterile gloves
2. Skin preparation e.g. chlorhexidine
3. A selection of catheters to unblock -3-5G French gauge tom-cat catheter; (others may be required if it is not possible to pass a urinary catheter e.g. IV catheter with stylet removed, tear duct cannula)
4. 3-5 French gauge indwelling catheter (this should be made of a soft, inert material which can remain in the urethra for several days whilst the cat is diuresed).There are various options.
5. 10 ml syringe
6. Three-way tap
7. Sterile saline
8. Sterile water-soluble gel
9. Non-absorbable suture material
10.Needle holders and forceps
11.IV drip set and empty fluid bag or commercial closed urine collection system
How do you prep a cat undergoing urethral catheterisation following a blockage?
Sedation or anaesthesia is usually essential on welfare
grounds. Occasionally in a severely collapsed patient sedation is not required. A cardiovascularly sparing sedation regime is appropriate e.g. ketamine and midazolam.
Anaesthesia may be preferred as with greater muscle relaxation, it may be easier to overcome urethral spasm and catheterise the patient.
Care should be taken when handling, the already possibly very inflamed penis and prepuce, not to cause further damage. It is important that this procedure is performed aseptically. Hair should be clipped away and the prepuce should be cleaned with skin
prep and rinsed. The skin prep should be appropriately diluted bearing in mind it may come into contact with delicate mucosa With the cat in dorsal or lateral recumbency, the penis should be extruded (by an assistant)
Describe the technique used for urethral catheterisation in a cat following a blockage from prep to aftercare?
Sedation or anaesthesia is usually essential ) on welfare grounds. Occasionally in a severely collapsed patient sedation is not required. A cardiovascularly sparing sedation regime is appropriate e.g. ketamine and midazolam.
Anaesthesia may be preferred as with greater muscle relaxation, it may be easier to overcome urethral spasm and catheterise the patient.
Care should be taken when handling, the already possibly very inflamed penis and prepuce, not to cause further damage. It is important that this procedure is performed aseptically. Hair should be clipped away and the prepuce should be cleaned with skin prep and rinsed. The skin prep should be appropriately diluted bearing in mind it may come into contact with delicate mucosa. With the cat in dorsal or lateral recumbency,
the penis should be extruded (by an assistant) and the lubricated catheter inserted into the urethral orifice. The prepuce should then be pulled caudally over the catheter to straighten the urethra to allow passage of the catheter (BSAVA, 2014). The catheter can then be gently advanced with a gentle ‘tapping’ applied to the end when resistance is encountered. No force should be applied if resistance is encountered due to the risk
of urethral trauma- localised urethral damage and inflammation could occur but, more seriously, a urethral tear or rupture could arise if excessive force is used (Findji, 2012). A syringe of sterile saline can be attached to the catheter, followed by intermittent injections of saline into the urethra, intended to retropulse the grit/mucous plugs back into the bladder. Once the catheter is in the bladder urine will flow freely from the catheter- it may be haemorrhagic and there may be grit like material in it. A sample should be obtained for analysis; and the bladder emptied before being flushed repeatedly with sterile 0.9% saline until the urine is clear.
The unblocking catheter is then removed, whilst gently flushing the last 10ml saline back into the bladder, to further retropulse any left-over grit. A soft, indwelling catheter should then be placed- this is much less likely to cause trauma to the urethra during placement. It should be sutured to the prepuce and attached to a closed urine collection system. It is important to have the urine bag lower than the patient’s bladder
to allow gravity collection of urine. Taping the urine-collection system to the cat’s tail prevents it from pulling on the prepuce thereby decreasing the potential for further stress and discomfort.
If it is not possible to alleviate the obstruction using a urinary catheter, there are several other options. Using a different size (typically 3.5 or 5FG) or different type of ‘catheter’ can be tried e.g. IV catheter (no stylet). Sometimes, careful repositioning of the cat can assist e.g. moving from dorsal to lateral recumbency. Sometimes a different set of hands does the trick, but in all cases patience and a gentle technique is essential. Adequacy of sedation and analgesia should also be consideredanaesthesia may be preferred for this reason. In most cases these alternative options will be successful
Is decompressive cystocentesis advised in a patient with a urethral obstruction?
Some authors advocate decompressive cystocentesis to reduce the pressure within the bladder. Whilst this is controversial due to potentialcomplications (leakage of urine into the abdomen, rupture of bladder), Cooper (2015) states that cystocentesis appears to be a safe procedure which may provide some benefits in the initial case management. Some sources suggest that decompressive cystocentesis should be carried out immediately on presentation. As this involves entry into a body cavity, it must be performed by a veterinary surgeon in the UK. If cystocentesis is performed, then a small gauge needle (25 g) should be used and the bladder emptied completely to avoid urine leakage and uroabdomen (Sant, 2012). Rarely, a surgically placed cystostomy tube may also be considered
What are the monitoring and nursing considerations of a cat following urethral catheterisation after a blockage?
In all cases the cat should have an Elizabethan collar applied to prevent it from removing the catheter. As stress is important in the aetiology of this condition,
however, it is important to place a collar that is well-tolerated by the patient e.g. a soft E-collar. Careful assessment of urine production, every hour, should be made to ensure the catheter is patent. Gentle palpation of the urinary bladder to assess its size can be useful. If urine production stops it must be reported promptly. It is important todetermine if this is due to a blockage in the catheter or due to oliguria/anuria from renal failure due to acute kidney injury. Continuing assessment of pain and provision of analgesia is important with e.g. buprenorphine. NSAIDs should NOT be used if the
cat is or was azotaemic
How can you help to minimise stress in a cat following urethral catheterisation after a blockage?
Appropriate nursing of cats with FLUTD is essential (Boor, 2013)- one main aim is to
minimise stress whilst hospitalised e.g. environmental enrichment and TLC; quiet, dedicated cat kennels; somewhere to hide, climb etc.; large kennel with litter tray and food/water dishes far apart; familiar litter substrate and use of synthetic F3 pheromone
preparations e.g. Feliway ®. Additional medication to help in management of stress may be required e.g. gabapentin or trazadone. It is important when nursing such patients to inform the veterinary surgeon promptly of any concerns re the stress in the patient.
How can water intake and nutrition help a cat following urethral catheterisation after a blockage during hospitilisation?
Increasing water consumption can aid in the flushing of crystals from the urinary bladder- increased consumption can be relatively easily achieved by feeding wet food and ensuring normal hydration. It is, however, not a good idea to change the diet of a
hospitalised cat as it may introduce food aversions or cause stress which may predispose to a recurrence. As these cats are commonly obese, it is important not to
cause hepatic lipidosis by inducing anorexia, which can become persistent, whilst in the hospital.
What diagnostic parameters should be monitored in a cat following urethral catheterisation after a blockage during hospitilisation?
Urea and creatinine, electrolytes (including potassium and phosphate), and urine output should be monitored on an ongoing basis. N.B. Whilst the cat may be
hyperkalaemic on presentation, they often subsequently become hypokalaemic especially if inappetant and if there is post-obstruction diuresis.
Urinalysis should be performed regularly. The volume of urine produced should be carefully measured and recorded - many cats develop significant post-obstructive diuresis.
What monitoring is required of a urinary catheter and collection bag in a cat following urethral catheterisation after a blockage during hospitilisation?
The urinary bag should be drained every 2-4 hours, or more frequently as required, and checked regularly for signs of blockage. Unless the catheter is blocked (decreased urine volume and increasingly distended bladder), the urinary catheter should not be disconnected from the tubing to keep the system closed, thus limiting the likelihood of bacterial contamination and ascending infection. If the catheter is blocked, it should be flushed using 0.9% sterile saline- the collection system should not be used for flushing as bacteria may be present in it (Ackerman, 2016). It is, of course, vital to keep the urinary bag below the level of the patient to prevent urine draining back into the bladder. It is important to monitor the cat’s reaction to the collection system and avoid the tubing becoming entangled. It is important that the patient is as comfortable as possible.
What medications are helpful for cats with urethral spasm following urethral catheterisation after a blockage?
Urethral spasm is common and may cause problems for the cat, both, with the catheter in place and once the catheter is removed. Drugs such as prazosin or phenoxybenzamine may be used to reduce urethral spasm. Acepromazine is also a very effective smooth muscle relaxant. However, because of its long-lasting effect and potential cardiovascular effects, careful assessment of the patient’s cardiovascular system is needed prior to administration.
Are antibiotics indicated for geline idiopathic cystitis?
For true feline idiopathic cystitis, antibiotics are not considered to provide any benefit - they may even increase the risk of recurrence by increasing the stress to the patient during administration. Antibiotics would only be a consideration in a patient with pyuria or significant bacteria on examination of urine sediment. Choice of antibiotic should be based on culture and sensitivity of a urine sample. N.B. It is important to be aware that the leucocyte square on urine dipsticks is not reliable for veterinary patients.
What usually causes the a urethral obstruction in cats?
male cat where it is usually associated with a fine silt or mucoid plug
What usually causes the a urethral obstruction in dogs?
This is more likely in a male dog due to their urethra being narrower than in a female. In the male dog, urethral obstruction is usually associated with a discrete urolith(s),
What breed of dog are predisposed to getting urate uroliths and why?
Dalmatians may be more predisposed because of their urate metabolism; urate urolith formation may also be a complication of portosystemic shunt
Why are dogs with a urethral obstruction less likely to have signs of post renal azotaemia compared to cats?
If back–pressure develops as a result of the obstruction, the glomerular filtration rate will be reduced and signs of post-renal azotaemia will develop. However, this tends to arise less commonly than in cats, probably since abnormal urination patterns are typically noted more quickly in dogs than cats. Hyperkalaemia is much less likely to be a complication in dogs with urethral obstruction than cats.
What are the clinical signs of urethral obstructionin dogs?
The clinical signs are like those seen in the male cat and include-
- stranguria (slow and painful discharge of urine)
- tenesmus
- dysuria
- haematuria
- pollakiuria
- anuria
- pain
- vocalisation
- unsettled
- behaviour change e.g. depression, aggression
- signs associated with post-renal azotaemia
What is the priority treatment when a dog presents in an emergency with a urethral obstruction?
As with the obstructed cat, the priority is identifying and managing life-threatening hypovolaemia, metabolic acidosis and electrolyte abnormalities (although significant hyperkalaemia is less likely).
What may urinalysis reveal in a dog with a urethral obstruction?
Urinalysis will often reveal struvite or calcium oxalate crystals, red blood cells, leucocytes and sometimes bacteria.
What may haematology reveal in a dog with a urethral obstruction?
Haematology may show no abnormalities or there may be an elevated leucocyte and neutrophil count. Occasionally, where large volumes of blood are lost through the urinary tract, the PCV may be decreased (as will the total protein levels) with evidence of a regenerative anaemia.
What may biochemistry reveal in a dog with a urethral obstruction?
Biochemistry may show findings suggestive of post-renal azotaemia.
What may an ECG reveal in a dog with a urethral obstruction?
ECG may demonstrate changes indicative of hyperkalaemia - bradycardia, peaked T waves, loss of P waves, wide QRS complexes and prolonged PR interval.
Radiography and ultrasonography will confirm the presence and location of radiopaque uroliths. They tend to lodge at the proximal end of the os penis or at the ischial arch in the male dog. Positive contrast urethrography may be required to identify structural abnormalities e.g. strictures, tumours or radiolucent calculi.
What initial treatment is required in a patient that present in an emergency for urtheral obstruction?
These patients will often present with systemic signs such as vomiting, hypovolaemia – they can sometimes present collapsed, like the feline patient. In this situation, stabilisation is the priority.
An intravenous catheter should be placed to enable administration of emergency treatment (IVFT)- some patients will be hyperkalaemic and uraemic (as described above for feline urethral obstruction).
What equipment in needed for urethral catheterisation in a dog?
Catheterisation
Urethral catheterisation should be performed, where possible, to relieve the obstruction. An aseptic technique is essential.
The equipment needed is as follows:
1. sterile gloves
2. antiseptic skin preparation to clean the prepuce e.g. chlorhexidine
3. 6-10 french gauge dog urinary catheter
4. three-way tap
5. kidney dish and sample pots
6. sterile 0.9% saline
7. sterile water-soluble gel
8. non-absorbable, monofilament suture material
9. needle holders and forceps
10. closed urine collection system
Describe the technique used when catheterising a dog that has a urethral obstruction?
Sedation or anaesthesia is preferable for this procedure (see Unit 2 Outcome 3). The dog should be placed in lateral recumbency and its prepuce should be cleaned. The urinary catheter should be opened and a feeding sleeve cut from the inner packaging- this allows for aseptic introduction of the catheter (BSAVA, 2014). The urinary catheter is lubricated with sterile water-soluble gel, sometimes containing lidocaine. The penis is protruded from the prepuce and the catheter is inserted into the urethra, at the ventral tip of the penis, with one hand whilst the other grasps the os penis to aid passage. The catheter should be kept sterile by using sterile gloves and keeping it within its sterile packaging as it is introduced. Any uroliths encountered may be retropulsed back into the urinary bladder, where possible, by careful, pulse flushing of using sterile 0.9 % saline (5-20 ml) through the catheter. The aim is to dilate the urethra around the obstruction and dislodge it. If this is not successful, a urethrotomy is likely to be required Once in place, the catheter can be sutured to the prepuce using non-absorbable, monofilament suture material. It should be connected to a closed collection system and managed as described for the cat
When is a urethrotomy indicated in a patient with a urethral obstruction?
This procedure may be necessary where it is impossible to unblock the urethra due to stricture formation, the presence of a large urolith, catheter induced trauma or where a dog re-presents frequently with urethral blockage and lower urinary tract disease. Urethrotomy should only be performed after stabilisation of the patient and removal of urine from the bladder e.g. by tube cystostomy. Tube cystotomy enables temporary urine diversion in the presence of urethral obstruction.
In most cases the urolith lodges at the proximal os penis. It may be palpated there -surgical removal of the urolith may be possible by performing a urethrotomy. A more permanent scrotal urethrostomy may be required in some patients but this would not be performed on an emergency presentation
What ongoing assessments are required in a patient following urethral catheterisation after an obstruction?
Ongoing assessments are the same as those described above for feline patients. The main priority is to ensure ongoing urine production, decrease pain and discomfort, dilute urine, ensure adequate, appropriate nutrition and address underlying causes.
What are the most common causes of urinary bladder rupture?
Blunt trauma such as road traffic accidents, kicks or falls are common causes of urinary bladder rupture. Bladder rupture may occasionally occur following cystocentesis especially if associated with urethral obstruction, although this is contentious. N.B. Any part of the urinary tract may be ruptured because of trauma- urethral rupture is a potential complication of urinary catheterisation in a ‘blocked’ patient. The patient may have comorbidities such as pelvic fracture.
What will a patient urinary status be if they have a urinary bladder rupture?
Generally affected patients have decreased or no urine output but it does depend on the size and location of the rupture as outlined previously. If the patient is producing urine the volume is likely to be decreased and there may be haematuria.
How will a patients biochemistry, electrolytes and blood gas be affected in patients with urinary bladder rupture?
The patient will develop a post-renal azotaemia, due to lack of excretion, and chemical peritonitis due to urine in the abdomen (uroabdomen). In addition to elevations in BUN and creatinine, the animal will rapidly become hyperkalaemic with a metabolic acidosis.
Uroabdomen is considered a medical rather than surgical emergency and is commonly managed without surgical intervention initially focusing on stabilising the patient
What are the clinical signs of urinary bladder rupture?
These can include-
- anuria/ oliguria (depends on the size and location of the tear-some patients will display normal urination)
- stranguria
- dysuria
- haematuria
- abdominal pain
- inguinal/ perineal bruising
- dullness and lethargy (signs secondary to post-renal azotaemia)
- hypothermia and other signs of shock
How might the clinical signs and history of a patient indicate urinary bladder rupture?
Clinical signs suggestive of urinary tract leakage may be present as above although they may be absent. There may be a history of blunt trauma or recent urethral catheterisation. The bladder may or not be palpable per abdomen depending on the size and location of the rupture- N.B. a palpable bladder does not rule out bladder rupture. A
What might a point of care ultrasound reveal in a patient with a urinary bladder rupture?
A POCUS free-fluid scan of the abdomen should be part of the minimum panel of diagnostics performed on a patient presenting with an ‘acute abdomen’, azotaemia or history of trauma. POCUS is a very effective means of confirming the presence of free abdominal fluid in these patients.
What might a biochemical analysis reveal in a patient with a urinary bladder rupture following an abdominocentesis?
If fluid is noted, then abdominocentesis should be performed by the veterinary surgeon. The fluid obtained should be analysed-including PCV/TP, biochemistry and cytology. Biochemical analysis of the fluid will confirm a diagnosis of uroabdomen- paired (abdominal fluid and blood) potassium and creatinine concentrations are measured. A ratio of creatinine in the effusion to serum creatinine above 2:1 is highly suggestive of uroperitoneum in dogs i.e. there is more than twice the level of creatinine in the effusion to blood (Stafford and Bartges, 2013). This measurement is less reliable in cats. A ratio of the potassium concentration in the effusion to serum potassium above 1.4:1 in dogs, and 1.9:1 in cats is also highly suggestive of of uroperitoneum. Urea is too soluble, so BUN cannot be used to diagnose uroabdomen. In addition, fluid ‘looking like’ urine cannot be used as diagnostic criteria for uroabdomen. Most transudates, regardless of the source, will “look like urine”. N.B. It is not uncommon for patients with acute kidney injury to develop a small volume retroperitoneal effusion; and a moderate to large volume abdominal effusion can rapidly develop in an overhydrated anuric animal.
What might radiography reveal in a patient with a urinary bladder rupture?
Radiography is useful once the patient is stabilised. Plain radiographs may show no evidence of a urinary bladder with loss of contrast and serosal detail due to the presence of free fluid. Tears in the bladder or urethra may be confirmed using an iodine-based positive contrast technique e.g. positive contrast urethra-cystography. Any leakage from the bladder or urethra will then be apparent. A non-ionic, iodine contrast media is preferred- as it is water-soluble, it will be absorbed and then excreted. If urine leakage from the kidneys or ureters is suspected then excretory/intravenous urography (IVU) may be considered rather than a lower urinary tract contrast study. The patient must, however, be adequately volume resuscitated and rehydrated before commencing an IVU
What is the initial priority during stabilisation of a patient with a urinary bladder rupture?
medical stabilisation of the patient is the initial priority- it is important to stabilise the patient haemodynamically prior to any anticipated surgical intervention. In addition to IVFT, management of acid-base and electrolyte abnormalities will be required as outlined previously. As urine is usually sterile, the peritonitis which develops secondary to uroabdomen may not be as serious as with other causes e.g. intestinal perforation. The post-renal hyperkalaemia and azotaemia, however, are potentially life-threatening.
How can therapeutic abdominocentesis help to assist a patient with a urinary bladder rupture?
Urethral catheterisation in a patient with bladder or urethral rupture can allow drainage of urine around the damaged area, depending on location. Therapeutic abdominocentesis by draining urine from the abdominal cavity can help in the management of hyperkalaemia (and azotaemia). This can often be performed in a conscious patient as it is not a painful procedure. In some patients this may involve placement of an abdominal drain but a drain is often not required (Forster and Humm, 2018). In some patients placement of an indwelling drainage catheter, ‘tube cystotomy’, may be required especially if there is a complicated urethral tear or bladder rupture.. Urine will take the route of least resistance as such a tube cystotomy may be indicated to facilitate easy excretion from the abdomen. This can allow the patient time to become stabilised before definitive surgical repair. Ongoing urinary diversion +/- peritoneal dialysis may be required in some patients until hyperkalaemia or co-existing injuries have resolved. Once the patient is stable, surgical repair of the bladder will be usually be necessary.
What can urethral rupture arise secondary to?
Urethral rupture may arise secondary to trauma e.g. fractured pelvis but may also be caused by catheterisation, especially in cats with FLUTD.
What life-threatening complications can occur with a urethral rupture?
As with bladder rupture, life-threatening hyperkalaemia, post-renal azotaemia and metabolic acidosis may develop if urine cannot be passed; additionally, there may be local perineal soft tissue damage and necrosis caused by urine leakage
How do you treat a urethral rupture and what complications are there associated with treatment?
Surgical management will be required for some cases of urethral rupture but life-threatening conditions must be managed initially as discussed previously. A complete avulsion (separation) of the urethra will require surgical repair (Welsh, 2011) as will patients who are dysuric. For minor lacerations, placement of a soft-indwelling urinary catheter allows for urine drainage whilst the urethra repairs. A urethral stricture is a possible complication, however, which may predispose the patient to further partial/complete urethral obstructions.
What is dystocia?
Difficulty in delivering the foetus (es) is a common emergency in veterinary practice
What are the two different types of dystocia?
There are two main types of dystocia- maternal and foetal.
Maternal dystocia occurs due to…?
The former occurs due to maternal factors such as a narrow pelvis; previous pelvic injury; primary or secondary uterine inertia (e.g. uterine stretching due to overlarge litter); and, rarely, uterine rupture or torsion
Foetal dystocia occurs due to…?
The latter occurs due to foetal factors e.g. single pup syndrome, foetal malformation/ conformation e.g. brachycephalic, foetal malposition, foetal malpresentation and foetal death.
What are the clnical signs of dystocia?
The clinical signs for most forms of dystocia include prolonged first or second stage parturition; cessation of second stage labour; or abnormal discharge/ discharge with no evidence of a foetus.
What is parturition thought to be initiated by?
Parturition is thought to be initiated by a series of hormonal changes associated with increased foetal secretion of cortisol
What happens during stage 1 of parturition in dogs and cats?
Stage 1 parturition:
During this stage, cervical relaxation and dilation occurs. In the bitch, first stage of labour is assumed to have started when altered behaviour is displayed e.g. nest building, restlessness, panting and shivering. She may be anorexic and apprehensive (Aldridge and O’Dwyer, 2013). The queen may show similar signs of restlessness, nesting and may be more vocal and aggressive than normal 2002). This stage averages 4 hours but can be much longer (up to 36 hours) in the bitch (Intervet, 2002) - it averages 24 hours in the queen however due to feline patients being a little more secretive may not be as evident (Intervet, 2002). Towards the end of stage 1, with cervical dilation, a cervical plug may be seen- this should be bright green in the bitch and darker coloured in the queen.
When is the first stages of labour in a bitch assumed to have occurred?
In the bitch, first stage of labour is assumed to have started when altered behaviour is displayed e.g. nest building, restlessness, panting and shivering
How long is stage 1 of parturition in the bitch?
This stage averages 4 hours but can be much longer (up to 36 hours) in the bitch
How long is stage 1 of parturition in the queen?
it averages 24 hours in the queen however due to feline patients being a little more secretive may not be as evident
What happens during stage 2 of parturition in dogs?
Stage 2 parturition: this is associated with intermittent and increasingly stronger uterine contractions. Passage of uterine/placental fluids (dark green-black in the bitch and red/brown in the queen) accompanies the contractions- between contractions, there may be vulvar licking of the placental fluids. Once the foetus is engaged within the pelvic canal, strong abdominal contractions start which should lead to delivery of a neonate (Intervet, 2002). The time between the onset of straining and delivery of the first foetus is very variable- it is generally assumed that less than one hour is normal. Between each foetus there may be rest periods where no straining occurs and these may last for 1-2 hours. Rest periods of over 3-4 hours would be abnormal (Intervet, 2002). Once abdominal straining re-commences it is expected that further foetuses will be delivered within 30 minutes (Intervet, 2002). Time from first to last birth can be up to 24 hours, occasionally longer, but is generally safely assumed to be around 4-5 hours, depending on the size of the litter.
What happens during stage 2 of parturition in cats?
In the queen, stage two is often quite fast and abdominal straining is not as obvious as the bitch (Intervet, 2002). A first kitten is usually delivered within one hour; with the interval between subsequent kittens usually being 5- 60 minutes. Occasionally, however, second stage in the queen can be split into two with a long interval (12-24 hours) between kittens
How soon are kittens usually delivered in a queen that is in the second stage of parturition and what is the interval time between each kitten?
A first kitten is usually delivered within one hour; with the interval between subsequent kittens usually being 5- 60 minutes. Occasionally, however, second stage in the queen can be split into two with a long interval (12-24 hours) between kittens
How much rest period may a bitch have between delivering puppies? What would be considered abnormal?
Between each foetus there may be rest periods where no straining occurs and these may last for 1-2 hours. Rest periods of over 3-4 hours would be abnormal
How long may a bitch be straining for on delivery of a first puppy? how soon should other puppies in the litter be delivered after this one?
The time between the onset of straining and delivery of the first foetus is very variable- it is generally assumed that less than one hour is normal. Between each foetus there may be rest periods where no straining occurs and these may last for 1-2 hours. Rest periods of over 3-4 hours would be abnormal (Intervet, 2002). Once abdominal straining re-commences it is expected that further foetuses will be delivered within 30 minutes
Within what time frame should a bitch deliver puppies from start to finish?
Time from first to last birth can be up to 24 hours, occasionally longer, but is generally safely assumed to be around 4-5 hours, depending on the size of the litter.
What occurs in stage 3 of parturition in dogs and cats?
Stage 3 parturition is the passage of the afterbirth (foetal membranes)- as this should occur after each birth, stage 2 and 3 should alternate. Pups and kittens may be born with intact membranes. Many bitches and queens will eat these membranes.
What information is important to gather in an emergency phone call in relation to parturition?
It is important to know what would be considered normal in relation to parturition and thus get a relevant history e.g.
• due date- if an expected due date has passed, the patient should be examined. Although length of gestation can be variable.
• breed/age/ litter number e.g. Siamese, Persian and brachycephalic, especially bulldog, breeds are more prone to dystocia (wikivet, 2015)
• the breed/ size of father
• previous dystocia
• presence and type of discharge e.g. foul smelling/frank haemorrhage would be significant
• membranes/ part of foetus protruding from the vagina
• what she is doing currently
• demeanour
• signs suggestive of systemic illness e.g. collapse
It is important to understand what prompted the owner to call for guidance and obtain a history. It is also important that the above areas are carefully considered. An elective caesarean prior to onset of active, stage two, labour is not generally considered appropriate due to the risk of foetal death. However, this may be requested by some breeders.
If a client calls in emergency hours in relation to parturition, what would require immediate veterinary attention?
Dystocia, and therefore requirement for immediate veterinary attention, is likely where there is-
• active abdominal straining for more than 30 minutes to one hour without delivery of a foetus
• evidence of second stage labour (e.g. uterine/placental discharge) but no sign foetus. Any significant green/ black discharge (before a first delivery), in the absence of visible abdominal contractions is of concern as it indicates placental separation (Lopate, 2013).
• presence of foetal membranes/foetus at the vulva but no straining
• evidence of foetuses still to be born but the resting phase, with no straining, has lasted longer than 2-4 hours
• weak or ineffectual straining of 2 hours duration
• straining that has ceased should also be investigated
significant haemorrhage at any stage
• acute abdominal pain
In addition, abnormal discharge (e.g. foul-smelling/ haemorrhagic) or signs of systemic illness in a pregnant animal warrant immediate attention.
What diagnostic equipment can help to assess foetal viability?
Ultrasonography and radiography can both be used to assess foetal viability and position and pelvic structure as well as foetal distress.
How can ultrasound help to determine foetal viability?
Ultrasound can be used to determine foetal viability- low heart rates (<180bpm) are consistent with foetal stress; the viability of the placenta and character of foetal fluids
How can radiography help to determine foetal viability?
Radiography demonstrates structural pelvic abnormalities, number, size and position of the foetuses
What will biochemistry reveal in a bitch with dystocia?
Biochemical analysis will allow determination of the plasma calcium level- this may be decreased with uterine inertia (calcium is involved in uterine muscle/
myometrial contractions); or, less frequently, hypocalcaemic tetany/paresis. Blood glucose and ketone levels may also need to be checked – some bitches present with hypoglycaemia or hyperglycaemia if gestational diabetes mellitus is present.
How can a non-obstructive dystocia may be managed medically?
A non-obstructive dystocia may be managed medically initially e.g. administration of calcium gluconate (causes increased strength of myometrial contractions) followed by oxytocin administration (causes increased frequency of myometrial contractions). If calcium gluconate is administered, ECG monitoring should ideally be performed to detect potential bradycardia. This treatment regime, however, would be contraindicated in obstructive dystocia.
When is a caesarean indicated in a patient with dystocia?
If medical management is unsuccessful or there is evidence/possibility of obstructive dystocia or foetal distress, a caesarean section (hysterotomy) is indicated.
Where malpresentation is the cause of dystocia, how can physical management help?
Where malpresentation is the cause of the problem, physical management, using KYTM or LubigelTM to lubricate the birth canal, may be used to manipulate the position of the foetuses.
What is (Cystic Endometrial Hyperplasia)?
pyometra
What bacteria is usually present in a bitch with a pyometra?
Recently it has been suggested that CEH and pyometra may be different conditions in the bitch (Hall, 2012). The bacteria associated with pyometra are typically coliform in nature e.g. E. coli but can be Staphylococcus, Streptococcus, Proteus and Pasteurella species
When does a pyometra usually develop in a bitch?
Pyometra usually develops during dioestrus in bitches (~ 4-6 weeks post-season) when the uterus is under the influence of progesterone and the animal is generally immunosuppressed;
When does a pyometra usually develop in a queen?
it tends to be immediately up to 4 weeks post-oestrus in queens
Why might endotoxaemia arise in a bitch with a pyometra?
Endotoxaemia may arise because of bacterial toxins being absorbed systemically from the uterus- these toxins often affect the kidneys and are responsible for some of the clinical signs
What two classifications are there in pyometra?
Pyometra is classified as open or closed based on whether the cervix is open or closed. In an open pyometra, pus will often discharge from the vulva.
what are the clinical signs of a pyometra?
Clinical signs These will depend on the underlying cause but could include: 1. signs of dystocia 2. unproductive straining at parturition 3. exhaustion 4. signs of pyometra 5. anorexia 6. lethargy 7. abdominal pain 8. signs of septic peritonitis following uterine rupture 9. collapse
What will happen if a uterine rupture occurs in a bitch with pyometra?
If secondary uterine rupture occurs straining will cease. Septic peritonitis and septic shock may then ensue as the uterine contents leak into the peritoneal cavity.
What can raiography and ultrasound reveal in a patient with a pyometra?
The abdomen may be distended. Radiography and ultrasound may demonstrate fluid-filled uterine enlargement suggest but is unlikely to confirm the condition. Radiography is unlikely to confirm this condition- although the lack of engagement of any of the foetuses in the birth canal may be suggestive. Radiographic evidence of uterine gas is suggestive of foetal death which can arise due to the decreased blood supply. v
How do you treat a pyometra and associated complications?
The treatment for uterine torsion is ovariohysterectomy and management of complications e.g. sepsis, peritonitis etc.is required. If the patient has clinical signs of shock, the addressing the haemodynamic status is the initial priority- initial medical management (see Unit 2 Outcome 1) is required, with intravenous fluids, oxygen supplementation and support of arterial blood pressure, prior to surgical intervention. Antibiotics are likely to be required as sepsis can develop, if not already present, because of the compromised blood supply to the uterus or vagina.
What is metritis and what is it generally caused by?
Metritis (inflammation of the uterus) is generally caused by a postpartum infection of the uterus with the same bacteria that are found in patients with pyometra e.g. E. coli, streptococci, staphylococci and Proteus sp
What is mastitis and what is it caused by?
Mastitis (inflammation of the mammary gland(s)) is also caused by bacterial infection in the postpartum period. Very occasionally mastitis can develop in a bitch who is lactating during false pregnancy
What are two common potentail complications in the immediate postpartum period?
Metritis and mastitis are both potential complications of the immediate postpartum period.
When does metritis usually occur postpartum?
Metritis usually occurs in the immediate post-partum period (1-7 days)- it is most likely to arise in older females.
What are the predisposing causes of metritis?
Predisposing causes are prolonged delivery, dystocia, retained foetuses or retained foetal membranes. It may also be associated with artificial insemination. If it arises during pregnancy it could be a cause of abortion or foetal death.
What are the clinical signs of metritis in dogs and cats?
Metritis- The patient will be systemically unwell with pyrexia, lethargy, anorexia, decreased milk production and possibly collapse. An often profuse, purulent, odourous, red-brown vaginal discharge develops soon after parturition. The discharge may be confused, in the first instance, with the normal post-partum discharge, especially the red coloured afterbirth ‘lochia’ of the queen. Occasionally, uterine rupture may occur in which case, there is likely to be rapid onset septic peritonitis and associated clinical signs (Brown, 2011). There may be hypovolaemia, dehydration, hypoglycaemia, signs of endotoxaemia and sepsis. Initially the offspring may be vocal and restless due to neglect and decreased milk intake. Ongoing lack of nutrition may result in them starting to show signs of ‘fading’
What are the clinical signs of mastitis in dogs and cats?
Mastitis-The affected patient may be lethargic, inappetent and painful- in some mild cases there are few clinical signs. In the most serious cases, clinical signs of sepsis may be present. The affected mammary glands are usually swollen, red, hard and painful; there may be skin ulceration, abscess formation or, in the worst cases, mammary gland necrosis. The milk from the affected gland may be altered and milk production may be decreased. As with metritis, in the more serious cases, the offspring may be unsettled, weak and crying due to lack of milk.
What may haemotology reveal in a patient with metritis or mastitis?
Haematology often shows a left shift with an overall leucocytosis and neutrophilia. Haemoconcentration may be present (↑ PCV and TP/TS).
What may radiography and/or ultrasound reveal in a patient with metritis?
With metritis, ultrasonography and radiography will confirm the presence of an enlarged fluid-filled uterus. Post-partum, the uterus normally decreases in size so this would be a significant finding. If there is uterine rupture, there may be radiographic/ultrasound signs of abdominal effusion- abdominocentesis would be indicated.
What may microscopic examination of vaginal discharge reveal in a patient with metritis?
Microscopic examination of the vaginal discharge will demonstrate bacteria and neutrophils; the bacteria present can be confirmed with culture and sensitivity.
What may microscopic examination of milk reveal in a patient with mastitis?
Mastitis is usually diagnosed based on compatible clinical signs and examination of the mammary glands. A sample of milk can be examined microscopically to identify bacteria and neutrophils. Culture and sensitivity may also be performed as required.
What treatment is required for a patient with metritis?
Initial management should be aimed towards managing endotoxic/septic/ hypovolaemic shock if present. Boluses of isotonic, crystalloid fluid therapy will be required to increase blood volume, rehydrate, dilute circulating endotoxins and maintain arterial blood pressure. If there is evidence of uterine rupture, the patient will need to be managed as for any case with septic peritonitis with surgery following initial stabilisation. Appropriate multimodal analgesia will be required.
The patient should be monitored for signs of worsening shock as discussed in Unit 1 Outcome 2. In addition, clotting times, blood gases and acid-base balance should be checked.
If septic mastitis or metritis is present what antibiotics are usually indicated?
If septic mastitis or metritis is present, broad spectrum intravenous antibiotics, usually cephalosporin or potentiated amoxicillin, are indicated. Drugs which are potentially harmful to growing neonates should be avoided due to the likelihood of trans-mammary transfer
What risk is there to a bitch that has metritis and recives oxytocin to stimulate uterine contractions?
With metritis, oxytocin may be administered to encourage contraction and emptying of the uterus- this, however, is potentially risky as the thin uterine wall may rupture. Many cases of metritis do not respond to medical therapy alone and ovariohysterectomy is required once the patient is stable.
What treatment will most cases of mastitis respond to ?
Most cases of mastitis will respond to symptomatic treatment e.g. warm compresses; in addition, ‘stripping’ of the affected mammary glands should be performed (Aldridge and O’Dwyer, 2013). If there is abscessation or necrotic tissue, surgical management is likely to be required. If the offspring are not feeding sufficiently, they may require supplementary feeding
Why does eclampsia/lactation tetany occur and in what time frame in pregnancy is it usually seen?
Hypocalcaemia, decreased plasma calcium, develops due to calcium being diverted to milk production more rapidly than the body can replace it- particularly likely if there is inadequate intake of calcium in food. Generally, the bitch, or more rarely the queen, is affected in the second or third week of lactation- peak lactation. Occasionally it occurs in weeks one or four of lactation and rarely, it occurs in the last two weeks of gestation.
What breeds does eclampsia/lactation tetany most commonly affect? in what other situations would a bitch be affected?
It most commonly affects toy breed dogs such as Chihuahuas or Yorkshire Terriers; but can affect any breed especially if there is a large litter or inappropriate calcium supplementation has been provided during pregnancy. The signalment and history are highly suggestive.
What are the clinical signs of eclampsia/lactation tetany?
The clinical signs depend on how advanced the condition is and can include-
- anxiety, aggression
- restlessness
- hyperaesthesia- oversensitive to stimuli
- vocalisation
- panting
- ataxia
- salivation
- stiff gait
- clonic-tonic muscle contractions
- hyperthermia
- seizuring/ tetany progressing to coma and death
What may biochemistry reveal in a patient with eclampsia/lactation tetany ?
Biochemical analysis will reveal a low blood calcium. The additional muscular activity may also cause hypoglycaemia.
What initial treatment is required in a patient with eclampsia/lactation tetany?
Placement of an intravenous catheter is essential- care must be taken during handling as the patient is hyperaesthetic. This will allow blood sampling to measure the ionised calcium level and allow IV calcium administration. 10% calcium gluconate solution should be administered by slow intravenous injection. Cardiac monitoring (by auscultation and ECG) should be performed throughout to detect arrhythmias that might arise, especially bradycardia.
Can the offspirng feed from the dam if she has developed eclampsia/lactation tetany?
The offspring may need to be hand reared during the first 24 hours of the acute stage of the condition but thereafter should be able to continue feeding from the dam- they should, however, be weaned as soon as it is feasible. For the remainder of the lactation period, the dam should be fed frequently a high-quality diet supplemented with oral calcium and vitamin D.
When might uterine haemorrhage be seen in a bitch?
Uterine haemorrhage
This may occur as a complication of parturition, following a caesarean, because of a coagulopathy or occasionally during pro-oestrus.
What signs are associated with uterine haemorrhage?
There will be signs associated with blood loss (lethargy, pale mucous membranes, rapid pulses etc.)- in the most serious cases hypovolaemic shock may develop. There may be a haemorrhagic vaginal discharge but, in some cases, the haemorrhage is entirely intra-uterine; or intra-abdominal if there is uterine rupture. Signs associated with septic peritonitis will develop if uterine rupture is present. Careful post-operative monitoring is essential for a patient who has had a caesarean, as intra-uterine haemorrhage is not easy to identify on physical exam until the blood loss is affecting the patient’s perfusion parameters.
What initial treatment is required in a patient with uterine haemorrhage?
Management of uterine haemorrhage is the same as for any bleeding patient i.e. provide oxygen and address the hypovolaemia with IVFT- blood product transfusions may be required with large volume blood loss. If there is any likelihood of uterine rupture, surgery will be required once the patient is sufficiently stabilised. In some cases, the only option may be removal of the uterus once the patient has been stabilised sufficiently.
Can the offspirng feed from the dam if she has developed uterine haemorrhage?
If the patient’s condition permits it, the offspring should be allowed to nurse as this promotes uterine involution
What species does uterine prolapse usually occur in and when does it usually arise?
Uterine prolapse is a rare condition in dogs and cats- when it arises it is usually a complication of the peri-parturient period This may arise during or following parturition in cats or dogs; and can be associated with dystocia, prolonged straining and hypocalcaemia. The prolapsed tissue is apparent at the vulva as a red, fleshy mass
What is the treatment of uterine prolapse?
If the condition develops, it is likely that surgery will be required especially if the patient is still pregnant.
Uterine prolapse needs to be differentiated from vaginal prolapse (Vetbook, 2013). As with all prolapses, the initial management involves minimising contamination, swelling and self-trauma- the patient should be supervised and have an Elizabethan collar applied. The prolapsed tissue should be covered with sterile, isotonic fluid (e.g. 0.9% saline) soaked, non-adherent dressings. If the prolapsed tissue has become inflamed and oedematous, hypertonic agents may be used to decrease the swelling e.g. hypertonic saline or mannitol.
As soon as possible, the patient will require general anaesthesia for reduction of the prolapsed tissue.
If replacement is not an option, then ovariohysterectomy will be required and would be curative
What species is acute prostatitis more common in?
Acute prostatitis can result in an emergency presentation (Davidson, 2014). It is more common in male dogs than male cats
What type of patient is most likely affected by acute prostatitis?
It can affect any male dog but is most likely in an entire, older male dog, especially those with testosterone-induced benign prostatic hypertrophy (BPH).
What is the cause of acute prostatitis and when does it usually present in an emergency?
It can affect any male dog but is most likely in an entire, older male dog, especially those with testosterone-induced benign prostatic hypertrophy (BPH). Occasionally neoplasia may be involved although commonly benign prostatic hyperplasia leads to trapping of prostatic fluids within cystic structures that can more easily become infected. Infection of the prostate gland is usually with coliform bacteria. Prostatitis can be acute or chronic. Infection may be ascending or haematogenous. This can be the cause of an acute abdominal emergency in a male dog.
What are the clinical signs of acute prostatitis?
Clinical Signs of Acute Prostatitis These include the following: 1. anorexia 2. pain 3. pyrexia 4. urinary tenesmus 5. faecal tenesmus 6. lethargy 7. vomiting 8. dysuria 9. passing blood at the end of urination 10. stiff/altered gait
Sometimes, a dog may present in collapsed, shocked state secondary to sepsis. The caudal abdomen, cranial to the pubis, may be intensely painful and the enlarged prostate may be palpable. Rectal examination is an important part of the veterinary surgeon’s clinical assessment- however, an enlarged prostate gland is often intra-abdominal rather than intra-pelvic. In addition, the patient may be too uncomfortable to permit this on initial presentation.
How do you obtain a definitive diagnosis in a patient with suspected acute prostatitis?
To obtain a definitive diagnosis for any prostatic disorder histopathologic evaluation is required although this may not be possible in all cases.
What may haematology reveal in a patient with acute prostatitis?
Haematology will demonstrate leucocytosis with a neutrophilia.
What may ultrasound reveal in a patient with acute prostatitis?
POCUS in the first instance can be very useful for confirming prostatic disease- prostatic enlargement, asymmetry and in more serious cases, free abdominal fluid may be present. Ultrasound will allow better visualisation of the internal architecture of the prostate than radiography- the prostate may appear hyperechoic with fluid-filled areas +/- evidence of abscessation.
Ultrasound guided fine-needle aspirates (FNA) of prostate tissue provide materials for culture, sensitivity and cytology.
What may urinalysis and prostatic fluid analysis reveal in a patient with acute prostatitis?
Both urine and prostatic fluid should be analysed. Prostatic material can be obtained following prostatic massage- although there is a chance of haematogenous spread following this procedure (Kutzler, 2013). Any urine/prostatic samples obtained should be examined microscopically as well as having culture and sensitivity performed- bacteria and leucocytes are likely to be identified. UTI is also likely to be present due to reflux of prostatic material into the bladder.
What may radiography reveal in a patient with acute prostatitis?
Lateral radiographs of the caudal abdomen will show an enlarged prostatic outline caudal to the bladder neck with cranial displacement of the bladder N.B. without contrast studies, however, it is not actually possible to differentiate the bladder from the enlarged prostate gland radiographically. Lateral, caudal abdominal radiography may also show lysis in the region of the L6-L7 vertebral bodies associated with spondylitis- a common sequel associated with haematogenous spread of bacteria from the prostate.
What is the treatment for acute prostatitis?
A systemically ill patient with required IVFT to treat hypovolaemia/shock and dehydration. An intravenous catheter should be placed and appropriate, bolus, crystalloid fluid therapy commenced. Ongoing patient monitoring and management of hypovolaemia/ shock and dehydration is required.
Broad spectrum antibiotics will be required- the blood–prostate barrier is altered due to inflammation meaning most antibiotics will penetrate the infected prostate (Davidson, 2014).
As this is a very painful condition, opioid analgesia is likely to be indicated.
Surgical management of a prostatic abscess may be required.
As with all emergency patients, meeting all the patient’s needs is essential and appropriate consideration should be given to the nursing required of the sick, painful patient who may have difficulty/ pain on urination and defaecation.
What patients are most likely affected by a prostatic abscess annd what are the causes of it?
This can develop as a complication of acute or chronic prostatitis. As the changes associated with benign prostatic hyperplasia (BPH) can predispose to this condition, it generally affects older, entire, male dogs. As with prostatitis, this condition may occasionally be associated with neoplasia. More commonly, however, benign prostatic hyperplasia leads to trapping of prostatic fluids within cystic structures that can easily become infected (Davidson, 2014). Coliform, staphylococcal or streptococcal species are often associated with abscess formation
What are the clinical signs of a prostatic abcess?
Clinical signs These are like acute prostatitis and include: 1. anorexia 2. pain 3. pyrexia 4. arched back/ stiff gait 5. passing blood at the end of urination 6. vomiting 7. dysuria 8. urinary tenesmus 9. faecal tenesmus 10. spondylitis 11. +/- collapse and septic shock If the abscess ruptures, then clinical signs of septic peritonitis will also develop.
How do you diagnose a prostatic abscess?
As with prostatitis, the signalment, history and physical examination may be suggestive. The prostate may be enlarged and irregular on the veterinary surgeon’s clinical examination.
Ultrasound examination will show discrete fluid filled cavities within the prostate indicative of abscess formation. Lateral radiography of the caudal abdomen will show an enlarged structure around the neck of the bladder – this is often much larger in size than with prostatitis
What tretament and nursing care are required for a patient with a prostatic abscess?
If signs of hypovolaemia/ shock are present, an intravenous catheter should be placed and appropriate, bolus, crystalloid fluid therapy commenced. Ongoing patient monitoring for and management of shock is required.
The treatment is similar to acute prostatitis- opioid analgesia and broad-spectrum antibiosis are required. Beyond the emergency period, surgical management +/- castration may be required
What is paraphimosis and what patients are affected by it ?
Paraphimosis is the inability to retract the erect penis back within the prepuce (WikiVet, 2012). There are several reasons for this but it most often occurs in male dogs following sexual stimulation- where they are unable to retract the glans penis into the prepuce.
What is the cause of paraphimosis?
The pathogenesis is not understood but it usually affects juvenile, hyper-excited dogs. There may be other causes e.g. trauma, infection, hypoplasia (too small preputial opening), foreign material e.g. hair, etc. Secondary self-mutilation is a serious potential complication. The condition is rare in the cat and only associated with abnormality of the prepuce
What are the clnical signs of paraphimosis?
Clinical signs are diagnostic-there is a protruded penis, often swollen and dark red in colour, that will not return into the prepuce. In severe (protracted) cases the penis may become necrotic due to ischaemic damage. In severe cases, localised swelling could lead to urethral obstruction.
What tretament and nursing care are required for a patient with a paraphimosis?
This condition is considered to be an emergency due to the potential risk of injury or necrosis of penile tissues which might necessitate amputation. The initial management involves prevention of further trauma, swelling and drying out of tissues- application of sterile, 0.9 % saline soaked, non-adhesive dressings may be of short-term benefit. Gentle cleansing, cooling of the surface, lubrication and careful return to to the prepuce is usually sufficient (Lewis and Reineke, 2018). The dog should be supervised and an Elizabethan collar applied to prevent further self-trauma.
The application of cold compresses may help to reduce swelling. If the penis is very swollen and oedematous, hyperosmotic solutions may be used to try to decrease swelling e.g. 50 % dextrose, mannitol solution or 7.2% hypertonic saline solution (Aldridge and O’Dwyer, 2013) although the potential irritation and discomfort form these has to be considered. Anti-inflammatories and opioid analgesics may be required in the most serious cases.
Often manipulation and reduction under sedation/ anaesthesia is required.
Following sedation of the patient (if required), most cases may be simply replaced following cleaning and lubrication of the penis- ensuring that any trapped hair or foreign material which could have contributed to the problem is removed.
In severe cases, surgery may be required- an incision into the prepuce may be performed to widen the preputial orifice and decrease the ligature effect. The worst cases may require amputation of the tip of the penis and reconstructive surgery to preserve the urethral opening. An indwelling urinary catheter may be required during the healing phase to prevent the risk of urethral obstruction.
What is a testicular/spermatic cord torsion?
Testicular Torsion- spermatic cord torsion
This is a rare condition but an emergency if it occurs. It arises secondary to rupture of the scrotal ligament (Lewis and Reineke, 2018). It generally affects an intra-abdominal (retained) testicle but may also be associated with testicular tumours. There is rotation of the testicle around the spermatic cord. This interrupts the blood supply to the testicle leading to ischaemic necrosis.
What are the clinical signs of testicular/spermatic cord torsion?
Patients with an intra-abdominal testicle will present with signs associated with an ‘acute abdomen’- lethargy, depression, abdominal pain, vomiting, anorexia, stiff gait, hypovolaemia/ shock etc. If a scrotal testicle is affected, it will appear swollen and the patient will have marked discomfort in the inguinal region. There may be discolouration of the overlying skin. Orchitis/ epididymitis is the main differential for a visibly swollen and painful testicle.
In each case, the patient’s condition will start to deteriorate significantly as ischaemic necrosis develops.
How do you diagnose testicular/spermatic cord torsion?
The diagnosis is likely to be confirmed when performing ultrasound examination of the ‘acute’ abdomen or examination of the scrotum.
What is Orchitis/ epididymitis, what type of patient is usually affected by it and what causes it?
This is a rare condition which can occasionally affect, usually, younger, intact, male dogs- it may be more common in breeding dogs. Orchitis can develop secondary to trauma, penetrating foreign body or infection. It may be secondary to systemic infection e.g. distemper virus or Brucella canis infection (Braund, 2014). As Brucella canis has zoonotic potential it is important to be aware of this possibility when handling, investigating and nursing affected patients.
What are the clinical signs of Orchitis/ epididymitis?
There is a sudden onset swelling of the affected testicle – possibly with an associated wound and there will often be signs of systemic illness with fever, lethargy, anorexia and vomiting. The condition is very painful- the patient may have a hunched stance, a stiff gait and be reluctant to lie down. The testicle will often be visibly swollen and inflamed with erythema of the overlying scrotal skin.
Other possible causes of a swollen, painful testicle include testicular torsion or abscess. Tumours will cause testicular enlargement but are not usually painful.
How do you diagnose Orchitis/ epididymitis?
The condition can be diagnosed by ultrasound, FNA of the affected testicle and analysis of semen samples. As the condition is painful, sedation may be required for any investigation. Microscopic examination of semen may demonstrate bacteria and leucocytes- culture and sensitivity should be performed if infection is possible. Haematology is likely to demonstrate a leucocytosis and neutrophilia.
What is the treatment for Orchitis/ epididymitis?
Antibiosis (for infected cases), analgesia and anti-inflammatories are likely to be required.
What nursing care is required for Orchitis/ epididymitis?
Nursing care
Cold compresses may be applied, with care, to decrease pain and swelling. It is important to ensure the patient is comfortable and has a deep bed.
