Patient signalment
Species: feline
Breed: domestic shorthaired
Age: 10 years
Sex: male neutered
History
The patient presented in an obtunded state with a bradycardia of 80 beats per minute. The bladder was large, distended and firm. Blood results revealed azotaemia and hyperkalaemia (Table 1). The patient was diagnosed with urethral obstruction and was stabilised prior to anaesthesia and a urinary catheter was placed to relieve the obstruction. The subsequent nursing care received at the out of hours hospital is the subject of this case report.
Table 1. Biochemistry and electrolyte results
| Test | Reference range | Date and time | ||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| 12/04 3.13PM | 12/04 4.20PM | 12/04 8.21PM | 12/04 11.33PM | 13/05 5.11AM | 13/04 10.16AM | 13/04 4.46PM | 14/04 1.17AM | 14/04 5.59PM | ||
| Sodium | 150–165 mmol/L | 157 | 153 | 150 | 168 | 180 | 167 | 165 | 168 | 165 |
| Potassium | 3.5–5.8 mmol/L | >10 | 10.0 | >10 | 5.7 | 5.3 | 4.6 | 4.3 | 3.6 | 3.5 |
| Na:K Ratio | 15 | 29 | 36 | 38 | 47 | 47 | ||||
| Chloride | 112–129 mmol/L | 108 | 109 | 113 | 119 | 123 | 118 | 121 | 123 | 120 |
| CREA | 71–212 μmol/L | High | 542 | 116 | ||||||
| UREA | 5.7–12.9 mmol/L | >46.4 | 36.1 | 8.9 | ||||||
Presentation
On arrival peripheral pulses were weak and thready. Mucous membranes were pale in colour, and capillary refill time was prolonged at 3 seconds. Respiration rate was 8 breaths per minute with a mild increased effort. Thoracic auscultation was clear. The rectal temperature was 33.2°C.
The patient presented from the primary practice with a 22-gauge catheter in the right cephalic vein and with an indwelling urinary catheter, a bung was placed on the end of the urinary catheter to allow for patient transportation. The veterinary surgeon prescribed intravenous compound lactate solution at an initial fluid bolus at a rate of 10 ml/kg over 15 minutes. The veterinary surgeon administered a bolus of calcium gluconate, 1 ml/kg over 20 minutes, and a longer-term treatment plan of glucose and soluble insulin was calculated. The urinary catheter was attached to a closed drainage collection system to relieve urine. The patient was admitted into hospital and had ongoing intensive care.
Feline urethral obstruction
Feline urethral obstruction is a common presenting emergency in small animal veterinary medicine. Feline urethral obstruction is reported to occur more commonly in young male cats due their relatively long and narrow urethra (Segev et al, 2011). Feline urethral obstruction can be caused by feline idiopathic cystitis, spasm, urethral pulse, stones, neoplasia or strictures (Gunn-Moore, 2013a). It can represent a life-threatening emergency. Patient stabilisation through appropriate management of hyperkalaemia, metabolic acidosis and uraemia are critical (Beal, 2018). Post-renal azotaemia caused by urethral obstruction can be irreversible and, in some cases, fatal without prompt, aggressive treatment (Taylor, 2013a). However, prognosis for survival is as high as 90–95% with timely appropriate treatment (St. Denis, 2020).
Nursing interventions
Three important areas for the care of the patient were identified:
- Monitoring of electrolytes
- Fluid balance
- Urinary catheter management.
Monitoring of electrolytes
Serum electrolytes levels may be abnormal as a result of post-renal obstruction or disruption (Beal, 2018). Electrolytes, specifically potassium, should be monitored every 4–24 hours depending on the individual patient's clinical signs (Webb, 2018).
The urethral obstruction can lead to acute kidney injury leading to post renal azotaemia. This can result in hyperkalaemia as the kidneys are unable to eliminate potassium (Gunn-Moore, 2013b). Serum potassium levels can increase with a relative decrease in urine output (Herold, 2017).
Potassium is the major intracellular cation (k+), and is important for maintaining the resting membrane potential of cells, particularly with muscle and nerve cells. The plasma concentrations of potassium are tightly controlled, as fluctuations can disrupt organ function and can be life-threatening. A rise in potassium (hyperkalaemia) can increase the resting membrane potential of cells; therefore, the cell is less negative and easier to polarise and more susceptible to over excitement. This increase can cause muscle and nerve excitability, of which the most serious consequence is cardiac arrhythmia and subsequent cardiac arrest (eClinpath, 2020).
Hyperkalaemia is a potentially life-threatening outcome of feline urethral obstruction, and derangement should be stabilised prior to further intervention (Beal, 2018). The patient's electrolyte levels showed an increase in potassium (Table 1). The registered veterinary nurse attached electrocardiogram (ECG) leads to the patient to monitor for changes in cardiac rhythm (Table 2). An ECG can be used to visualise cardiac arrhythmias, which are the most serious consequences of hyperkalaemia. However, the ECGs of hyperkalaemia patients with urethral obstruction do not always display these signs consistently, therefore the ECG results should be interpreted alongside serum electrolyte levels (Sabino, 2017).
Table 2. The sequence of ECG changes with increasing levels of potassium
| 1. | Peaked T waves |
| 2. | Reduced R wave amplitude, prolonged P-R interval, and reduced QT interval |
| 3. | P waves reduced in amplitude, widen and then become absent – ‘atrial standstill’ |
| 4. | Widening of the QRS complex and bradycardia |
| 5. | Ventricular fibrillation, systole and cardiac arrest. |
Source: adapted from Hibbert (2013)
Calcium gluconate can be administered intravenously to counteract the effects of the hyperkalaemia on myocardial contraction (Boag, 2018). Although the administration of calcium gluconate is cardio-protective, it has no effect on the serum potassium levels (Aldridge and O'Dwyer, 2013). The effects of the calcium gluconate last approximately 20 minutes; however, it is the first-choice therapy in severely affected animals because of the quick onset (Boag, 2018). These patients require rapid stabilisation of the cardiovascular system, to allow urethral catheterisation which may require sedation or general anaesthesia depending upon the patient (Foster and Humm, 2018). The cardiogenic effects of hyperkalaemia can greatly increase anaesthetic risk (Aldridge and O'Dwyer, 2013). The administration of calcium gluconate can provide a timeframe in which the patient is stabilised for anaesthesia to relieve the urethral obstruction. Calcium gluconate has the potential to cause bradyarrhythmias; therefore, monitoring with an ECG during administration is desirable (Hibbert, 2013). The registered veterinary nurse used a syringe driver to administer the calcium gluconate over 20 minutes. The patient's ECG was continuously monitored during administration, and any abnormalities reported to the veterinary surgeon.
An infusion of dextrose alongside soluble insulin can be administered to treat severe hyperkalaemia. The insulin acts to lower serum potassium by promoting the uptake of potassium intracellularly along with glucose (Boag, 2018). It is important that fluids are supplemented with glucose 12–24 hours post-insulin treatment and blood glucose levels are monitored (Hibbert, 2013; Boag, 2018). The registered veterinary nurse monitored the patient's blood glucose levels regularly, via venous sampling or ear prick (Table 3). A continuous glucose monitor is a small sensor that can continuously measure interstitial glucose. Measurements can be taken via an electronic device to prevent multiple venous sticks (Taylor, 2022). However, as a result of the higher financial costs and short duration of usage it was decided that this method was not suitable for this case. The patient was monitored for signs of hyperglycaemia and hypoglycaemia as both can have a detrimental effect to the patient. Hyperglycaemia can cause glycosuria, diuresis, water loss and an increase in plasma osmolarity which can result in increased extracellular water if the patient receives fluids (Loose, 2017). Hypoglycaemia can cause weakness, ataxia, depression, tremors, seizures and death (Taylor, 2013b). The registered veterinary nurse monitored patient's mentation for signs of change, which could have been caused by hypoglycaemia. The patient's urine output was regularly measured, and a urine dipstick performed to check for glycosuria.
Table 3. Blood glucose results
| Test | Date and Time | ||||||
|---|---|---|---|---|---|---|---|
| Glucose | 12/043.13PM | 12/048.25PM | 12/0410PM | 12/0411.30PM | 13/045AM | 13/0410.16AM | 14/045.59PM |
| 7.85 | 3.1 | 2.9 | 7.9 | 11.9 | 19.4 | 5.62 | |
Hypokalaemia can occur post-obstruction as a result of transcellular shift of fluid, and increased losses through diuresis (Barton and Kirby, 2017). Clinical signs of hypokalaemia can include weakness, lethargy, ileus and anorexia, and in cats ventroflexion of the neck may be seen (Boag, 2018). Patients may require potassium supplementation to restore serum potassium levels (Foster and Humm, 2018).
The patient's electrolyte levels showed an increase in sodium levels. Hypernatremia can be a result of post-obstructive diuresis, glycosuria and renal medullary washout (Barton and Kirby, 2017) – these are all considered a differential for the feline urethral obstruction patient. Hypernatremia can result in osmotic shrinkage of cells in the central nervous system. Clinical signs include dull mentation, seizures and coma (Lacovetta, 2017). The patient's mentation was closely monitored and interpreted alongside the sodium results. The registered veterinary nurse observed the decline in the patient's mentation, and the blood results which were communicated to the veterinary surgeon. This resulted in the patient being prescribed a 0.45% saline and 2.5% glucose infusion. Rapid correction of serum sodium levels can result in clinical signs that are more severe than the sodium abnormality itself. Serum sodium should be correct slowly with a maximum change of 0.5 mmol/l sodium per hour in either direction (Boag, 2018). Repeated blood samples (Table 1) were taken to allow trends to be monitored and acted on.
The registered veterinary nurse was required to take multiple blood samples from the patient to monitor their progress. The placement of a central venous catheter would have been beneficial as this can be left in situ for a longer period in comparison to the peripheral catheters. Central venous catheters allow for non-invasive blood draw benefiting the patient's comfort and ease of use for clinicians (Gray, 2018). For placement of a central venous catheter, sedation or anaesthesia is nearly always required (Aldridge and O'Dwyer, 2013). However, it was decided that the risk of anaesthetising or sedating the patient outweighed the benefits. It may be beneficial in future cases for central lines to be placed during urinary catheterisation, using one anaesthesia or sedation period.
Fluid balance
Fluid therapy is often a key component of a patient's treatment plan when hospitalised. The choice of fluid type and dose depends on the individual patient and their condition. The patient's hydration status, haemodynamic stability, electrolyte balance and the resources available in practice should all be considered (Lyons and Waddell, 2017). The fluid therapy plan can be divided into three different phases resuscitation, rehydration, and maintenance (Kirby and Rudloff, 2017). When creating a fluid therapy plan it should be tailored to the individual to ensure treatment goals are met (Box 1). It is important that fluid therapy plans are constantly reassessed and evolved depending on the patient's clinical status and response to treatment (American Animal Hospital Association, 2013). The goal of fluids therapy for feline urethral obstruction patients are to support the intravascular volume, dilute serum potassium and to correct metabolic derangements (St. Denis, 2020).
Box 1.Considerations when approaching fluid therapy
- What is the type and severity of the fluid volume deficit and what is the clinical effect on the patient?
- What is the type of fluid defect and therefore replacement fluid required?
- How will fluid be given?
- At what rate should fluids be given?
- How will response to fluid therapy be monitored?
- What ongoing losses and maintenance requirements will the patient have?
- What complications may be encountered?
Source: adapted from Taylor (2013c)
Hypovolaemic patients exhibit different clinical signs to dehydrated patients (Box 2) and require different treatment (Taylor, 2013c). Hypovolaemia is the decreased volume of fluid in the vascular system, with or without whole body fluid depletion. Dehydration is the depletion of wholebody fluid. Both dehydration and hypovolaemia can occur simultaneously or individually (American Animal Hospital Association, 2013). Dehydration requires more gradual replacement, whereas hypovolaemia requires rapid volume replacement (Boag and Hughes, 2018).
Box 2.Hypovolaemia versus dehydration in the catHypovolaemia
- Hypovolaemia is reduced intravascular volume
- Hypovolaemia results in tachycardia, a normal heart rate or bradycardia (usually seen in cats), hypotension and slow capillary refill time
Dehydration
- Dehydration is a reduction predominantly in interstitial fluid volume
- Dehydration results in skin tenting and dry mucous membranes, but no change in heart rate or pulse quality
Source: adapted from Taylor (2013d)
In this case, the patient presented in a state of hypovolaemic shock. The clinical signs included bradycardia, weak peripheral pulses, pale mucous membranes and increased capillary refill time. The veterinary surgeon prescribed an intravenous compound lactate solution at an initial fluid bolus at a rate of 10 ml/kg/15 minutes.
The choice of fluids is dependent on the veterinary surgeon; however, the registered veterinary nurse should understand the medication prescribed to allow them to monitor and evaluate the patient's status. A study by Drobatz and Cole (2008) concluded that the use of both 0.9% sodium chloride and balanced crystalloid solutions are appropriate for feline urethral obstruction patients. The potassium containing fluids had no effect on the normalisation of blood potassium.
Bolus fluid therapy is the administration of fluids over a defined time frame, with the aim of restoring intravascular volume, and therefore perfusion parameters (Table 4) to within normal limits (Boag and Hughes, 2013). A physical examination should be performed regularly on patients receiving intravenous fluid therapy, with an emphasis on monitoring the degree of dehydration and perfusion parameters (Mattox, 2017). Boag and Hughes (2013) recommend patients are assessed every 15 minutes when receiving fluid boluses. The registered veterinary nurse recorded the patient's perfusion parameters (Figure 2) allowing for trends to be recognised and evaluated. The patient's pulse quality improved after the initial bolus; however, the capillary refill was still prolonged and repeat bolus fluid therapy was needed.
Table 4. Resuscitation endpoints targeted with fluid resuscitation in cats
| Parameter | High normal | Low normal |
|---|---|---|
| Level of consciousness | Alert, responsive | Alert, responsive |
| Heart rate (bpm) | >160 | >160 |
| Mucous membrane colour | Pink | Pale pink |
| Capillary refill time (seconds) | 1–2 | ≤2 |
| Peripheral pulse intensity | Strong | Palpable central and peripheral pulses |
| Rectal temperature (°c) | 37.2–38.3 | 36.6 |
| Indirect blood pressure (mmHg) Mean | 80–100 | 60–80 |
| Urine output (ml/kg/hour) | 1–2 | 1.0 |
| Lactate (mmol/l) | ≤2 | Declining trend to <2 |
Source: adapted from Kirby and Rudloff (2017)
Replacement fluid therapy was commenced after the initial volume resuscitation. The patient's biochemistry results showed an increase in renal parameters (Table 1). Post-renal azotaemia occurs when there is an obstruction to urine outflow, as seen in patients with urethral obstruction. The management of the acute kidney injury depends on the initial cause – in this case relieving the urethral obstruction. Aggressive fluid therapy is needed to promote diuresis and reverse azotaemia (Balakrishnan and Drobatz, 2013).
Anuria and oliguria are potential complications of acute kidney injury, and the presence of these parameters can indicate the severity of the renal injury (Herold, 2017). Treatment is directed towards converting anuria or oliguria into polyuria though the use of fluid therapy and/or diuretics (Aldridge and O'Dwyer, 2013). The presence of anuria or oliguria places the patient at a high risk of volume overload. Careful monitoring of fluid infusion rates, urine output, central venous pressure, blood pressure, packed cell volume, total protein and body weight is desirable to avoid fluid overload associated with oliguria or anuria (Herold, 2017).
Prolonged aggressive fluid therapy can result in medullary washout and the loss of urine concentrating ability. Fluid therapy should be tapered depending on the patient's clinical condition, and to re-establish the medullary solute gradient (Balakrishnan and Drobatz, 2013).
Post-obstruction diuresis is condition that occurs in over 50% of feline urethral obstruction cats (Balakrishnan and Drobatz, 2013). Post obstruction diuresis is a result of several complications of feline urethral obstruction: the accumulation of osmotically active substances in the blood, pressure necrosis, medullary washout and antidiuretic hormone resistance (Balakrishnan and Drobatz, 2013). The urine production of these patients can increase by up to 74% (St. Denis, 2020). It is important the patient's urinary output is measured, and ‘ins and outs’ of fluid infused and urine produced should be matched to prevent hypovolaemia and/or dehydration (Balakrishnan and Drobatz, 2013). The patient's urine production was intermittently measured throughout the hospitalisation. The urine was collected, and the ml/kg produced per hour was calculated and compared to the intravenous fluid therapy rate. The urine production was much greater than fluid therapy rates. This was communicated to the veterinary surgeon and adjustments were made accordingly. On reflection it would have been beneficial to measure the urine production at set intervals to ensure prompt detection of complications.
The registered veterinary nurse should understand the parameters for perfusion, and assess the patient's response to intravenous fluid therapy (Mattox, 2017). Information regarding the patient should be communicated effectively between members of the clinical team.
Urinary catheter management
A variety of complications can arise during or after the placement of a urinary catheter (Table 5), and should be considered before placement (Oosthuizen, 2011).
Table 5. Possible complications of indwelling urinary catheters
| Inflammation and/or strictures |
| Urinary tract trauma and/or rupture |
| Haematuria |
| Infection |
| Mechanical difficulties such as knotting or kinking |
Source: adapted from Walton (2023)
The patient should be monitored closely, and any complications be communicated to the veterinary surgeon (Oosthuizen, 2011). Catheter-associated urinary infections are a major health concern in human medicine. It is estimated that 40% of nosocomial infections in human hospitals are urinary catheter-related (Hugonnard et al, 2013).
A study by Hugonnard et al (2013), suggested a third of cats develop significant bacteriuria during catheterisation. However, the study was unable to differentiate between cath-eter-induced bacteriuria and those present for other reasons.
Closed urinary collection systems should always be used to prevent the catheter being open to the outside air and introducing infection. The closed system prevents urine scaling, prevents back flow of urine and improves patient's welfare (Aldridge and O'Dwyer, 2013). Closed systems can be classified as a urinary collection bag, or a sterile bung on the catheter to allow for intermittent draining (Oosthuizen, 2011). A urinary collection bag was used in this case. Aldridge and O'Dwyer (2013) recommend that closed systems should be broken as infrequently as possible, as this is the greatest risk of introduction of bacteria into the system. However, Bloor (2013) recommends the urine bag should be drained every 4 hours. Nevertheless, both sources explain the importance of maintaining asepsis, and the use of protocols to reduce the risk of hospital-acquired infections (Table 6). Oosthuizen (2011) recommends that to reduce the risk of infection, the urinary catheter should be regularly cleaned with a chlorhexidine solution and checked frequently for signs of contamination. On reflection it may have been beneficial for a standard operating procedure regarding urinary catheter patients to be implemented.
Table 6. Recommended methods to reduce risk of hospital acquired infections
| Hand hygiene |
| Cleaning and disinfection |
| Surveillance |
| Patient management |
| Antimicrobial stewardship |
| Education and training |
Source: adapted from Bloor (2018)
The amount of urine produced should be calculated and recorded. The normal urine output of a healthy patient is 1–2 ml/kg/hour (Orpet and Welsh, 2010). If there are concerns regarding the urine flow the catheter can be flushed. This should be performed aseptically to reduce the risk of infection (Aldridge and O'Dwyer, 2013). Additional checks to the urine should be made and noted such as the colour, turbidity and sediment checks (Hibbert, 2018). Based on the evidence and recommendations it would be beneficial to create a standard operating procedure regarding urinary catheter management which could be regularly audited.
Outcome
The strong, clear communication between the team was paramount for the successful treatment of this patient. The veterinary surgeon and registered veterinary nurse should be aware of the potential complications, monitoring and nursing this type of patient should receive and how these parameters and trends develop the treatment plan.
For future practice it is advisable to create a standard operating procedure for the management of urinary catheters. The literature available is variable, but creating a protocol within the practice that could be audited would be ideal to create an evidence-based approach. It would be beneficial to consider the options for vascular access that are available, and the appropriate method for the individual patient and case. Continuing professional development in the use of a variety of vascular access methods, as well as creating protocols for their use in practice would be advantageous for future cases.
The patient was discharged after 4 days of hospitalisation, when biochemistry and electrolyte blood parameters had returned to normal. The patient was urinating with no signs of discomfort. The patient continued to have follow up assessments with the clinic nurse to manage the home environment and prevent reoccurrence.
Conclusions
Registered veterinary nurses provide an extremely important role in the care of the emergency hospitalised patient. The monitoring and evaluation of the care received can allow treatment plans to be adapted to the individual patient. The communication between the veterinary surgeon and registered veterinary nurse is paramount in providing a high quality, efficient care to patients.