Between a Urolith

and a Hard Place:

Acute Upper Urinary
Tract Disease and
Beyond...

ISFM FELINE CONGRESS 2023

Veterinary Proceedings
DUBLIN 29 June – 2 July, 2023 #ISFMRocksDublin
 Dublin, 29 June – 2 July

Hello and welcome to Dublin!

Welcome and thank you for joining us for our 2023 congress,
whether you are with us in lively Dublin or joining us virtually from
the comfort of your own home after the event.

Our fabulous lineup of veterinary ‘rock stars’ cover the ECC,

internal medicine, and surgical and non-invasive surgical worlds
of veterinary medicine. They will be covering imaging, medicine,
surgery, critical care, nutrition and, as always, a cat friendly
approach to managing urinary tract disease and urolithiasis.
Nathalie Dowgray
As well as the fantastic feline content, those of you joining us in
Head of ISFM
Dublin will be able to fully enjoy the ‘craic’ with the ISFM team at the
Hill’s Pet Nutrition Welcome Reception on Thursday evening and with
a pint (or a half) of Guinness on Friday evening in the exhibition hall.

This year we are taking advantage of the space the Clayton Hotel
has to offer and are trying something new! As well as doubling the
number of masterclasses, we are also running a second Clinical
Practice Stream on Thursday, Friday and Saturday. These lectures
are designed to be practical, ‘take back to the clinic’ sessions to
help those of us in primary care practice with our day-to-day work.
Can’t be two places at once? Don’t worry; both the main stage and
the Clinical Practice sessions are being recorded so what you don’t
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 Dublin, 29 June – 2 July

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 Dublin, 29 June – 2 July

The line-up: THURSDAY, 29 JUNE

MAIN STAGE Proceedings
page no.

08.30 Opening
08.45 Diagnosis of upper urinary tract disease: more than azotaemia 12–16
Soren Boysen and Serge Chalhoub
09.45 Management of acute kidney injury: just fluids and furosemide? 17–25
Soren Boysen and Serge Chalhoub
10.30 Coffee break
11.15 Pathophysiology of feline urolithiasis; those pesky rocks: why do they form in
the first place? 26–30
Myles McKenna Sponsored by Zoetis
12.00 ZOETIS SYMPOSIUM
Feline arthritis: easing the pain – 2 years’ experience with Solensia® 31–34
Martha Cannon
13.00 Lunch break
14.00 Imaging of the upper urinary tract: Ultrasound and beyond 36–42
Tom Maddox
15.00 State of the art: Dialysis for AKI, where are we with advanced renal medicine? 43–50
Serge Chalhoub
16.00 Coffee break
16.45 Panel discussion: The severely azotemic cat presenting at midnight on a n/a
busy shift, oh and the owner has no money!
Soren Boysen, Serge Chalhoub, Myles McKenna
17.45 HILL’S SYMPOSIUM
Urolithiasis: The amazing things nutrition can do 51–53
Jody Lulich
18.45 Welcome reception

MEETING ROOM 1: MEETING ROOM 2:

09.00–10.30 MASTERCLASS 09.00–10.30 MASTERCLASS
Advanced surgery of the urinary tract Understanding feline body
Laura Owen language in the clinic, what are
these cats trying to tell us?
11.15–12.00 Abstract presentation
Goncalo Da Graça Pereira
Yaiza Gomez-Mejias

MEETING ROOMS 1& 2: CLINICAL PRACTICE STREAM Proceedings

page no.

14.00–14.30 Fluids and CRIs for felines: making the maths easy 130–134
Laura Jones
14.30–15.00 Behavioural considerations to reduce the risk of urinary disease 135–137
Goncalo Da Graça Pereira
15.00–15.30 Post discharge: at-home management of complex cases 138–140
Laura Jones
15.30-16.00 Hospitalisation and post discharge: behavioural considerations for cats 141–143
Goncalo Da Graça Pereira
16.45-17.45 Abstract presentation
Nathalie Dowgray

#ISFMRocksDublin 5
 Dublin, 29 June – 2 July

The line-up: FRIDAY, 30 JUNE

MAIN STAGE Proceedings
page no.

08.00 The role of diet in preventing and managing urolithiasis 55–59

Cecilia Villaverde Sponsored by Pro Plan
09.00 Hypercalcaemia in cats and its role in urolithiasis 61–66
Myles McKenna Sponsored by Zoetis
10.00 Coffee break
10.45 Diagnosis of feline urolithiasis: those pesky rocks, how do I find them? 67–72
Serge Chalhoub
11.45 BOEHRINGER INGELHEIM SYMPOSIUM
From acute and visible to chronic and hidden: the benefits of early 73–74
management for cats’ kidneys
Thierry Francey, Teresa Rehme, Roswitha Dorsch
12.45 ABCD Awards – Young Scientist Award
13.00 Lunch break
14.00 Feline ureteral obstructions – diagnosis and management 76–82
Allyson Berent (joining us live virtually from New York)
15.00 SUBs 101 – technical aspects and trouble shooting 83–88
Laura Owen
16.00 Coffee
16.30 CEVA SYMPOSIUM
Use of antimicrobial in the managing of urinary tract infections 89–92
Roswitha Dorsch
17.30 PANEL DISCUSSION
Urolithiasis in cats: those pesky rocks, ongoing treatment and management n/a
Serge Chalhoub, Goncalo Da Graça Pereira, Laura Jones, Myles McKenna,
Cecilia Villaverde
18.30 Drinks reception

MEETING ROOM 1: MEETING ROOM 2:

08.30–10.00 MASTERCLASS 08.30–10.00 MASTERCLASS
Practical emergency tricks and tips Cat friendly interactions: practical
for feline upper urinary cases: the cat handling for the clinic
good, the bad and the squashed Goncalo Da Graça Pereira, Alex
Soren Boysen, Serge Chalhoub Taylor
10.45–11.45 Abstract presentation 10.45-11.45 IDEXX MASTERCLASS
Samantha Taylor Islands in the Stream? Urinary
crystals, casts and more*
Yvonne McGrotty

MEETING ROOMS 1& 2: CLINICAL PRACTICE STREAM Proceedings

page no.

14.00–15.00 What tube and when? Feeding tube management and care 144–148
Cecilia Villaverde
15.00–16.00 Critical care aspects of managing an acute renal injury 149–155
Laura Jones

* This is a free masterclass sponsored and hosted by IDEXX. Space is limited to 40 people and seats will be allocated on a first come, first served basis.

#ISFMRocksDublin 6
 Dublin, 29 June – 2 July

The line-up: SATURDAY, 1 JULY

MAIN STAGE Proceedings
page no.

08.30 PANEL DISCUSSION

Ethics of advanced procedures in cats: just because we can, does it mean n/a
we should?
Soren Boysen, Serge Chalhoub, Karen Hiestand, Laura Jones
09.30 ROYAL CANIN SYMPOSIUM
A success story: How to recruit and retain staff as well as clients through a 94–95
cat friendly approach
Cyril Berg, Marc-Antoine Rappart, Clémentine Doucet
10.30 Coffee break
11.15 Beyond the bladder 1: an update on urethral obstruction 97–101
Soren Boysen, Serge Chalhoub
12.00 Beyond the bladder 2: urethral obstruction – managing the aftermath 97–101
Soren Boysen, Serge Chalhoub
12.45 Beyond the bladder Q&A n/a
Soren Boysen, Serge Chalhoub
13.00 OTA: minimally invasive management of stone disease in cats 102–103
Allyson Berent (oining us live virtually from New York)
14.00 AFTERNOON OFF

MEETING ROOMS 1& 2: CLINICAL PRACTICE STREAM Proceedings

page no.

07.15-08.15 Wake up to inappetence, practical solutions for the cat that won’t eat 156–157
both in the clinic and at home
Sam Taylor Sponsored by Dechra
11.00-12.00 Nutritional intervention case studies: when food makes a big difference 158–161
Cecilia Villaverde

12.00–12.45 Tubes everywhere! Practical management of SUBS, catheters and urine 162–166
bags!
Laura Jones

ABSTRACTS
Abstracts can be found at the back of the proceedings, pp 168–195.

#ISFMRocksDublin 7
 Dublin, 29 June – 2 July

The line-up: SUNDAY, 2 JULY

SUNDAY, 2 JULY Proceedings
page no.

08.30 Urinary tract surgery in general practice: tips and tricks from a busy referral
practice to take back to your clinic 104–111
Laura Owen
09.30 PANEL DISCUSSION n/a
Euthanasia decision making: when is enough enough when we could do
more?
Nathalie Dowgray, Sam Taylor, Karen Hiestand
10.30 NORBROOK SYMPOSIUM
Drugs and cats: when are they small dogs and when are they not? 112–115
Jill Maddison
11.30 Coffee break
12.00 Hocus POCUS: the role of ultrasound in the critical feline patient, anyone can
learn these magic techniques... 117–128
Soren Boysen, Serge Chalhoub
14.00 CONGRESS CLOSES

MEETING ROOM 1: MEETING ROOM 2:

08.30–09.55 MASTERCLASS 08.30–10.30 MASTERCLASS
Ultrasound in critical cat cases: Nutrition masterclass
POCUS and more masterclass Cecilia Villaverde
Soren Boysen, Serge Chalhoub

10.05-11.30 MASTERCLASS
Ultrasound in critical cat cases:
POCUS and more masterclass
Soren Boysen, Serge Chalhoub

ABSTRACTS
Abstracts can be found at the back of the proceedings, pp 168–195.

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#ISFMRocksDublin 8
 Dublin, 29 June – 2 July

Meet our veterinary ‘rock’ stars speakers

The Headliners
Søren Boysen Di DVM, Dipl. ACVECC
Søren is a Professor of Veterinary Emergency and Critical Care at the University of Calgary,
Faculty of Veterinary Medicine. He obtained his DVM from the University of Saskatchewan in
1996, completed a small animal internship at the Atlantic Veterinary College, and a residency
at Tufts University, becoming a diplomate of the American College of Veterinary Emergency
and Critical Care in 2003. He is the former Chief of small animal emergency and critical care
at the University of Montreal (2003-2009). A member of several ECVECC, ACVECC and VetCOT
committees he continues to actively promote the global advancement of veterinary ECC.
Extensively published and a recipient of numerous teaching and research excellence awards,
he has become an internationally recognized speaker. He and his colleagues from Tufts
published the first small animal focused assessment with sonography for trauma (FAST) exam,
and with colleagues at the University of Calgary, adapted veterinary point of care ultrasound
for use in non-trauma patients. With the help of many great colleagues from around the world,
he continues to develop ultrasound training techniques and workshops for non-specialist
practitioners. Along with point of care ultrasound, his research interests include hemorrhage,
coagulation, and perfusion.

Serge Chalhoub BSc, DVM, DACVIM (SAIM)

Serge Chalhoub graduated from the Faculté de médecine vétérinaire (FMV) of the Université de
Montréal in 2004. Serge followed this with a one-year rotating small animal clinical internship at
the same institution. Serge pursued a residency in small animal internal medicine at the Animal
Medical Center (AMC) in New York City. He stayed on at the AMC as their first renal/hemodialysis
fellow and then as a staff doctor. Dr. Chalhoub is an Associate Professor (Teaching) at the
University of Calgary’s Faculty of Veterinary Medicine (UCVM) and has been on faculty since
2012. He was the recipient of the 2013 and 2021 Canadian Veterinary Medical Association’s
Teacher of the Year Award, the 2015 University of Calgary Team Teacher of the Year Award,
and the 2017 Carl J. Norden Distinguished Teacher Award. He has authored and co-authored
numerous scientific articles and book chapters on veterinary point of care ultrasound, renal
and urinary medicine, and lectures around the world on these topics.

Laura Owen BVSc CertSAS AFHEA DipECVS MRCVS European & RCVS Specialist in
Small Animal Surgery
Laura graduated from the University of Bristol in 2001. After a three year period in first opinion
practice, she completed a rotating Internship at the Royal Veterinary College, London, followed
by a Small Animal Surgical Residency at the University of Bristol. She moved to Cambridge as a
Clinical Surgeon in the soft tissue department in 2009 and obtained the ECVS Diploma in Small
Animal Surgery in 2010. She currently holds the position of Associate Professor in Small Animal
Surgery and continues to enjoy all aspects of soft tissue surgery, with particular interests in
urology, wound management & reconstructive surgery and minimally invasive techniques.

Allyson Berent DVM, DACVIM (SAIM) Veterinary Specialist in Internal Medicine,

Medical Device Development, Urology an Interventional Endoscopy
Dr. Allyson Berent graduated from Cornell University College of Veterinary Medicine in 2002 and
then from 2002-2003 Dr. Berent completed a small animal rotating internship at the University
of Minnesota. This was followed by a residency in small animal internal medicine at the Matthew
J. Ryan Veterinary Hospital of the University of Pennsylvania from 2003-2005. From 2005-2006
Dr. Berent completed the first veterinary fellowship in Interventional Radiology at the Veterinary
Hospital of the University of Pennsylvania and the Hospital of the University of Pennsylvania, and
a fellowship in Endourology at Thomas Jefferson University. She served as Adjunct Assistant
Professor in Internal Medicine and Interventional Radiology/Interventional Endoscopy at the
Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania helping to establish the
first Interventional Radiology/Endoscopy service in veterinary medicine. In 2009 Dr. Berent joined
the Animal Medical Center in New York City as the director of the Interventional Endoscopy
Service where she co-founded the first full time Interventional Radiology and Endoscopy
program for veterinary medicine in the world. Dr. Berent has received numerous teaching and
research awards throughout her career. Dr. Berent also serves as Adjunct Professor at Purdue
University and University of Guelph-Ontario Veterinary College.

#ISFMRocksDublin 9
 Dublin, 29 June – 2 July

Fabulous supporting lectures from:

#ISFMRocksDublin 10
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Purrfect Play Every Day

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 Dublin, 29 June – 2 July

Diagnosis of upper urinary tract disease:

more than azotemia
Serge Chalhoub DVM, Dipl. ACVIM (SAIM)
Søren Boysen DVM, Dipl. ACVECC
Faculty of Veterinary Medicine, University of Calgary

Learning objectives:

◆ Recognize the clinical signs of upper urinary tract disease

◆  nderstand the different causes of upper urinary tract disease
U
(e.g. pyelonephritis, acute kidney injury, ureteral obstruction)
◆ Interpret clinical pathology findings in azotemic patients
◆ Discuss application of imaging of such cases in the emergency and critical care
situation*
*Note: a detailed discussion of imaging and urolithiasis (advanced and in clinic) is covered in other talks

Introduction
Upper urinary tract disease can be challenging to diagnose. Clinical signs may be vague
(fever, abdominal discomfort, “ain’t doing right”, etc.), especially in cats. We will focus more on
the conditions that lead to acute azotemia and also to some degree of pelvic distension, and
benign ureteral obstruction (BUO).

Causes
The main causes of upper urinary tract disease in cats include chronic conditions such as
chronic kidney disease (CKD) and polycystic kidney disease (PKD), and acute conditions such
as pyelonephritis, toxicities (lilies, ethylene glycol, other toxins such as NSAIDs), and BUO. We will
focus on BUO and pyelonephritis.

BUO
BUO is being increasingly recognized in cats. The incidence of BUO is unknown but likely
represents a significant proportion of cats, especially those presenting with acute and chronic
azotemia. This condition is important to recognize as these cats are generally considered
to have a good to excellent prognosis, despite previous considerations on this. The majority
of cats with BUO have been documented to have partial obstructions, which is likely why
decompression, even after a chronic obstruction, can still result in an improvement in renal
function. Based on animal models, a ureteral obstruction results in decreased renal blood flow
due to the increased hydrostatic pressure in the nephrons, which encourages progressive
intrinsic kidney damage. Rapid recognition and relief of an obstruction are crucial in order to
preserve nephron function and thus overall renal function. The majority of cats presenting with
BUO do have concurrent intrinsic renal dysfunction, either in addition to the obstruction or as
a result of the obstruction, which emphasizes the need to preserve as much renal function as
possible, as quickly as possible.

In a study by Kennedy and White (2022), of 168 cats (28 cats with BUO and 140 control cats
without BUO), only diet was identified as a risk factor for developing BUO. Cats eating exclusively
dry food were 15.9 times as likely to develop a BUO than cats fed a moist food diet. Considering
that the predominant stone type in the upper urinary tract is calcium oxalate, feeding a moist

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diet for prevention could reduce the incidence of these stones, as has been documented in
the lower urinary tract. Interestingly, total plasma calcium was not associated with a greater
risk for calcium oxalate BUO in this study compared with other studies, although case numbers
were low and further studies are needed. However, ionized calcium was not studied, and
ionized calcium was shown to increase the risk of subcutaneous ureteral bypass (SUB) device
mineralization (see later sections).

Causes of BUO
The most common reported cause of feline BUO is calcium oxalate urolithiasis. However,
ureteral strictures have been documented more recently in a large number of cats.

Causes of BUO:
◆ Calcium oxalate urolithiasis
◆ Ureteral strictures
◆ Dried solidified blood
◆ Neoplasia
◆ Iatrogenic: surgical trauma
◆ Pyelonephritis
◆ Fibrosis
◆ Mucus plugs

PYELONEPHRITIS
This is a condition usually secondary to an ascending urinary tract infection, and most often
related to Escherichia coli. Pyelonephritis rarely occurs in isolation, meaning there is often a
comorbidity that leads to it developing (CKD, lower urinary tract infection, diabetes mellitus,
hyperadrenocorticism, etc.). Pyelonephritis is more severe than lower urinary tract infections as
it leads to systemic clinical signs, azotemia, and other changes.

Clinical signs of upper urinary tract disease

Clinical signs are vague. We will not discuss chronic conditions. Most cats presenting with
acute upper urinary tract disease will have a variety of clinical signs that will depend on the
primary cause. Most will likely have clinical signs related to acute azotemia (more on this later).
Pyelonephritis may or may not lead to fever. Most cats will likely develop lethargy, inappetence,
and possibly abdominal discomfort.

Diagnosis
Patient history is one of the most important tools in determining what is going on and also
identifying risk factors for developing azotemia. Acute azotemia can be pre-renal (rarely
causing severe azotemia), renal, or post-renal in origin. Acute azotemia patients merit a
complete blood count (CBC), chemistry panel, urinalysis, urine culture, and medical imaging.
The urine specific gravity (USG) is very helpful in determining the cause, but it is important to be
careful in its interpretation. For instance, certain pre-renal causes will have isosthenuric or even
hyposthenuric USGs.

Azotemia is simply a reflection of increased nitrogenous waste products in the body, and it
indicates a drop of glomerular filtration rate (GFR) by the kidneys. The causes of azotemia
can be acute or chronic, and also pre-renal, renal, or post-renal in origin. It is important not to
assume that all azotemia is the kidney’s fault.

ACUTE AZOTEMIA
Azotemia should not be ignored. Proper reference ranges are important (creatinine above

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140–160 mmol/L in a dog or cat), with

isosthenuria, is indicative of renal
dysfunction), and USG needs to be
addressed. Grey zone USG (see later)
needs to be qualified with hydration.
Azotemia is not a diagnosis; it is
merely a descriptive term that needs
to be qualified with a cause and also
whether it is acute or chronic.

Acute kidney injury (AKI) is damage

that occurs to the kidneys, but
this does not necessarily lead to a
severe drop in GFR nor does it lead to
azotemia. However, it is important to
recognize and to try to identify when
present. Unfortunately, even though
creatinine is the better marker, it has
poor sensitivity, even with newer reference ranges. It is poorly correlated to GFR in mild cases of
renal dysfunction. However, studies have shown that any change in creatinine from its baseline
can not only indicate AKI (even before changes in USG) but also estimate prognosis.

The current International Renal Interest Society (IRIS) AKI staging system bases its staging on
changes in creatinine:

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RENAL AZOTEMIA
This is where the kidneys are the cause of the azotemia, which is secondary to parenchymal
damage due to ischemic, glomerular, or tubular damage. This can be because of pre-renal
or post-renal azotemia. In cats, common causes are toxins, pyelonephritis, and ischemia.
Decreased GFR is the result, and isosthenuria or hyposthenuria is present.

There are a lot of medications that can cause acute renal azotemia/AKI, but the most common
are aminoglycosides, NSAIDs, and ACE inhibitors. In terms of toxins, there are many: ethylene
glycol, vitamin D, lilies, and myoglobin/hemoglobin are some of them. Other causes of acute
renal azotemia/AKI include ischemia, proteinuria, and renoliths.

POST-RENAL AZOTEMIA
This includes anything that blocks urine from leaving the body below the level of the kidneys:
uroliths, urethral disease, neoplasia, ureteroliths, feline lower urinary tract disease (FLUTD),
urethral obstructions, blood clots, debris, congenital disease, inflammatory diseases, and
acquired strictures. Isosthenuria or hyposthenuria is present.

Ureteroliths and BUOs are becoming more recognized as a cause of renal disease and acute
azotemia, especially in cats. Even unilateral cases have been shown to cause azotemia.
Unfortunately, these stones in cats are most often calcium oxalate and have been there for
some time, which often means that renal damage is present and the ureters are already
damaged/strictured.

Elevations in serum creatinine concentration have been documented to be present in over

95% of cats with BUO, regardless of whether they are unilaterally or bilaterally obstructed. It is
important to recognize that not all obstructed cats are azotemic.

Urine is often neglected when evaluating cats with acute azotemia, yet it can greatly help
us in determining what is going on with the kidneys. USG is very important in that regard, but
it is important to realize that strict reference ranges are difficult to provide, and it is always
important to evaluate the patient’s hydration status. A USG above 1.035 in cats indicates good
concentrating ability, and if these patients are azotemic then the azotemia is likely pre-renal
in origin. USG between 1.015 and 1.030 is termed the grey zone, which means the USG may be
adequate if the patient is well hydrated. If the patient is dehydrated with a grey zone USG,
then this USG is inappropriate and renal disease should be considered. Isosthenuria is a USG
between 1.008 and 1.015 and indicates a lack of ability to concentrate and dilute urine. USG
below 1.008 is termed hyposthenuria, and this may be appropriate (the kidneys are trying
to dilute urine on purpose) or inappropriate (central diabetes insipidus, secondary diabetes
insipidus to toxins/medications, etc., and secondary to a loss of antidiuretic hormone receptors
from chronic kidney disease).

Urinalysis can also help us identify specific causes of upper urinary tract disease. For instance,
ethylene glycol intoxication will lead to an acidic urine pH and calcium oxalate crystals, NSAIDs
and other tubular damage-causing intoxications may or may not lead to urine casts, and
pyelonephritis may lead to an active sediment with bacteria. Unfortunately, urinalysis and urine
culture can be poorly sensitive.

MEDICAL IMAGING
A diagnosis of upper urinary tract disease requires medical imaging. Abdominal
ultrasonography is the most available and reliable diagnostic tool in most cases.
Abdominal radiographs are often helpful to support identification of the underlying cause

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 Dublin, 29 June – 2 July

(e.g. ureterolithiasis) but is not sensitive enough as the main modality for diagnosis.

When it comes to BUO, there is significant agreement between ultrasound and surgical findings
in determining the etiology and location of a ureteral obstruction, but this is most accurate if
the obstruction is caused by a ureterolith, and less so when it is caused by a stricture, dried
solidified blood stones, or a purulent plug. Most cats with BUO have evidence of concurrent
hydronephrosis and hydroureter, but it may not be clearly associated with an obstructive lesion
visualized on ultrasound. This does not rule out a ureteral obstruction, and one should always be
considered in the face of luminal dilation.

In one study, the ultrasonographic size of the feline renal pelvis and ureter were evaluated in
control cats and then compared with those with suspected CKD, BUO, and pyelonephritis. 66.6%
of cats with CKD had measurable renal pelvic dilation compared with 30.0% of normal cats,
84.6% of cats with pyelonephritis and 100% of cats with BUO. There was no statistically significant
difference in renal pelvis size (as measured in the X plane) between cats with CKD and control
cats, or those with CKD and pyelonephritis. Interestingly, cats with a BUO had significantly
greater renal pelvic dilation compared with those with CKD and normal cats, but not compared
with those with pyelonephritis. There was no significant difference in proximal ureteral width
between normal cats and those with CKD, or between cats with pyelonephritis and those with
a BUO. However, there was a significant difference in proximal ureteral width between cats with
CKD and those with pyelonephritis or a BUO. Normal cats had a significantly smaller ureteral
diameter than those with a BUO or pyelonephritis.

In addition, it is possible for a cat with BUO to present with minimal pelvic dilation (2–5 mm),
and therefore if a patient does not have evidence of a large degree of renal pelvic dilation, the
clinician should not exclude a diagnosis of BUO.

Point-of-care ultrasound (POCUS), which can be done by any practitioner, can also assist a
clinician with the diagnosis of acute ureteral obstructions, specifically with BUO caused by
ureteral obstructions. A study from the Royal Veterinary College demonstrated that using
POCUS, and looking a short-axis renal pelvic dilation, could identify ureteral obstructions if
the renal pelvis was >13 mm in diameter. Therefore, a short-axis renal pelvis >13 mm confirms
ureteral obstruction, but <13 mm does not exclude it.

Other medical imaging findings will depend on the cause. For instance, cats with ethylene
glycol toxicity may present with bright kidneys and also a medullary rim sign. Renal AKI causes
may lead to “swollen” kidneys which appear larger on ultrasound when measured. Debris may
be seen in the renal pelvis with pyelonephritis. Ureteral dilation may be seen with any cause of
BUO.

Conclusions
Upper urinary tract disease requires a combination of history, clinical findings, laboratory
analysis (specifically a CBC, chemistry panel, urinalysis, and culture) and medical imaging for
diagnosis. For non-specialists, POCUS can help diagnose ureteral obstructions.

References
◆ Kennedy AJ, White JD. Feline ureteral obstruction: a case-control study of risk factors (2016–2019). J Feline
Med Surg 2022; 24(4): 298–303.
◆ Syme H, Jepson R. Clinical approach and laboratory evaluation of renal disease. In: Ettinger S, Feldman
E, Cote E (Eds). Textbook of Veterinary Internal Medicine. 8th ed. eBook. Available from: Elsevier eBooks+.
Elsevier - OHCE, 2017.

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 Dublin, 29 June – 2 July

Management of acute kidney injury: just fluids and

furosemide?
Serge Chalhoub DVM, Dipl. ACVIM (SAIM)
Søren Boysen DVM, Dipl. ACVECC
Faculty of Veterinary Medicine, University of Calgary

Learning objectives:

◆  nderstand the order of treatment priorities when facing an acute upper urinary
U
case
◆ Understand the staging of acute kidney injury and why it is useful
◆ Understand fluid and electrolyte support
◆ Understand the role of diuretics
◆ Understand what additional therapies are indicated (e.g. antiemetics, analgesia)

Introduction
Azotemia is simply a reflection of increased nitrogenous waste products in the body (and we
measure this readily by blood urea nitrogen (BUN) and creatinine, but there are many other
waste compounds), and it indicates a drop of glomerular filtration rate (GFR) by the kidneys.
The causes of azotemia can be acute or chronic, and also pre-renal, renal, or post-renal in
origin. It is important not to assume that all azotemia is the kidney’s fault. Acute kidney injury
(AKI) can also occur from pre-renal and post-renal azotemia, and can lead to severe AKI (a
significant and detrimental drop in GFR) as well as chronic kidney disease (CKD). All three
forms of azotemia can coexist (a patient can be dehydrated, have CKD, and have a ureteral
obstruction), which makes differentiating them sometimes challenging.

Azotemia
We have to be careful when calling these
nitrogenous waste products “kidney
markers” or more commonly “kidney
enzymes”, both among ourselves and even
when it comes to describing what is going
on to owners. These “kidney markers” that
we use to talk about kidney function (and
help estimate GFR) are not produced
by the kidneys. They are, however,
eliminated by the kidneys. We can use the
nitrogenous waste products that are more
predictably and constantly eliminated by
the kidneys as markers of kidney function.
This can be done daily and cheaply. The
main nitrogenous waste products we use
are BUN and creatinine.

BUN is nitrogen in the form of urea, and is the by-product of protein metabolism by the liver
via the urea cycle. Protein waste products are converted to urea. This production is variable
and depends on proper liver function and the availability of substrate (protein). For instance,

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with gastrointestinal bleeding, more protein is brought to the liver from blood digestion in the
gut, and BUN increases. With starvation or liver failure, BUN decreases. BUN is eliminated by the
kidneys. However, this elimination is not constant. Some BUN is reabsorbed by the tubules to be
used for medullary tonicity. Therefore, BUN is not the most reliable marker of renal function.

Creatinine is formed from the breakdown of creatine phosphate, a rapid energy reserve of
the muscles, and is relatively constantly produced. It is also relatively constantly eliminated,
with little tubular reabsorption. Therefore, creatinine is a much better everyday marker of renal
function. However, its validity depends on muscle mass and can vary. For instance, Greyhounds
will have a higher normal creatinine level. A late-stage IRIS CKD patient will have less muscle
mass, which means their creatinine will be “falsely” lower (underestimating azotemia and renal
function).

Uremia is the term used to describe the illness of being in renal failure, and should not be
used interchangeably with azotemia. Uremia is secondary to azotemia, and is the effect of
the circulating nitrogenous waste compounds on the body. Clinical signs of uremia include
anorexia, lethargy, nausea, gastrointestinal erosions/ulcers, vomiting, chills, peripheral
neuropathy, seizures, coma, and even death.

Acute azotemia
Azotemia should not be ignored. Proper reference ranges are important (creatinine above
140–160 mmol/L in a dog or cat), with isosthenuria, is indicative of renal dysfunction), and
urine specific gravity (USG) needs to be addressed. Grey zone USG (which can be loosely
defined as a USG between 1.015 and 1.030) needs to be qualified with hydration. Azotemia is not
a diagnosis; it is merely a descriptive term that needs to be qualified with a cause and also
whether it is acute or chronic.

AKI is damage that occurs to the kidneys, but this does not necessarily lead to a severe drop in
GFR nor does it lead to azotemia (>70% loss of function). However, it is important to recognize
and to try to identify. All causes of azotemia (pre-renal, renal, post-renal) can lead to AKI, but
not all causes of AKI are associated with acute azotemia. Unfortunately, even though creatinine
is the better marker, it has poor
sensitivity, even with newer
reference ranges. It is poorly
correlated to GFR in mild cases
of renal dysfunction. However,
studies have shown that any
change in creatinine from its
baseline can not only indicate
AKI (even before changes
in USG), but also estimate
prognosis. This has led to
studies looking at survival and
prognosis for AKI patients.

In the staging system pictured

left, patients falling into stages
1–3 during hospitalization were
less likely to survive.

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In this staging system,

patients that were
presented to the hospital
following AKI and acute
azotemia (>1.6 mg/dl in
USA values, or 140 µmol/L
in Canadian values)
were followed closely
based on their outcome
and creatinine changes.
Dogs in level 1 within 2
days were 3 times more
likely to die within 90
days. Those in level 2
within 2, 3, or 7 days were
3 times more likely to die
within 30–90 days. Cats
in level 2 within 3 or 7
days were 3 times more
likely to die within 30
days, and 4 times more likely to die if placed at this level in 7 days. If placed in level 2 within
2–3 days, they were more likely to die within 90 days.

Finally, this leads us to the current International Renal Interest Society (IRIS) staging system:

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These staging systems bring about the importance of not ignoring changes in creatinine,
especially over a short period of time. Over a longer period of time, creatinine changes, even if
still within the normal range, should be investigated and not ignored. Unfortunately, GFR studies,
especially in the acute setting, are not realistic.

Acute azotemia (of any type) or AKI that is prolonged, severe, or ongoing will lead to severe AKI,
where GFR is significantly decreased and will lead to significant detrimental changes to the
patient. Once in severe AKI, regardless of cause, the general prognosis for renal recovery is 50%.
This means 50% of patients do not recover. Of the 50% that do, half are left with CKD that should
be manageable. There are exceptions to this rule. Renal recovery depends on identifying the
cause of the damage, removing or administering the appropriate treatment, supporting the
entire body (very important), giving the kidneys time to try to recover, and luck. Renal recovery
may take many days to weeks, and can even go on for up to 6 months (but most of the
recovery happens in the first few weeks).

The earlier AKI is recognized, the better the chance at preventing permanent renal damage.

Approaching acute azotemia

Patient history is one of the most important tools in determining what is going on, and also for
identifying risk factors for developing azotemia: examples include heart disease, existing renal
disease, recent anesthesia, dehydration, low perfusion, hypotension, hypoadrenocorticism, heat
stroke, pancreatitis, and diabetes mellitus.

It is also important to identify clues that might indicate if the azotemia is acute or chronic in

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nature (evidence of weight loss, cachexia, renal structural damage, chronic clinical signs that
are progressing, changes on lab work that might indicate acute disease, etc.).

The next steps involve identifying whether the azotemia is pre-renal, renal, or post-renal.
Although azotemia can be a combination of all three, typically one factor is more responsible
for the majority of azotemia. Acute azotemia patients merit a complete blood count, chemistry
panel, urinalysis, urine culture, and medical imaging. The USG is very helpful in determining
the cause, but it is important to be careful in its interpretation. For instance, certain pre-renal
causes will have isosthenuric or even hyposthenuric USGs.

Pre-renal azotemia
With pre-renal causes the azotemia is usually mild to moderate and USG is usually
concentrated. Examples include dehydration, hypotension, shock, heart disease/heart failure,
acute hemorrhage, and certain endocrinopathies such as diabetes mellitus, hyperthyroidism,
hyperadrenocorticism, and hypoadrenocorticism. With diabetes mellitus, USG can be
isosthenuric or even hyposthenuric because glucose is very hyperosmolar and will pull water
through the kidney. Diabetes mellitus can also lead to urinary tract infections (UTIs), which
may impact USG. Hyperthyroidism accelerates GFR so USG can be low. With Cushing’s disease,
cortisol can block antidiuretic hormone (ADH) receptors, which prevents the kidneys from
concentrating the urine. Lastly, with Addison’s disease, the lack of sodium reabsorption can
affect the medullary tonicity and the ability to concentrate urine. Therefore, USG can be low.

If left untreated, pre-renal azotemia can lead to renal damage and renal azotemia if it leads
to renal perfusion issues. This may become irreversible. However, pre-renal azotemia is usually
preventable.

Renal azotemia
This is where the kidneys are the cause of the azotemia, which is secondary to parenchymal
damage due to ischemic, glomerular, or tubular damage. This can be because of pre-renal
or post-renal azotemia. In cats, common causes are toxins and ischemia, whereas in dogs
infections and ischemia are common causes. Decreased GFR is the result, and isosthenuria or
hyposthenuria is present.

There are a lot of medications that can cause acute renal azotemia/AKI, but the most common
ones are aminoglycosides, NSAIDs, and ACE inhibitors. In terms of toxins, there are many:
ethylene glycol, vitamin D, raisins/grapes, lilies, and myoglobin/hemoglobin are some of them.
More common infectious diseases include pyelonephritis, Lyme disease (more a cause of
severe glomerulonephritis and proteinuria that leads to severe AKI), and leptospirosis. Other
causes of acute renal azotemia/AKI include ischemia, heat stroke, proteinuria, and renoliths.

Post-renal azotemia
This includes anything that blocks urine from leaving the body below the level of the kidneys:
uroliths, prostatic disease, urethral disease, neoplasia, ureteroliths, feline lower urinary tract
disease (FLUTD), urethral obstructions, blood clots, debris, congenital disease, inflammatory
diseases, and acquired strictures. Isosthenuria or hyposthenuria is present.

Ureteroliths are becoming more recognized as a cause of renal disease and acute azotemia,
especially in cats. Even unilateral cases have been shown to cause azotemia. Unfortunately,
these stones in cats are most often calcium oxalate and have been there for some time, which
often means that renal damage is present and the ureters are already damaged/strictured.

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Treatment of acute azotemia

The earlier acute azotemia is identified and treated, the better. Trying to determine which
type (or types) of acute azotemia is present is key and stresses the importance of lab work,
urinalysis, and medical imaging. Post-renal causes are often overlooked.
Many of these patients will be unstable, especially oliguric/anuric patients.

Intravenous fluid therapy, often with a balanced isotonic crystalloid fluid, is indicated. If the
patient is dehydrated or hypovolemic, then this needs to be addressed immediately with
appropriate boluses of fluid and calculation of dehydration deficit.

It is very important to monitor what the fluids are doing through serial physical examinations
(weight of patient, skin tent, respiratory rate, central venous pressure if available) and urine
output. Urine output needs to be a minimum 1–2 ml/kg/hour (and much more if on IV fluids,
ONCE hydration has been restored). Urine output can be monitored via a urinary catheter (and
calculating ins and outs) or by measuring urine on pee pads. This is an often overlooked but
very simple and critical step to include.

What is even more important is not to drown our patients. It is important to remember that
azotemia is a syndrome and a reflection of trash that is not being eliminated. IV fluids serve
ONLY to rehydrate or restore perfusion to a patient, and to maintain renal perfusion. They do
NOT serve to “FLUSH” the kidneys and to get “RID” of azotemia. Therefore, once a patient is
hydrated and well perfused, if the azotemia reaches a baseline plateau, there is NO INDICATION
to increase the IV fluid rate. This can harm and drown the patient by causing fluid overload. It is
important to treat the patient, not the numbers. More IV fluids do not repair renal function; only
the kidneys can repair themselves. We often aim to manage the more acute clinical symptoms
of uremia (vomiting, ulcers, dehydration), which may occur early in the course of therapy, and
often before the azotemia is resolved.

Fluid therapy can be guided and monitored not only with a urinary catheter, but also using
point-of-care ultrasound (changes in caudal vena cava diameter, cardiac chamber size and
contractility, signs of fluid overload such as B lines, gallbladder halo sign, abdominal or pleural
effusion, etc.). This will be covered in another lecture.

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If a patient is oliguric or anuric despite hydration being restored, or the patient is already
overhydrated from being oliguric or anuric, then this is an emergency situation. If possible, the
patient should be referred to a specialty hospital for potential dialysis (hemodialysis or even
peritoneal dialysis). If not available, diuretic therapy can be attempted to restore some degree
of urination. It is important to note that dialysis and diuretics serve only to buy time to keep a
patient stable while the kidneys heal (or not); they do not fix the kidneys and may not improve
outcome (they improve outcome only by keeping the rest of the body stable while the kidneys
try to repair themselves). Furosemide and mannitol are the main diuretics used, but mannitol
should not be used if the patient is overhydrated as the risk of heart failure is high. Dialysis is
much more effective, and in certain instances can even remove certain toxins from the blood.
Peritoneal dialysis, although labor-intensive, is also effective.

Specific antidotes and treatments should be given as soon as possible. With pyelonephritis,
broad-spectrum antibiotics (e.g. ampicillin-sulbactam and enrofloxacin) should be started
immediately after taking a urine culture. Urethral obstructions should be relieved as soon as
possible.

Anuric patients unfortunately die quickly, and the prognosis is poor if urine is not produced
following hydration of the patient, or if dialysis is not available, regardless of the cause.

If a patient is found to have a ureteral obstruction, then the sooner the patient is referred for
a potential procedure the better. This includes patients with mild but acute azotemia (classic
case: cat has decreased appetite, lab work indicates a creatinine of 240 µmol/L (2.2mg/dl)
with a USG of 1.012 and x-rays show ureteroliths). There are no concrete data in cats, but in
dogs if complete ureteral obstructions are relived within 4 days, then almost full return of GFR
is possible. After 14 days that drops to under 50%, and after 40 days there is little recovery that
can be achieved. Procedures include ureteral stents, subcutaneous ureteral bypass (SUB)
placement, and ureteral surgery. If a procedure is not possible, then medical management is
a second (but much less ideal) option for cats. There is a small chance that some degree of
renal function may return, at least enough for stable CKD that is compatible with life. Medical
treatment involves administration of IV fluids sufficient to maintain renal perfusion until
creatinine stabilizes. If creatinine stabilizes at a reasonable plasma concentration (good control

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of clinical signs despite persistent azotemia), there is a chance the cat can be treated at home,
similar to any CKD patient. Unfortunately, there is a chance that the azotemia will not improve.

Nutrition is very important. As early as possible, if a patient is not eating, then consider a
nasogastric/nasoesophageal tube or E-tube and start nutrition. These tubes can also be used
to give water and medications.

Uremia leads to nausea, and treating nausea is beneficial to a lot of these patients. Dolasetron/
ondansetron and Cerenia are very effective.

Hypertension is also a possible consequence of AKI. However, it is important to be careful, as

hypertension may be an appropriate reaction to the kidney trying to maintain renal perfusion. If
hypertension is excessive (>180–200 mmHg), then treatment can be considered (ACE inhibitors,
calcium channel blockers).

Hyperkalemia is often a consequence of AKI. It is important to rule out Addison’s disease

first, but if the hyperkalemia is secondary to AKI this usually means the patient is anuric or
oliguric, and this needs to be treated. Urine output needs to be restored, and if hyperkalemia is
causing arrhythmias or bradycardia, then without dialysis or return of adequate urine output
the prognosis is poor. Treatment of hyperkalemia should involve IV fluids and may include
rapid insulin and dextrose or bicarbonate. Calcium gluconate will not decrease potassium
concentrations, but it may stabilize cardiac disturbances and buy time for other therapies to
decrease potassium levels in severely affected patients.

If renal recovery occurs, it is important to monitor for post-obstructive/post-AKI diuresis. This

occurs because all of the built-up azotemia pulls water out of the kidneys once the kidneys start
to return to normal GFR, and patients can become dehydrated and hypoperfused very quickly.
Proper monitoring of ins/outs and hydration, and matching IV fluids to losses, will prevent this.

Transfusions may sometimes be necessary. Acute azotemia can lead to severe non
regenerative anemias (due to a combination of lack of erythropoietin (EPO), acute
inflammation, uremia, and bleeding).

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Prognosis
If the creatinine decreases by ±50% within 24–48 hours of treatment, then the patient generally
has a good prognosis and a chance of continued renal recovery. It is important to continue
to monitor the patient constantly (weight, blood pressure, creatinine, electrolytes, packed cell
volume), and to continue treatments as necessary (IV fluids to maintain hydration and renal
perfusion, nutrition, anti-nausea medications, etc.). Once azotemia baseline is achieved, then IV
fluids are tapered by 25% every day and creatinine is monitored.
If the creatinine stays stable or continues to decrease, fluids are further tapered. If the creatinine
increases or reaches a new lower plateau, then the patient is transitioned to enteral (E-tube)
or subcutaneous fluids if possible and if this will maintain hydration. If hydration cannot be
maintained by enteral or subcutaneous means, then the patient may have a poor quality of life.

Renal recovery can take days or weeks. Unfortunately, after 1–2 weeks, if there is no
improvement or only mild initial improvement that fails to continue, then the odds are renal
function will remain significantly impaired, regardless of the initiating cause of the acute
azotemia. Pyelonephritis usually has a more favorable prognosis (70–80% return to renal
function), whereas toxicity due to raisins/grapes, lilies, or ethylene glycol usually has a poorer
prognosis.

Pertinent reference:
International Renal Interest Society: http://www.iris-kidney.com/

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Pathophysiology of feline urolithiasis: those pesky

rocks – why do they form in the first place?
Myles McKenna MVB, MVetSci, MVetMed, DACVIM (SAIM), DECVIM-CA
Director of the Global Clinical Consultation Service for Zoetis Diagnostics

Sponsored by

Summary:
Uroliths are solidified aggregates of mineral and non-mineral crystalloids,
usually named based on their mineral composition, with calcium oxalate and
struvite (magnesium ammonium phosphate) being the two most commonly reported types
in cats. Urolithiasis is responsible for 10–20% of all cases of feline lower urinary tract disease
and may be life-threatening in cases of ureteral or urethral obstruction.

Urolith structure
Each urolith is composed of three main parts:

NIDUS
This is the area of initiation of growth, usually (but not always) located towards the centre of
the urolith. Usually, the nidus is composed of organic minerals, but less commonly it may be
composed of foreign material such as suture material. Identifying the nidus is important when
uroliths are being analysed, as the mineral composition of the nidus is generally the primary
focus of preventive measures.

BODY
his composes the “bulk” of the urolith. If it is not possible to locate the urolith nidus, the mineral
composition of the body should be the focus of preventive measures.

SHELL
This is the outer “crust” of the urolith. It is common for the mineral composition of the crust to
be different from that of the body and nidus, which may reflect recent changes to the patient’s
diet, health status or medications.

Compound uroliths are defined as uroliths with an identifiable nidus that contain one or more
layers of minerals in the body or shell that are different from the minerals in the nidus. Mixed
uroliths are defined as uroliths without an identifiable nidus that are composed of more than
one mineral (neither of which composes >70% of the urolith).

Urolith formation
There are two phases of urolith formation: nucleation and growth.

NUCLEATION PHASE
The nucleation, or initiation, phase involves the formation of a crystal “embryo”, which is
essentially where tiny aggregates of crystals or crystalloids (crystal-like structures) form, which
ultimately will become the urolith nidus. Crystals are defined as orderly collections of molecules
arranged in a lattice structure, a structure which allows their continued growth. They are neutral
compounds derived from the interaction of a cation (e.g. calcium) and an anion (e.g. oxalate).
The exact inciting factor and sequence of events that lead to the formation of the crystal

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embryo are unknown, but the main requirement is that the urine must be supersaturated with
lithogenic (stone-forming) crystalloids.

What is supersaturation?
A supersaturated solution is one that is more saturated with a particular substance at a given
temperature than would be normally expected. In the case of urine, supersaturated urine
contains a greater concentration of a particular crystalloid (e.g. calcium or ammonium) than
the associated solvent (water) would normally be able to keep in solution. At high levels of
supersaturation with a crystalloid, the urine is no longer able to keep it in solution, resulting in
the crystalloid precipitating into a solid form – a crystal salt. Urine pH affects the ionisation of
many crystalloids in urine and thus impacts their solubility. Urine pH commonly varies during
the course of a day, meaning that the urine may be supersaturated with a crystalloid at certain
times of the day but not at other times.

Nucleation can be classed as either homogeneous or heterogenous. Homogeneous

nucleation occurs spontaneously in highly supersaturated urine, where identical crystalloids
spontaneously aggregate and join together to form the nidus. Heterogeneous nucleation
occurs in the presence of a foreign material, such as suture material, which acts as a catalyst
for nucleation; the nidus will therefore be composed of a mixture of organic and inorganic
material. A lower degree of supersaturation is required for heterogenous nucleation to occur
than for homogeneous nucleation. The nucleation stage is the primary target of many urolith
prevention strategies aimed at preventing the supersaturation and precipitation of crystalloids.

GROWTH PHASE
Once the crystal embryo has formed, for it to continue to grow into a urolith it is necessary for
crystals to continue to aggregate and join to the crystal embryo, and for the crystal embryo
to remain in the urinary tract without being voided. Ongoing supersaturation of the urine
with crystalloids leads to ongoing crystal aggregation and ultimately urolith growth. Various
molecules in the urine can act as inhibitors of lithogenesis. Some of these molecules, such as
citrate and pyrophosphate, form soluble salts with minerals such as calcium, thereby reducing
the quantity of the mineral that is able to precipitate and interact with other minerals, such as
oxalate. Other inhibitor molecules, such as nephrocalcin and glycosaminoglycans, interfere
with the ability of minerals to combine with each other or prevent crystals from adhering to
the urinary tract mucosa. Whether or not a crystal embryo will grow into a urolith depends on
where the balance lies between promoting factors (supersaturation) and inhibitor molecules.
Ultimately, if supersaturation is severe and ongoing, the protective actions of these inhibitor
molecules will be overridden and a urolith will form.

Relative prevalence of feline urolith types

Across multiple studies from several countries, the two most common types of uroliths in cats
are struvite (magnesium ammonium phosphate) and calcium oxalate, which between them
account for >90% of all uroliths submitted for analysis.1–3 Struvite uroliths were by far the most
commonly reported urolith type until the 1990s, but over time calcium oxalate has overtaken
struvite as the most common, with calcium oxalate now accounting for 40–50% of all uroliths
submitted for analysis, very closely followed by struvite.2,4 There are several theories for this
change in the relative prevalence of struvite vs calcium oxalate uroliths over time:
◆ The widespread use of commercial struvite prevention diets that are restricted in
magnesium and acidifying.5 Dietary acidification promotes calciuria (a risk factor
for calcium oxalate formation), while urinary magnesium is known to inhibit the
formation of calcium oxalate crystals in humans and rats (it is unknown if this is

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the case in cats)

◆ An increased ability of veterinarians to diagnose and treat struvite uroliths
medically without needing to submit the uroliths for analysis (leading to a
submission bias for uroliths that do not resolve medically, such as calcium
oxalate)6
◆ The increasing age of the cat population (calcium oxalate uroliths are more
common in older cats)6
◆ A change in the prevalence of cat breeds over time (certain breeds are at a higher
risk of calcium oxalate vs struvite urolithiasis)6

STRUVITE UROLITHS
Feline struvite uroliths typically form in sterile urine, unlike in dogs, where they are most
commonly associated with urinary tract infections. The ability of cats to form struvite uroliths
in the absence of infection may be explained by this species’ greater ability to strongly
concentrate its urine, leading to greater levels of supersaturation of urine with lithogenic
minerals. Several specific risk factors for the development of struvite uroliths have been
identified in cats:
◆ Dietary and metabolic factors: diets with high concentrations of magnesium,
ammonium, phosphate, sodium and chloride are associated with an increased
risk of struvite urolithiasis. Struvite uroliths are more likely to form if urine pH is
consistently elevated (twice the risk if urine pH is consistently 6.5–6.9 vs 6–6.2)5
◆ Infection: although infection-related struvite uroliths are rare in cats, they can
occur, and are usually associated with urease-producing bacterial species (e.g.
Staphylococcus and Proteus species)5
◆ Age: struvite uroliths tend to affect younger cats, with a peak incidence between 2
and 7 years of age5
◆ Sex: female cats are at increased risk6
◆ Obesity: obese cats are at increased risk1
◆ Breed: studies in different geographical regions have reported certain breeds to be
at increased or decreased risk of struvite uroliths, with some conflicting results that
may be due to geographical differences or differences in study methodology.1,3,4

CALCIUM OXALATE UROLITHS

Multiple risk factors for calcium oxalate urolith formation in cats have been identified or
proposed:
◆ Dietary and metabolic factors: cats fed diets low in moisture, sodium and
potassium diets or diets formulated to maximize urine acidity are at increased risk
of calcium oxalate urolithiasis. Formation of calcium oxalate uroliths is more likely
if urine pH is consistently decreased (three times the risk if urine is pH consistently
6–6.2 vs 6.5–6.9)5
◆ Hypercalcaemia: this can lead to hypercalciuria and is a predisposing factor for
calcium oxalate urolithiasis. Hypercalcaemia has been observed in 35% of cats
with calcium oxalate uroliths.7 It is important to note that hypercalciuria can result
from other causes too, for example, due to the administration of glucocorticoids,
furosemide, urinary acidifiers and vitamin C or D.
◆ Age: older cats (7–10 years) are most commonly affected6
◆ Sex: males, in particular neutered males, are at increased risk6
◆ Breed: certain breeds of cats are predisposed, including Persians, Himalayans, and
Burmese1,2,4
◆ In human medicine, decreased serum concentrations of citrate, a calcium oxalate

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crystallization inhibitor, have been associated with an increased risk of calcium

oxalate urolith formation; however, there are limited data on this potential risk
factor in cats.

URATE UROLITHS
Urates are generally regarded as the third most common type of feline urolith, albeit much less
prevalent than struvite or calcium oxalate uroliths. Affected cats are usually young (1–6 years)
and are more commonly male. A genetic association between the Egyptian Mau breed and
urate urolithiasis has been reported in some geographies, although a specific genetic mutation
has not yet been identified.8 Hepatic disease or portosystemic shunts may result in a reduced
ability to convert ammonia to urea and uric acid to allantoin, and thereby cause urate uroliths
to form.

XANTHINE UROLITHS
Xanthine uroliths are rare and may occur as a result of a defect in the activity of the enzyme
xanthine oxidase (leading to an inability/reduced ability to convert xanthine to uric acid), or
secondary to chronic allopurinol administration (a medication which inhibits xanthine oxidase).

CYSTINE UROLITHS
Rare; may occur due to a defect in the COLA transporter in the proximal tubule of the nephron,
resulting in abnormal amounts of cystine and dibasic amino acids (ornithine, lysine and
arginine) entering the urine. This stone type has been associated with acidic urine.

SILICATE UROLITHS
Very rare; usually related to increased intake of silica in the diet or from drinking water with a
high silicate content. This stone type has been associated with acidic urine.

CALCIUM PHOSPHATE UROLITHS

Calcium phosphate is often found as a minor component of calcium oxalate or struvite uroliths;
it is much less common for uroliths to be primarily composed of calcium phosphate. This urolith
type is sometimes associated with primary hyperparathyroidism.

DRIED BLOOD CLOT UROLITHS

Uncommon; usually associated with inflammatory disease of the urinary tract causing the
formation of a blood clot, which serves as a nidus for crystal deposition.

What about nephroliths?

Upper urinary tract uroliths (nephroliths and ureteroliths) are overwhelmingly calcium
oxalate in composition (with calcium oxalate uroliths representing 98% of all such uroliths
in one study9). In conjunction with the supersaturation of urine with calcium, it has been
hypothesized that the presence of “Randall’s plaques” in the kidneys may be of importance in
the pathophysiology of upper urinary tract calcium oxalate urolith formation in cats. Randall’s
plaques are very common in humans with calcium oxalate nephroliths, and essentially are
plaques of calcium phosphate that are located within the basement membrane of the loop of
Henle. These calcium phosphate plaques are believed to serve as a nidus for calcium oxalate
nucleation and subsequent calcium oxalate urolith formation. Despite being discovered
in human medicine almost a century ago, little is known about how or why these plaques
form. To date, there is very little published data on the histopathological findings in cats with
calcium oxalate nephrolithiasis. However, recent data suggest the likely presence of calcium
phosphate deposits in feline renal tissue adjacent to the renal tubules, suggesting that a similar
pathogenesis to Randall’s plaques in humans may occur in our feline patients.10

#ISFMRocksDublin 29
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References

1. Burggraaf ND, Westgeest D, Corbee RJ. Analysis of 7866 feline and canine uroliths submitted
between 2014 and 2020 in the Netherlands. Res Vet Sci 2021; 137: 86–93.
2. Kopecny L, Palm CA, Segev G, et al. Urolithiasis in cats: evaluation of trends in urolith composition
and risk factors (2005-2018). J Vet Intern Med 2021; 35(3): 1397–1305.
3. Breu D and Müller E. Feline uroliths: analysis of frequency and epidemiology in Germany (2016-
2020). Tierärztliche Praxis 2022; 50(2): 102–111.
4. Cannon AB, Westropp JL, Ruby AL, et al. Evaluation of trends in urolith composition in cats: 5,230
cases (1985–2004). J Am Vet Med Assoc 2007; 231(4): 570–576.
5. Lekcharoensuk C, Osborne CA, Lulich JP, et al. Association between dietary factors and calcium
oxalate and magnesium ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc 2001;
219(9): 1228–1237.
6. Lekcharoensuk C, Lulich JP, Osborne CA, et al. Association between patient-related factors and risk
of calcium oxalate and magnesium ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc
2000; 217(4): 520–525.
7. Midkiff AM, Chew DJ, Randolph JF, et al. Idiopathic hypercalcemia in cats. J Vet Intern Med 2000;
14(6): 619–626.
8. Appel SL, Houston DM, Moore AE, et al. Feline urate urolithiasis. Can Vet J 2010; 51(5): 493–496.
9. Kyles AE, Hardie EM, Wooden BG, et al. Clinical, clinicopathologic, radiographic, and ultrasonographic
abnormalities in cats with ureteral calculi: 163 cases (1984–2002). J Am Vet Med Assoc 2005; 226(6):
932–936.
10. Tang PK, Jepson RE, Chang YM, et al. Risk factors and implications associated with renal
mineralization in chronic kidney disease in cats. J Vet Intern Med 2022; 36(2): 634–646.

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SYMPOSIUM

Feline arthritis: easing the pain – 2 years’

experience with Solensia®
Martha Cannon BA VetMB DSAM(Fel) FRCVS
RCVS Specialist in Feline Medicine
Oxford Cat Clinic, UK

Arthritis is a painful condition which affects the majority of the older pet cat population, with a
prevalence of around 60% in cats over 6 years old (Slingerland et al., 2011), rising to around 90%
of cats over 12 years old (Hardie et al., 2002). The joints most commonly affected are the hips,
stifles, tarsi and elbows (Lascelles et al., 2010). Spondylosis of the thoracic and lumbar spine
is also very common. However, despite arthritis being recognised as a significant problem
for more than 20 years, many affected cats are currently untreated, even within the sub-
population of pet cats whose owners regularly access veterinary services.

Identifying and overcoming some of the factors that prevent cats from receiving treatment is
an important step in improving the well-being of older pet cats.

Barriers to treatment include:

◆ Under-recognition of the problem by both owners and vets.
◆ Owners’ misconception that their cat is “stiff” rather than in pain, and that this is an
inevitable consequence of ageing.
◆ Owners’ misconception that there is nothing that can be done to treat the problem.
◆ Lack of time in the consulting room to engage the client and discuss all the many
treatment options that are available.
◆ Concern on the part of both vets and owners about the potential adverse effects
of treatment, especially chronic use of non-steroidal anti-inflammatory drugs
(NSAIDs) in older cats and cats with renal compromise.
❖ Both osteoarthritis and chronic kidney disease (CKD) are common in older cats,
and they commonly occur together. One recent study identified that 70% of
cats recruited to studies of degenerative joint disease also had concurrent CKD
(Marino et al., 2014).
◆ The inherent difficulty in administering daily medication to cats.
◆ Cost of treatment.
The last two factors are not only a barrier to starting treatment but can also be a significant
factor in low long-term compliance – a recent survey of cat owners indicated that around 50%
of owners who start treatment do not continue to administer the treatment in the long term
(Zoetis Pet Owner Feline Journey Market Research, 2020).

Common reasons cited for stopping treatment included:

◆ Limited efficacy: owners did not perceive a significant benefit when using the
recommended treatment.
◆ Adverse effects: gastrointestinal adverse effects are common in cats receiving

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NSAIDs, while opioids and gabapentin (not licensed for use in cats, but commonly
prescribed for this indication) can induce sedation.
◆ Difficulty dosing their cat on a regular basis.
◆ Difficulty in remembering to give the treatment.
◆ Lack of conviction that their cat is in pain and in need of treatment rather than
“just slowing down in their old age”.

How can we encourage owners to treat their affected cat?

Owners often recognise changes in their cat’s gait, behaviour and quality of life, but they do not
associate them with pain, and they do not consider them a reason to visit their vet because
they consider them an inevitable part of ageing. We need to open the conversation and allow
owners to share their concerns about their cat’s reduced quality of life to open the way for a
treatment plan, and we need to have confidence that our advice will be valued. Even in the age
of the internet and social media influencers, owners still trust their vet as a most valued source
of information:

When a vet identifies the signs as attributable to the pain of arthritis, owners are likely to listen
and be open to advice on when and how to treat.

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We must also be aware that our own perceptions, and indeed misconceptions, of what owners
will accept and be willing to afford can have a major impact on how we present the wide range
of treatment options to an owner. Owners consistently report that they are prepared to pay for
treatment that will improve their elderly cat’s quality of life, especially if they perceive it to be
safe, and if delivering the treatment is not stressful for their cat or themselves. In a recent global
survey of cat owners, only around 30% of owners reported difficulty in bringing their cat to the
vet (Zoetis, information on file), so the opportunity to see elderly cats regularly and to educate
owners to help their arthritic cats is there.

Vets need to become confident in making a diagnosis of arthritis based on gait and
behavioural changes and to make positive recommendations for effective, stress-free, well-
tolerated treatment options.

Frunevetmab (Solensia®, Zoetis)

Frunevetmab is an anti-Nerve Growth Factor (Anti-NGF) monoclonal antibody which has
recently been licensed for use in cats and offers a valuable addition to the array of treatment
options for feline arthritis.

It is indicated for the long-term management of arthritis in cats, including those with IRIS stage
1 and 2 CKD. It is administered once a month by subcutaneous injection, thus overcoming
difficulties in dosing and removing the requirement for owners to dose their cats every day.
Unlike NSAIDs, it is not metabolised by the liver or kidneys, and it can be used in cats with
other concurrent diseases that require treatment with corticosteroids. Where necessary, it
can be used in conjunction with other analgesics and nutraceuticals as part of a multi-modal
approach to chronic pain management, but in the absence of long-term data caution is
recommended when using it concurrently with NSAIDs.

During the pivotal clinical trial for Solensia®, 76% of cat owners reported sustained improvement
in signs of pain when their cats were treated. The only adverse effect identified was focal skin
lesions (alopecia, pruritus, dermatitis), usually at sites separate from the site of injection.

FIELD EXPERIENCE WITH SOLENSIA®

Solensia was launched in the UK market in May 2021. A retrospective analysis of its use in our
two-branch cat-only first-opinion and referral medicine practice in Oxford, England, indicates
that it is a well-tolerated, effective option for treatment in many cases, and that it is generally
well accepted by owners.

A retrospective analysis of the practice management system identified 75 cats that had
received at least 1 injection of Solensia® for management of chronic osteoarthritis in the period
May 2021–March 2023. Four cases were lost to follow up as their owners moved away from the
area before the effect could be assessed. Five cats did not receive a second injection because
they had severe, unrelated concurrent diseases which led to euthanasia within 2 weeks of the
first injection. These 7 cases have been excluded, leaving 66 cases included in the analysis
summarised below:
◆ 49 owners (74.2%) reported a positive response to treatment.
◆ Adverse effects were suspected in 7 cats (10.6%):
❖ Pruritus occurred in 3 cats (3.4%).
❖ Gastrointestinal signs (reduced appetite or vomiting) occurred in 4 cats (6.1%).
❖ 1 cat was “not quite right” for 24 hours following the injection.
❖ 1 cat developed a tremor 5 days after the first injection of Solensia. The tremor

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resolved within 36 hours and did not recur after a second injection. However, this
cat also suffered transient gastrointestinal (GI) signs (vomiting) within 1 week of
each injection, so treatment was not continued.
◆ The majority (71.4%) of cats whose owners perceived a positive response to the
first injection received 3 or more injections.
◆ 12 cats (18%) received only a single injection; reason(s) cited for not continuing
with treatment were:
❖ 8 = Lack of effect.
❖ 3 = Adverse effects.
❖ 1 = Cost (this owner also reported no recognisable improvement).
❖ 1 = Unwell for other reasons. The Solensia® was effective, but the owner chose
not to continue in the face of other unrelated problems.
❖ 1 = No record of the reason. The owner reported a positive effect but did not
continue treatment.
◆ 6 cats (9%) received only two injections; the reason(s) cited for not continuing
treatment were:
❖ 4 = Lack of effect.
❖ 1 = Adverse effects.
❖ 1 = No record of the reason. The owner reported a positive effect but did not
continue treatment.
◆ 2 owners (3%) ceased treatment after 3 and 5 months, respectively, due to a
perceived reduction in efficacy.
◆ 59 cats (89%) had at least one other chronic concurrent disease.
• The most common concurrent conditions were:
• CKD = 32 cats.
• Chronic GI disease = 21 cats.
• Hyperthyroidism = 11 cats.

Conclusion
Solensia® provides a valuable addition to the range of treatments, including NSAIDs,
nutraceuticals and other unlicensed analgesic agents, that are available for long term
management of osteoarthritis in cats. It is effective in a high proportion of cases, and is well
tolerated and well accepted by many owners for long-term use.

References
◆ Hardie EM, Roe SC, Martin FR. Radiographic evidence of degenerative joint disease in geriatric cats: 100
cases (1994–1997). J Am Vet Med Assoc 2002; 220(5): 628–632.
◆ Lascelles BDX, Henry JB, Brown J, et al. Cross-sectional study of the prevalence of radiographic
degenerative joint disease in domesticated cats. Vet Surg 2010; 39(5): 535–544.
◆ Marino CL, Lascelles BD, Vaden SL, et al. Prevalence and classification of chronic kidney disease in cats
randomly selected from four age groups and in cats recruited for degenerative joint disease studies. J
Feline Med Surg 2014; 16(6): 465–472.
◆ Slingerland LJ, Hazewinkel HAW, Meij BP, et al. Cross-sectional study of the prevalence and clinical features
of osteoarthritis in 100 cats. Vet J 2011; 187(3): 304–309.

#ISFMRocksDublin 34
The material featured in this
advertisement is based on approved
labelling in Ireland.

Frunevetmab

BACK WHERE
I BELONG
Come and talk to us
at the Zoetis Stand

Solensia — A New Era in Pain Management

The FIRST and ONLY monoclonal antibody therapy for cats
with osteoarthritis (OA)1

• 86% of cat owners would

treat their cat for OA pain
if recommended by their
vet2

• Start the conversation

by directing them to
zoetispets.com
Name: Solensia. Active ingredient: frunevetmab. Target species: cats. Indication: For alleviation of pain associated with osteoarthritis. Contraindications: Do not use
in animals under 12 months and/or under 2.5 kg body weight. Do not use in cases of hypersensitivity to the active substance or to any of the excipients. Do not use in
animals intended for breeding, or animals that are pregnant or lactating. Adverse events: Focal skin reactions. Manufacturer: Zoetis. Read the SPC or package label
before use.
References: 1. Solensia SPC 2. Zoetis Study TI-06572 (based on responses of 270 UK cat owners)
Solensia® contains Frunevetmab. Solensia is licensed for the alleviation of pain associated with osteoarthritis in cats. POM
Approved labelling for registered products can be different in various countries around the world and not all products featured in this advertisement are approved
for use in every country around the world. As an example, Solensia® is approved in the EU, the UK, Canada, Australia and the US.
Date of preparation: April 2023 • MM-25850
 Dublin, 29 June – 2 July

Imaging of the upper urinary tract:

ultrasound and beyond
Prof Thomas W. Maddox
BVSc, PhD, PGCertHE, CertVDI, DipECVDI, FHEA, MRCVS

Summary:
The modalities commonly used for imaging of the upper urinary tract (including in primary
care and referral settings) will be assessed, including a review of normal appearance and
important findings. The choice of modality will be discussed, with consideration of when a
technique offers a benefit to the patient.

Introduction
Most of the imaging modalities typically available for veterinary use can be used successfully to
image the upper urinary tract, and in many situations the information obtained from different
techniques can be complementary. However, there are often occasions where one modality is
preferred over the others, and making the decision as to which is most suitable depends on the
clinical signs and range of differential diagnoses being considered.

There are many indications for imaging the upper urinary tract in cats. Specific indications
include (but are not limited to):
◆ Haematuria
◆ Dysuria
◆ Anuria
◆ Pyuria
◆ Assessing the integrity of the urinary tract post trauma/uroabdomen
◆ Acute or chronic renal failure
◆ Renal colic
◆ Urinary incontinence
◆ Weight loss (suspected protein-losing nephropathy)
◆ Investigation of abdominal masses/organomegaly.

In cats with signs of lower urinary tract disease, it may still be prudent to scan the upper urinary
tract as some conditions affect multiple sites (urolithiasis) and lower urinary tract infections
can ascend to result in pyelonephritis.1

Imaging modalities
Radiography is almost universally available to those in primary care situations (although not
all of the possible techniques are commonly performed), with ultrasound also widely available.
Computed tomography (CT) is increasingly available, but magnetic resonance imaging (MRI)
is most performed in referral settings. All of these modalities can be of some value in imaging
the upper urinary tract.

Radiography: Plain radiography has limited value in assessing the urinary tract but can be
useful for assessment of the kidneys. At least one laterolateral and a ventrodorsal radiograph
should be obtained (the latter is particularly required for any renal measurements). The kidneys
are more consistently visualised in cats than dogs and are typically located between lumbar
vertebrae L1 and L4. Their size is normally 1.9–2.6 x the length of L2 but can measure as larger in
un-neutered cats.2

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The kidneys should be evaluated according to radiographic signs (number, location, size, shape
and opacity). Most commonly, only structural changes will be apparent, so either changes in
shape or size (often a combination of both) and the pattern of these changes can be used to
inform differential diagnoses (see Table 1). Alterations in opacity can be readily seen if there is
mineralisation within the renal silhouette, which can represent renoliths or renal parenchymal
mineralisation (such as nephrocalcinosis or dystrophic mineralisation). In cats, it should also be
noted that the fat in the renal hilus can sometimes be appreciated as a central region of slight
radiolucency. Changes in number and location are less frequent but can be seen in cases of
severe dysplasia or ectopic kidneys.

Table 1. Differential diagnoses for changes in renal size and shape. While based around
changes seen with radiography, this can be applied to other modalities too.

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Although the ureters are soft tissue opacity and should theoretically contrast well with the
fat of the retroperitoneal space, they are generally far too small to be visible. However, their
normal anatomical location is known and so abnormalities in the corresponding regions should
raise suspicion of ureteral disease. The only abnormalities likely to be directly visible on plain
radiographs are calculi. Urinary calculi can have varying radiopacity (see Table 2), and some
may be poorly visible. However, most calculi in cats are calcium oxalate1 and so can usually be
detected when present in the kidneys and ureters. Occasionally, nipples overlying the kidneys or
region of the ureters can be mistaken for calculi. The retroperitoneal space should be assessed
for detail, as loss of contrast or streaking in this region suggests retroperitoneal effusion, which
can be seen with renal or ureteral rupture.

Table 2. Types of urolith and their typical radiographic opacities

The ureters should be very evident after the administration of intravenous iodinated contrast
given as part of an intravenous urogram (IVU) or excretory urography, and this procedure will
also result in opacification of the kidneys. It is a prerequisite that plain radiographs are obtained
prior to performing any type of contrast study. Various contrast agents are available (see Table
3), with the non-ionic and low-osmolarity agents being considered safer. The dose is normally
600–800 mgI/ml, which for most preparations equates to a volume of around 2 ml/kg. As well
as opacifying the renal pelvis, pelvic recesses/diverticuli and ureters, the technique provides a
crude estimate of renal function.3,4

Table 3. Examples of iodinated contrast agents available for use.

None of these are specifically licensed for veterinary use

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Antegrade pyelography represents an alternative to the IVU and can be used when there
are concerns over intravenous contrast causing further harm to kidney function or if reduced
renal function suggests there would be poor opacification of the renal pelvis and ureters.5
The technique involves injection of contrast directly into the renal pelvis (bypassing the renal
parenchyma) under fluoroscopic or, preferably, ultrasonographic guidance.6 As the contrast is
not diluted there is excellent opacification of the collection system, and it can be an especially
useful technique to demonstrate ureteral obstruction or rupture.7

There is often hydronephrosis present when this technique is indicated; injection should be
made with a narrow-gauge (<22 G) needle through a thin part of the cortex, taking care to
avoid the hilar and interlobular vessels. Urine can be aspirated for analysis and a similar
volume of iodinated contrast (>250 mgI/ml) carefully introduced, with ventrodorsal and
lateral radiographs subsequently obtained. Subcapsular and perirenal leakage of contrast
are common complications but are not often significant, but subcapsular and intrapelvic
haemorrhage are potentially more serious.5

Urine samples should generally be obtained prior to performing any form of contrast study as
the contrast media can potentially affect the results of any urinalysis, possibly inhibiting some
bacterial growth and altering specific gravity for up to 24 hours.

Ultrasound: The soft tissue resolution of ultrasound makes it an excellent modality for imaging
the kidneys in particular. It provides highly detailed imaging of the renal architecture and
vascularity, with ready distinction between fluid and soft tissue. Both kidneys are easy to image
in the cat due to their slightly more caudal location, but their mobility does mean it is important
to verify whether you are examining the left or the right kidney; the use of high-frequency (>8
MHz) linear probes is preferred.

Normal feline kidneys are 30–43 mm in length and should be symmetrical. The renal cortex is
usually isoechoic to the liver (may be slightly hyperechoic in obese cats) and measures 2–5
mm in thickness.8,9 The medulla is hypoechoic and there should be good corticomedullary
distinction. The renal sinus is hyperechoic due to peripelvic fat and fibrous tissue; the actual
renal pelvis may not be apparent unless dilated.

Doppler ultrasound allows assessment of renal vascularity, and pulsed-wave (PW) Doppler
can allow more quantitative measurements such as calculation of the resistive index (RI).10
Elevations in RI have been documented with ureteral obstruction and most acquired renal
disease, but its relatively non-specific nature has meant that it is not often used in clinical
practice.11–13

It can be challenging to identify the ureters if they are normal; however, if enlarged or dilated
they can be seen more readily and with experience it is usually possible to follow mild to
moderately dilated ureters from the renal pelvis to the ureterovesical junction.14,15 Ureteroliths
can be identified as echogenic structures within the lumen that usually cast a distal acoustic
shadow.

As for most organs, ultrasound affords the opportunity to perform ultrasound-guided sampling
for needle aspirates or biopsies. As the kidneys are very vascular organs, it is sensible to
use Doppler to interrogate the sample region and reduce the risk of renal haemorrhage.
Pyelocentesis can be carried out under ultrasound guidance, or the same approach can be
used for injection of contrast during antegrade pyelography. There needs to be a moderate

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degree of pelvic dilation for these techniques to be feasible.5,6,16

Computed tomography: Although CT shares some limitations with radiography (relatively poor
soft tissue resolution), to an extent its cross-sectional nature overcomes this, and the depiction
of soft tissues can be further enhanced through the use of contrast media. Essentially, to image
the upper urinary tract accurately, an IVU is performed but with CT rather than radiography,
with the advantage that multiple studies and projections are not normally required.

For contrast-enhanced CT, the same dosages and contrast agents as used for an IVU are
recommended. If a pressure injector can be used, then an early arterial and later venous phase
can potentially be acquired, although arterial phase images will show no enhancement of the
ureters and the normal post-contrast venous phase is normally sufficient for examination of
the kidneys. The kidneys enhance very strongly and so mineralisation is likely to be obscured,
meaning that careful inspection of the pre-contrast images is imperative.

Overall assessment of the kidneys is similar to radiography, although the ability to accurately
distinguish between fluid and soft tissue helps further inform the differential diagnoses.
Most renal disease can be assessed adequately with CT; lesions with a fluid content can be
recognised by their hypoattenuation prior to contrast, and normally show poor enhancement
relative to the strong enhancement of the surrounding renal parenchyma. Similarly, nodules
and mass lesions can be easily recognised by their differential contrast enhancement.

There is good visualisation of the ureters after contrast administration, and normally the
ureterovesical junction can be identified, with definitive assessment of contrast entry into the
bladder.17,18 However, occasionally dynamic imaging of the ureterovesical junction is needed to
confirm or exclude normal opening of the ureters into the bladder.19

Magnetic resonance imaging: MRI is rarely considered for primary imaging of the urinary
tract. The high soft tissue resolution of this modality does mean the kidneys can be depicted
very clearly and there is good distinction of the urinary bladder wall, with the advantage that
contrast administration is not generally required. However, there is little published information
on the MRI appearance of normal or diseased kidneys in the cat, and imaging of the ureters is
difficult with this modality: even post-contrast they are difficult to detect.

Choice of modality
The choice of modality may be largely dictated by what is available at the time when imaging
is required, particularly in the emergency setting. For the upper urinary tract, employing a
combination of plain radiography and ultrasound is usually sensible as a first-line approach.
Ultrasound is preferred if renal parenchymal disease is suspected, especially if intravenous
urography is contra-indicated or not available.

CT does not offer any significant advantage over ultrasound for evaluation of the kidneys and
may result in further kidney injury through the use of contrast. Consequently, it is generally not
considered particularly beneficial for cases of suspected renal disease, although it can be
useful to assess renal masses if resection is being considered. If there is a suspicion of ureteral
disease (especially ectopia), then CT can be very useful,20 especially if there is not access to a
relatively experienced ultrasonographer. CT will also allow the detection of lower concentrations
of iodinated contrast and so may be advantageous for patients with poor concentrating ability.

An important consideration if planning to perform either a radiographic IVU or a contrast-

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enhanced CT is contrast-induced renal failure.21 This is a rare but serious consequence of

intravenous iodinated contrast administration, although it is usually self-resolving.22,23 There
are several proposed risk factors (see Table 4). Of these, pre-existing renal disease is clearly
an important consideration for cats. The human literature suggests that patients with serum
creatinine levels >200 μmol/l should be considered high risk, but the equivalent has not been
fully established for either dogs or cats. There are suggestions in the literature not to perform
IVU if creatinine levels are >350 μmol/l,24 but this stems more from the fact that the study quality
will be compromised by poor renal function rather than explicitly considering patient safety.
However, only 5% of renal function is necessary for the excretion of iodinated contrast. Anuria
and dehydration should be considered absolute contra-indications for contrast administration.

Table 4. Risk factors for the development of contrast-induced renal failure

(extrapolated from the human literature)

If use of contrast is unavoidable in a high-risk patient, then the potential harm can be reduced
by keeping the contrast volume to a minimum (400 mgI/kg has been shown to result in
adequate opacification), using non-ionic, low/iso-osmolar contrast agents such as iohexol or
iotrolan, and administering intravenous fluid therapy. The development of contrast-induced
renal failure can be recognised by a good initial nephrogram followed by steadily increasing
renal opacity and a delayed or absent pyelogram phase.

Conclusion
Most of the available imaging modalities have something to offer when imaging the upper
urinary tract in cats, and often using a combination of techniques is the most appropriate
method. If there are no concerns regarding contrast administration, then CT is probably the
single modality that is most informative overall. However, if a contrast examination is not
possible, then the combination of radiography and ultrasound will provide a similar level of
information.

References
1. Geddes RF, Davison LJ, Elliott J, et al. Risk factors for upper urinary tract uroliths and ureteral
obstruction in cats under referral veterinary care in the United Kingdom. J Vet Intern Med 2023;
37(2): 567–577.
2. Shiroma JT, Gabriel JK, Carter RL, et al. Effect of reproductive status on feline renal size. Vet Radiol
Ultrasound 1999; 40(3): 242–245.
3. Latham C. Practical contrast radiography. 1. Contrast agents. In Practice 2005; 27(7): 348–352.
4. Baines E. Practical contrast radiography 3. Urogenital studies. In Practice 2005; 27(9): 466–473.
5. Etedali NM, Reetz JA, Foster JD. Complications and clinical utility of ultrasonographically guided
pyelocentesis and antegrade pyelography in cats and dogs: 49 cases (2007–2015). J Am Vet Med

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 Dublin, 29 June – 2 July

Assoc 2019; 254(7): 826–834.

6. Delaney FA and Dennison S. Sonography-guided pyelocentesis and pyelography in cats: the
sonographer’s role. J Diagn Med Sonog 2010; 26(3): 116–120.
7. Adin CA, Herrgesell EJ, Nyland TG, et al. Antegrade pyelography for suspected ureteral obstruction in
cats: 11 cases (1995–2001). J Am Vet Med Assoc 2003; 222(11): 1576–1581.
8. Yan GY, Chen KY, Wang HC, et al. Relationship between ultrasonographically determined renal
dimensions and International Renal Interest Society stages in cats with chronic kidney disease. J
Vet Intern Med 2020; 34(4): 1464–1475.
9. Griffin S. Feline abdominal ultrasonography: what’s normal? what’s abnormal? The kidneys and
perinephric space. J Feline Med Surg 2020; 22(5): 409–427.
10. Rivers BJ, Walter PA, O’Brien TD, et al. Duplex Doppler estimation of Pourcelot resistive index in
arcuate arteries of sedated normal cats. J Vet Intern Med 1996; 10(1): 28–33.
11. Tipisca V, Murino C, Cortese L, et al. Resistive index for kidney evaluation in normal and diseased
cats. J Feline Med Surg 2016; 18(6): 471–475.
12. Evangelista GC, Dornelas LRSM, Cintra CCV, et al. Evaluating feline lower urinary tract disease:
Doppler ultrasound of the kidneys. J Feline Med Surg 2023; 25(1): 1098612X221145477.
13. Evangelista GCL, Viana AGA, Neves MM, et al. Resistivity and pulsatility indexes in feline kidney
disease: a systematic review. Vet Radiol Ultrasound 2022. 63(3): 306–318.
14. Merindol I, Vachon C, Juette T, et al. Benign ureteral obstruction in cats: outcome with medical
management. J Vet Intern Med2023; 37(3): 1047–1058.
15. Vitello G, Bacon J, Earley NF. Ultrasound diagnosis and medical management of presumed
segmental ureteritis in a cat. Vet Rec Case Reports 2022; 10(3): e416.
16. Lemieux C, Vachon C, Beauchamp G, et al. Minimal renal pelvis dilation in cats diagnosed with
benign ureteral obstruction by antegrade pyelography: a retrospective study of 82 cases (2012–
2018). J Feline Med Surg 2021; 23(10): 892–899.
17. Brzozowska M, Marzec M, Czerski A, et al. Unilateral extramural ureteral ectopia in a cat:
ultrasonographic and computed tomography findings. Vet Rec Case Reports 2021; 9(4): e2180.
18. Samii VF, McLoughlin MA, Mattoon JS, et al. Digital fluoroscopic excretory urography, digital
fluoroscopic urethrography, helical computed tomography, and cystoscopy in 24 dogs with
suspected ureteral ectopia. J Vet Intern Med 2004: 18(3): 271–281.
19. Schwarz T, Bommer N, Parys M, et al. Four-dimensional CT excretory urography is an accurate
technique for diagnosis of canine ureteral ectopia. Vet Radiol Ultrasound 2021; 62(2): 190–198.
20. Testault I, Gatel L, Vanel M. Comparison of nonenhanced computed tomography and
ultrasonography for detection of ureteral calculi in cats: a prospective study. J Vet Intern Med 2021;
35(5): 2241–2248.
21. Mehran R and Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at
risk. Kidney Int 2006; 69(Suppl 100): S11–S15.
22. Griffin MA, Culp WTN, Palm CA, et al. Suspected contrast-induced nephropathy in three sequential
patients undergoing computed tomography angiography and transarterial embolization for
nonresectable neoplasia. J Am Vet Med Assoc 2021; 259(10): 1163–1170.
23. Goic JB, Koenigshof AM, McGuire LD, et al. A retrospective evaluation of contrast-induced kidney
injury in dogs (2006–2012). J Vet Emerg Crit Care 2016; 26(5): 713–719.
24. Dennis R, Kirberger RM, Barr F, et al. Handbook of Small Animal Radiological Differential Diagnosis
E-Book. Elsevier Health Sciences, 2010.

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Dialysis for AKI: where are we with advanced renal

medicine?
Serge Chalhoub DVM, Dipl. ACVIM (SAIM)
Søren Boysen DVM, Dipl. ACVECC
Faculty of Veterinary Medicine, University of Calgary

Acknowledgment:
Special thank you to Dr. Chalhoub’s Nephrology Fellowship mentor Dr. Cathy Langston for the
use of her dialysis notes.

Learning objectives:
◆  Explain the process and options for dialysis in cats
◆ Understand which cases are suitable for these therapies
◆ Understand the complications of these procedures
◆ Explain potential future developments in advanced renal
support in small animals

Introduction
Acute kidney injury (AKI) is damage that occurs to the kidneys, but this does not necessarily
lead to a severe drop in glomerular filtration rate (GFR) nor does it lead to azotemia (>70% loss
of function). However, it is important to recognize and to try to identify. All causes of azotemia
(pre-renal, renal, post-renal) can lead to AKI, but not all causes of AKI are associated with acute
azotemia. Unfortunately, even though creatinine is the better marker, it has poor sensitivity, even
with newer reference ranges. It is poorly correlated to GFR in mild cases of renal dysfunction.
However, studies have shown that any change in creatinine from its baseline can not only
indicate AKI (even before changes in urine specific gravity [USG]) but can also estimate
prognosis. This has led to studies looking at survival and prognosis for AKI patients.

In this staging system, patients falling into stages 1–3 during hospitalization were less likely to
survive.

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In this staging system,

patients that were
presented to the hospital
following AKI and acute
azotemia (>1.6 mg/dl in
USA values, or 140 µmol/L
in Canadian values)
were followed closely
based on their outcome
and creatinine changes.
Dogs in level 1 within 2
days were 3 times more
likely to die within 90
days. Those in level 2
within 2, 3, or 7 days were
3 times more likely to die
within 30–90 days. Cats
in level 2 within 3 or 7
days were 3 times more
likely to die within 30
days, and 4 times more
likely to die if placed at this level in 7 days. If placed in level 2 within 2–3 days, they were more
likely to die within 90 days.

Finally, this leads us to the current International Renal Interest Society (IRIS) staging system:

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These staging systems bring about the importance of not ignoring changes in creatinine,
especially over a short period of time. Over a longer period of time, creatinine changes, even if
still within the normal range, should be investigated and not ignored. Unfortunately, GFR studies,
especially in the acute setting, are not realistic.

Acute azotemia (of any type) or AKI that is prolonged, severe, or ongoing will lead to severe AKI,
where GFR is significantly decreased and will lead to significant detrimental changes to the
patient. Once in severe AKI, regardless of cause, the general prognosis for renal recovery is 50%.
This means 50% of patients do not recover. Of the 50% that do, half are left with CKD that should
be manageable. There are exceptions to this rule. Renal recovery depends on identifying the
cause of the damage, removing or administering the appropriate treatment, supporting the
entire body (very important), giving the kidneys time to try to recover, and luck. Renal recovery
may take many days to weeks, and can even go on for up to 6 months (but most of the
recovery happens in the first few weeks).

The earlier AKI is recognized, the better the chance at preventing permanent renal damage.

Management of AKI
The medical management of AKI is discussed in detail in other lectures. Renal replacement
therapies (RRT) are often considered, and it is important to understand when RRT would be
indicated in cats with AKI.

AKI secondary to pre-renal causes (such as dehydration) rarely if ever merits a discussion
on RRT. Urethral obstruction also rarely merits a conversation on RRT as the azotemia and AKI

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usually resolve. Direct renal AKI and post-renal causes, specifically ureteral obstructions, could
be considered reasons to consider RRT; however, the current trend for ureteral obstructions has
been to proceed with the placement of a subcutaneous ureteral bypass as soon as possible
instead of starting RRT, and to relieve the obstruction. Thus, the most common causes to
consider RRT in cats include pyelonephritis and direct renal toxicities such as lilies or ethylene
glycol. However, as discussed later, severe azotemia is not usually the deciding factor: the main
factors include urine production and patient stability.

Why RRT?
In humans, the reasons to proceed with RRT differ from those in veterinary medicine. They
will tend to start RRT much sooner than veterinary patients. The reasons for this difference
in veterinary medicine include financial considerations, complications in cats, training, and
availability.

ANURIA AND OLIGURIA

In cats, RRT is often considered in situations where the patient is anuric or oliguric, or has severe
systemic effects from azotemia. If the decrease in urine volume is due to renal AKI, appropriate
medical management should be used, including ensuring adequate volume expansion prior to
assuming anuria or oliguria. With anuria and oliguria, diuretics have not been shown to improve
outcome. Previously, it was standard procedure to treat with at least one diuretic before
determining whether a veterinary patient should be treated with RRT, but this is no longer the
case.

If optimizing volume status and blood pressure (and potentially the use of diuretics) do not
cause adequate urine production, RRT may be helpful. In addition to absolute anuria (urine
output <0.08 ml/kg/hr) or oliguria (<0.5 ml/kg/hr), relative oliguria is a potential reason for RRT.
Relative oliguria is a condition in which urine output is ≥0.5 ml/kg/hr but does not increase in
response to volume loading. Continued fluid diuresis in this setting will lead to volume overload.
If adequate urine production is not established, RRT should be started before further sequelae
appear.

VOLUME OVERLOAD
Life-threatening volume overload can develop in oligoanuric patients or in patients with a
relative oliguria, and also in patients that are treated aggressively with IV fluids, especially if
there is minimal monitoring of fluid therapy. Pulmonary edema can develop in overhydrated
patients. In the absence of urine production, the body has very limited methods of removing
excess pulmonary water. RRT could also be indicated in this setting, although it is rarely used
simply for fluid overload. Pleural effusion is more effectively treated with thoracocentesis. In a
study by Berent et al. (2018) on the outcome of cats with subcutaneous ureteral bypass devices
placed for ureteral obstruction, the main negative prognostic indicator pre-surgery was if the
patient was in fluid overload.

HYPERKALEMIA
Anuric or oliguric patients, patients with severe renal impairment, are at risk of hyperkalemia.
Emergency treatment (i.e. insulin dextrose, bicarbonate, calcium gluconate) will provide
temporary stabilization. If urine production cannot be established, RRT is indicated.

AZOTEMIA
Progressive azotemia or azotemia that does not resolve is an indication for RRT when combined
with anuria or oliguria and clinical signs related to uremia. However, severe azotemia in itself is

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not the sole deciding factor. Patients that have severe azotemia but that have adequate urine
production, and whose clinical signs of uremia can be managed, may not benefit from RRT.

Patient considerations
RRT involves prolonged and intimate contact with the patient. Therefore, cats with aggressive
temperaments cannot safely undergo RRT unless they can be sedated. In addition, cats need to
weigh at least 2.5 kg, and the reality is that the larger the patient, the better RTT will be in terms
of catheter placement and for the treatment itself. Lastly, the patient’s systolic blood pressure
needs to be maintained above 80 mmHg. If this is not possible, then peritoneal dialysis should
be considered.

Main types of RRT

RRT includes peritoneal dialysis (PD), an intracorporeal technique, and extracorporeal renal
replacement therapies (ERRT), which include intermittent hemodialysis (IHD) and continuous
hemodialysis (CRRT). IHD and CRRT are closely related techniques. In general, IHD is faster and
more efficient at clearing small solutes, such as urea, potassium, and some toxins such as
ethylene glycol. If rapid metabolic control or removal of a large amount of uremic toxins in a
short period of time are desired, IHD is superior.

In the initial treatment of AKI, rapid urea clearance may not be desired. Rapid shifts of
potentially osmotically active agents (i.e. urea, sodium) can lead to dialysis disequilibrium
syndrome (DDS). In people, CRRT was preferred over IHD in hemodynamically unstable patients,
but recent evidence has failed to show superiority of one modality over another. Another factor
in deciding between IHD and CRRT involves the availability and training of personnel. In theory,
CRRT may be easier to apply and proceed with. Lastly, CRRT may be the initial treatment of
choice for unstable cats for the first 48–72 h, then IHD can be considered for shorter and quicker
treatments.

PD is another option. For AKI, it will require 24-hour nursing. Because of complications
associated with PD (catheter occlusion, difficulty in controlling fluid balance, inefficient control
of uremia), it is unlikely that PD would be preferred over CRRT or IHD except in certain situations.
One of those is uroabdomen, in which a peritoneal catheter will be placed and maintained.

The most likely reason for us to choose PD would be a patient that is too hemodynamically
unstable even for CRRT. PD might be an acceptable option for the extraordinarily small patient
(<2 kg) and in situations where machine RRT is not available. A 2009 study (Dorval and Boysen,
2009) identified that PD was effective at helping to stabilize patients with severe azotemia and
urine volume decreases.

Other considerations
Cost is an important consideration. RRT can be quite expensive. Depending on the institution,
costs per treatment may vary from $2000 to $5000, with a rough estimate of $20,000-30,000 for
2 weeks of RRT.

Prognosis is also an important consideration. The survival rate for dogs and cats with AKI
treated with dialysis is approximately 50%. This statistic includes patients that survive the
initial insult but are later euthanized due to failure to recover adequate renal function for
discontinuation of dialysis. The etiology of AKI has a large impact on the outcome. RRT patients
with obstructive and infectious etiologies may have a probability of survival as high as 90%,
whereas some patients with toxic etiologies (particularly ethylene glycol or lily intoxication)
have only a 20% chance of survival.

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Some patients will show definite signs of recovery within a week, and we expect the majority of
patients to show renal recovery within 3–4 weeks. The client should be committed emotionally
and financially to at least 2 weeks of therapy. If there are no signs of renal recovery after 2–3
weeks of treatment, the likelihood of sufficient recovery to allow eventual discontinuation of RRT
fades.

Eatroff et al. (2012) evaluated the long-term outcome of patients with AKI treated with IHD,
and to determine whether renal function, as determined by serum or plasma creatinine
concentrations, is associated with long-term survival. The paper was a retrospective case series
with 20 cats and 35 dogs treated with IHD for AKI that survived longer than 30 days following
the last IHD treatment. Results: For all-cause mortality, the median survival time was 1,823 days
(95% confidence interval: 841, 4,667) for cats and 1,049 days (95% confidence interval: 893, 1,931)
for dogs. When only renal-related causes of death were taken into account, the median survival
time was not reached for cats or dogs. Survival time for all-cause mortality was inversely
associated with the lowest creatinine concentration within the 30 to 90 day period following the
last IHD treatment (p < 0.01 for cats and dogs). Conclusions and Clinical Relevance: Veterinary
patients that are diagnosed with AKI, treated with IHD, and survive greater than 30 days after
the last IHD treatment have a good long-term prognosis and frequently die from causes that
are unrelated to renal impairment.

Complications
Complications of treatment include adverse cardiac and respiratory events associated with
anesthesia for catheter placement, bleeding due to systemic administration of anti-coagulant
during each RRT treatment, thrombosis of the vena cava due to the indwelling dialysis catheter,
DDS (neurologic sequela associated with the first few treatments in cases of severe azotemia),
hypotension, failure of renal recovery, and sudden death. Additional risks of which the owner
must be informed include those associated with the administration of human erythropoiesis-
stimulating agents, and respiratory complications associated with the underlying disease
(acute lung injury or acute respiratory distress syndrome, pulmonary thromboembolism,
pulmonary edema and pleural effusion in cases of oligoanuria).

Important terminology
DIFFUSION
Diffusion is defined as the movement of particles from an area of higher concentration to an
area of lower concentration. Particles in solution have kinetic energy causing movement, and
smaller particles tend to have more movement than larger particles. If two identical solutions
are separated by a membrane that is permeable to a substance, individual particles may
cross the membrane in either direction, and although the individual particles on either side
of the membrane may change, there is no net change in the concentration of particles. If,
however, the concentration on one side is lower, there will be net diffusion from the higher
concentration to the lower concentration. Over time, the two solutions will equilibrate to the
same concentration on both sides. With dialytic therapies (including extracorporeal and
peritoneal forms), the solution on one side of the membrane is the blood, and dialysate is
the solution on the other side of the membrane. By constant replenishment of the dialysate,
a large concentration gradient is maintained and equilibrium is never reached, so diffusive
clearance continues. Extracorporeal therapies have a constant dialysate flow, although the rate
of dialysate flow generally varies dramatically between intermittent and continuous therapies.
Extremely fast dialysate flow rates maximize diffusive clearance, whereas continuous therapies
in a diffusive clearance mode typically use lower dialysate flow rates. PD involves instillation of

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a discrete volume of dialysate that is periodically removed and replaced with fresh dialysate.
During the dwell time, diffusion occurs.

ULTRAFILTRATION
As opposed to diffusion, in which a concentration gradient causes solute movement,
ultrafiltration involves a hydrostatic pressure gradient that causes water movement. By creating
negative pressure on the side opposite the blood compartment, water is “pulled” out of the
blood. This is sometimes desirable, for instance, in fluid overload situations.

OVERVIEW OF ADEQUACY
Prescribing the dose of dialysis requires an ability to predict the adequacy of treatment. The
most commonly used measure of clearance in veterinary hemodialysis is the urea reduction
ratio (URR), which can be calculated by the formula:
(pre-treatment BUN – post-treatment BUN)/pre-treatment BUN.

The most commonly used measure of dialysis dose in humans (which is also used in veterinary
medicine) is Kt/V, a dimensionless unit of measurement that incorporates the dialyzer
clearance, time on dialysis, and volume of distribution.

Vascular access
Temporary catheters are used for acute RRT. Temporary catheters should more precisely be
called non-tunneled, non-cuffed catheters. Temporary catheters are placed via the Seldinger
technique either by ultrasound guidance, fluoroscopy, or blind.

Anti-coagulation
Patients undergoing machine RRT need some form of anti-coagulant to make sure that when
the blood leaves the patient it does not clot in the circuit. Clotting of blood can result in large
blood loss and could be detrimental to the patient. As such, clotting times are closely monitored
to make sure there is enough anti-coagulant. Anti-coagulation may be systemic (e.g. heparin)
or regional (citrate).

When to discontinue RRT

The decision to wean and stop RRT is usually based on either the patient starting to produce
adequate urine, or the patient being more stable, or the initial cause of AKI having resolved.
Most of the time, the decision is based on urine output and azotemia improvement. Sometimes,
acute RRT is replaced with more chronic therapy (e.g. 3 times a week) for multiple weeks until
the patient reaches an acceptable renal function baseline, or in rare cases (and even more rare
in cats), chronic dialysis can be considered. For cats, chronic dialysis is rarely prescribed due to
their higher rate of complications compared with dogs. In this instance, renal transplantation
could be considered.

Conclusions
RRT is an effective management strategy for the AKI cat that is anuric/oliguric or has severe
azotemia affecting its stability. Many factors need to be considered prior to starting RRT,
including the likely prognosis.

References
◆ Berent AC, Weisse CW, Bagley DH, Lamb K. Use of a subcutaneous ureteral bypass device for treatment of
benign ureteral obstruction in cats: 174 ureters in 134 cats (2009–2015). J Am Vet Med Assoc 2018; 253(10):

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 Dublin, 29 June – 2 July

1309–1327.
◆ Dorval P, Boysen SR. Management of acute renal failure in cats using peritoneal dialysis: a retrospective
study of six cases (2003–2007). J Feline Med Surg 2009; 11(2): 107–115.
◆ Eatroff A, Langston CE, Chalhoub S, et al. Long-term outcome of cats and dogs with acute kidney injury
treated with intermittent hemodialysis: 135 cases (1997–2010). J Am Vet Med Assoc 2012; 241(11): 1471–1478.
◆ Langston CE, Poeppel K, Mittleberg E, Eatroff A. Veterinary Dialysis Handbook. 2nd ed. Animal Medical Center;
2014.

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SYMPOSIUM

Urolithiasis: the amazing things nutrition can do

Jody P. Lulich DVM, PhD, DACVIM
Director – Minnesota Urolith Center

In 2022, the Minnesota Urolith Center analyzed over 21,000 urolith submissions from cats.
Of these, 50% were composed of struvite, 37% were calcium oxalate, 7% were urate, and 6%
consisted of a variety of smaller numbers of stones (compound, mixed, silica, cystine, drug
metabolites, etc.). In the Republic of Ireland and Northern Ireland, 68% of feline stones were
composed of struvite, 23% were calcium oxalate, and 2% were urate.

Naturally occurring urolithiasis is affected by many risk factors, some of which are known and
some of which are unknown. Factors known to be associated with feline uroliths include:
◆ breed;
◆ sex;
◆ age;
◆ anatomical and functional abnormalities of the urinary tract;
◆ abnormalities of metabolism;
◆ urinary tract infections; and
◆ diet and its influence on the excretion of calculogenic precursors, urine
concentration, and urine pH.
Each of these factors may have different effects on different types of uroliths. Each contributing
or protective factor may play either a limited or a significant role in the development or
prevention of different types of uroliths. Recognition and avoidance of highly significant dietary
risk factors for urolithiasis may minimize urolith formation and their recurrence.

Therapeutic nutrition is the best strategy for managing struvite diseases

Some veterinarians prefer to remove feline struvite stones surgically. This is often due
to the perception that surgical management is more effective, alleviates clinical signs
quicker, bypasses the need to predict urolith composition, and eliminates the chance of
urethral obstruction as uroliths decrease in size with nutritional dissolution. These are often
misperceptions. Over 100 cats from six published studies had their stones medically dissolved;
some stones dissolved in as little as 6 days and in most other cases struvite stones dissolved
by 2 to 3 weeks of therapy.1–6 The cost for care was much lower than the cost for surgery, and
for many cats, pain medication was not needed. Lastly, no cat developed a urethral obstruction
during stone dissolution. This is in contrast to surgical stone removal, where 15% of patients had
stones left at the time of surgery, placing those cats at risk for urethral obstruction.7

It is interesting that over time, idiopathic cystitis, which was once confined to non-obstructed
lower urinary tract disease in cats, has now become implicated as the overwhelming cause
for urethral obstruction. This is likely related to the fact that most cats with urethral obstruction
are not investigated for the underlying cause of obstruction prior to treatment, resulting in their

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disease being classified as idiopathic as opposed to a specific etiology. This has led to the
application of unproven and potentially ineffective treatments (e.g. prazosin, environmental
enrichment, among others).8 Recent reports indicate that following an initial de-obstruction,
re-obstruction occurs in up to one-third of treated cats in the first 30 days.9 Prevention has
largely been directed at avoiding stress and multimodal enrichment, even though, in controlled
studies, inducing stress in cats with idiopathic cystitis has not been associated with causing
urinary signs or urethral obstruction.10 Clearly, more studies are needed. However, controlled
studies have shown that feeding struvitolytic foods prevented re-obstruction in a small study
of 20 cats followed for 1 year.11 This overwhelmingly positive effect may be related to the
observation that over 90% of urethral plugs submitted for analysis were composed of struvite.
Therefore, nutritional prevention of struvite prevented urethral obstruction.

The role of struvite crystalluria and urinary signs in cats with idiopathic cystitis is controversial.
However, one case report identified profound struvite crystalluria in association with idiopathic
lower urinary signs that resolved with prescription food, returned when the prescription food
was stopped, and resolved again when the prescription food was re-instituted.12 Urinalyses and
ultrasonography of the bladder revealed that the absence of crystalluria during consumption
of the therapeutic food correlated with the absence of clinical signs. The research and clinical
studies provide applicable and practical evidence that the use of therapeutic diets to control
struvite is the primary strategy for the control of feline struvite stones, urethral plugs and
crystalluria-associated lower urinary tract disease.

What these studies did not provide was an indication as to how long therapeutic diets should
be fed. Data from the Minnesota Urolith Center indicated that of over 10,000 struvite submissions
in 2022, 87% were from cats 9 years old or younger, an indication that struvite likely decreases
as cats age (Figure 1).

Figure 1. Prevalence of cats with struvite uroliths by age

The role of diet and calcium oxalate stones is complex

Nutritional risk factors have been identified in cats with calcium oxalate stones (e.g. over-
acidification of urine, increased urinary excretion and concentration of calcium, feeding dry
foods, vitamin B6 deficiency, higher protein consumption, strategies resulting in increased
vitamin D) but it is unknown whether these associations are primarily responsible for stone

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formation. This is because most studies were retrospective and not controlled, measured
risk indirectly (e.g. relative supersaturation) instead of directly (e.g. calcium oxalate stone
formation), studied risk in healthy young cats that were not at risk for calcium oxalate stones
and were disease free at the time of evaluation, or evaluated diet ingredients as if their quantity
was controlled when in actuality the association to calcium oxalate stones was a diet effect
and not an individual nutrient response. However, hypercalciuria has been a consistent finding
in most cats with calcium oxalate stones; the origin of this metabolic risk factor is unknown, but
approximately one-third of cats are hypercalcemic. The cause of calcium oxalate stones in
animals with a normal serum calcium concentration is poorly understood.

Would better nutritional control of kidney disease minimize feline uroliths?

In humans, calcium oxalate stones typically form over mineralized sections of the renal pelvis
that are exposed to the urinary space. We have observed similar findings in cats.13 This may
indicate that the origin of feline calcium oxalate is not just a reflection of the composition of the
urine but initiated by ectopic mineralization of the kidney. It is unknown whether these changes
result from normal aging, genetic mutations, serum–tissue calcium perturbations or nutritional
excesses. Maintaining renal health may delay and prevent renal mineralization, and nutritional
changes to reduce urine concentration appear to be logical approaches to reduce calcium
oxalate stone formation and recurrence.

References
1. Osborne CA, Lulich JP, Kruger JM, et al. Medical dissolution of feline struvite urocystoliths.
J Am Vet Med Assoc 1990; 196: 1051–1063.
2. Houston DM, Rinkardt NE and Hilton J. Evaluation of the efficacy of a commercial diet in the
dissolution of feline struvite bladder uroliths. Vet Ther 2004; 5: 187–201.
3. Houston DM, Weese HE, Evason MD, et al. A diet with a struvite relative supersaturation less than
1 is effective in dissolving struvite stones in vivo. Br J Nutr 2011; 106: S90–S92.
4. Lulich JP, Kruger JM, Macleay JM, et al. Efficacy of two commercially available, low-magnesium,
urine-acidifying dry foods for the dissolution of struvite uroliths in cats. J Am Vet Med Assoc 2013;
243: 1147–1153.
5. Tefft KM, Byron JK, Hostnik ET, et al. Effect of a struvite dissolution diet in cats with naturally occurring
struvite urolithiasis. J Feline Med Surg 2021; 23: 269–277.
6. Torres-Henderson C, Bunker J, Contreras ET, et al. Use of Purina Pro Plan Veterinary Diet UR Urinary
St/Ox to dissolve struvite cystoliths. Top Companion Anim Med 2017; 32: 49–54.
7. Lulich JP, Osborne C, Polzin D, et al. Incomplete removal of canine and feline urocystoliths by
cystotomy. J Vet Intern Med 1993; 7: 124.
8. Hanson KR, Rudloff E, Yuan L. et. al. Effects of prazosin on feline recurrent urethral obstruction.
J Feline Med Surg 2021; 23: 1176–1182.
9. Beeston D, Humm K, Church DB, et al. Occurrence and clinical management of urethral obstruction
in male cats under primary veterinary care in the United Kingdom in 2016. J Vet Intern Med 2022;
36: 599–608.
10. Stella J, Croney C and Buffington T. Effects of stressors on the behavior and physiology of domestic
cats. Appl Anim Behav Sci 2013; 143: 157–163.
11. Osborne CA, Caywood DD, Johnston GR, et al. Perineal urethrostomy versus dietary management
in prevention of recurrent lower urinary tract disease. J Small Anim Pract 1991; 32: 296–305.
12. Bell ET and Lulich JP. Marked struvite crystalluria and its association with lower urinary tract signs
in a cat with idiopathic cystitis. Aust Vet J 2015; 93: 332–335.
13. Alford A, Furrow E, Borofsky M, et al. Animal models of naturally occurring stone disease.
Nat Rev Urol 2020; 17: 691–705.

#ISFMRocksDublin 53
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 Dublin, 29 June – 2 July

SYMPOSIUM

The role of diet in preventing and managing

urolithiasis
Cecilia Villaverde BVSc, PhD, DACVIM (Nutrition), DECVCN
Consultant in Clinical Nutrition for Expert Pet Nutrition and the Veterinary Information
Network (VIN)

Summary:
Feline urolithiasis is relatively common, and dietary management is crucial for prevention (and,
in some cases, dissolution) of this condition. There are several aspects to consider in order to
choose the best dietary management depending on the stone type, and this lecture will discuss
these, including strategies to dilute the urine.

Introduction
The most common uroliths in cats are struvite (magnesium ammonium phosphate) and
calcium oxalate, with purine-based uroliths in a distant third place. Dietary management,
together with medical and other types of management (e.g., surgical), is an important part
of the treatment and prevention of these calculi.1
For a urolith to form, the urine must be supersaturated in the precursors, which must be in
a specific chemical form to bond and crystallise. Other aspects, such as the presence and
concentration of inhibitors, urinary pH, and urine specific gravity (USG), will also affect the
process. All of these aspects need to be considered in order to assess dietary management.

Goals of nutritional management

◆  ecrease USG to both decrease the concentration of precursors and increase the
D
frequency of urination, therefore reducing the chance of crystallisation.
◆ Decrease the urinary concentration of precursors and, if possible, increase the
urinary concentration of inhibitors.
◆ Promote a urinary pH that promotes solubility of the specific urolith.

Nutritional assessment
Before choosing the best feeding plan (including the diet, allowance, and feeding method),
a nutritional assessment2 is required, including a detailed diet history. This will give us enough
information to ensure that the diet is complete and balanced, considers any comorbidities
or sensitivities of the patient, and is palatable. Identifying the diet at diagnostics will also help
us decide how aggressive dietary management needs to be. In addition, some therapeutic
diets might have already been attempted and might be therefore ruled out for the case. The
assessment will also help us decide on the daily allowance to maintain (or reach, if needed) an
ideal body condition score.

Role of urine dilution

Independently of the feeding plan, promoting a dilute urine is potentially helpful with all uroliths,
although there is a lack of studies. It is a common recommendation to aim for a USG <1.030.3
There are several ways we can promote a low USG:

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◆  sing a wet diet or adding water to the food (dry or wet)

U
There are no prospective clinical trials on the effect of increasing water intake
alone (independent of mineral content, urinary pH and other dietary factors) on
urolithiasis treatment and prevention. One epidemiological study4 found that high-
moisture diets were associated with a lower risk of calcium oxalate urolithiasis;
however, this association was not seen in struvite-forming cats and this study of
course has the limitation of being retrospective.

One study5 fed the same diet, varying in moisture content, to healthy cats for
three weeks in a crossover design. The four treatments were achieved by adding
water to a dry cat food to obtain a moisture content of 6.3%, 25.4%, 53.2% or 73.3%.
Even though the cats fed the 73.3% moisture diet drank less water than the other
groups, their overall water intake (coming from both diet and drinking water) was
higher. The cats fed the highest-moisture diet also urinated more and their urine
had a lower USG (1.036 for the 73.3% diet vs 1.052–1.054 for the others), which was
likely due to the higher total water intake. These cats also had a lower relative
supersaturation (RSS) for calcium oxalate, which could represent a lower risk of
urolithiasis formation. However, the cats in the study were non-stone formers,
therefore conclusions cannot be drawn regarding the effect of this strategy on
urolithiasis.

As water is cheap and very safe, adding water to the diet to decrease USG is very
useful (feeding wet food is easier, but also requires a higher budget). I like to
aim for a moisture content of 80% or more. For wet foods with around 70% water
content, this means adding water at a 1:1 (v:v) ratio. For dry foods at around 10%
moisture, this means adding water at a 5:1 (v:v) ratio (grossly, two cups of water
per cup of dry food).

◆  sing a salt-enriched diet

U
There are some studies in healthy cats suggesting that salt-enriched diets,
supplemented with sodium6 or potassium7 chloride, can promote diuresis by
stimulating thirst. This is very useful in cats that cannot or will not eat wet food.
The effect can be less potent than adding water and might not be sustained over
time3. Urinary diets with added salt have sodium levels of about 2–3.5 g/1000 kcal
(as a comparison, most maintenance diets provide around 1 g/1000 kcal).

◆ Promoting (drinking) water intake

Some strategies include providing multiple water stations, using moving water
sources (although one small study8 that looked at this did not see differences in
water consumption, it seems that there are individual preferences) or flavouring
the water.

Two studies using a nutrient-flavoured water resulted in increased water intake

and decreases in USG in healthy cats9,10, which is helpful, although this has not been
specifically looked at in stone formers yet.

Diet choice
STRUVITE
Diets with a RSS for struvite below 1 have been shown to dissolve struvite uroliths in cats.11
Antibiotic treatment will be needed in cases associated with urinary tract infections. Overall,
diets for urolith dissolution provide moderate amounts of the precursors (magnesium,

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phosphate, protein), promote low USG and acidify the urine, the latter being the most critical
characteristic. As such, these diets must be fed exclusively, as the use of treats or other foods
can alter the urinary pH and interfere with the diet. Dietary dissolution is preferred to surgery, as
it is less invasive,3 but it can fail if the uroliths are not struvite or are of mixed composition.
Preventative diets have similar strategies; currently, most diets are formulated for both
dissolution and prevention in cats (with some exceptions). Treats might be allowed in these
circumstances (maximum 10% of the daily calories).

A diet history is essential to know whether the patient will require a preventative veterinary
diet in the long term or not. In fact, most diets for struvite dissolution and prevention are also
formulated/marketed for calcium oxalate prevention (“dual” diets). For example, in a young
cat fed a dry diet, with only one episode of urolithiasis, it might be sufficient to switch to a
maintenance wet diet from a reputable manufacturer and work on promoting water intake.
In other cases, a veterinary urinary diet will be required for prevention as well. In case of
comorbidities, some brands have multifunction diets or veterinary diets with secondary urinary
claims; both types include diets for obesity management, which is desired as overweight has
been associated with urinary disease.12

CALCIUM OXALATE
Calcium oxalate uroliths cannot be dissolved with dietary approaches; the main role of diet
is in prevention. However, there is a lack of research backing up specific strategies to prevent
calcium oxalate urolithiasis in cats. While there are some studies supporting a positive effect
of certain diets on calcium oxalate RSS5,13,14, there are no data yet on their effects on rates of
recurrence. Currently, the main efforts are geared towards promoting a dilute USG throughout
the day. Other strategies for these diets include moderate (but not deficient) calcium and
vitamin D, low-oxalate ingredients, and low precursors of oxalate (e.g., vitamin C). High-oxalate
ingredients to avoid include potatoes, spinach and other vegetables.

Some studies suggest that some protein sources rich in certain amino acids, such as
hydroxyproline, can increase endogenous oxalate synthesis and urinary excretion.15,16 Therefore,
it is recommended to avoid chewy treats in these cats, as well as vitamin C-containing
supplements. Unfortunately, there is no easy way to check the amino acid profile of feline diets.
The protein content of these diets is usually average (not low, but high protein levels are
uncommon). In theory, high-protein diets (of animal origin) can promote more acidification
as they are rich in sulphur, which can in turn promote higher excretion of calcium. However,
epidemiological data4 found that higher-protein diets had a protective effect in cats, which
could be due to an effect increasing the urine volume, but interpretation of these studies is
difficult and separating out effects between diets is extremely complex. It is also notable that
protein content and urinary pH do not always necessarily correlate. At this point there are no
recommendations on the best protein (or fat or carbohydrate) content for calcium oxalate
prevention.

Commercial diets for calcium oxalate prevention are mainly the same as for struvite; therefore,
they will promote acidification. In the past, renal diets (which alkalinise the urine) were
recommended, and they can still be tried if “regular” urinary diets do not help to minimise
recurrence, although the effect of pH on calcium oxalate is much less clear than for struvite,17
and these stones can form at any physiological urinary pH. A common recommendation is to at
least avoid “excessive” acidification.3

The best choice of diet will depend on the cat’s diet and clinical picture at diagnosis (was the

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diet dry or wet, from a reputable manufacturer or not, high in oxalate ingredients, what was
the cat’s USG, etc.). In some cases, a veterinary urinary diet might not be needed. If the rate of
recurrence does not decrease, changing to a different urinary diet product/brand and focusing
on USG is indicated. A renal diet (promoting alkalinisation) can be tried as well, but clinical
evidence is also limited with this strategy.

Supplementation with potassium citrate is potentially helpful as citrate is considered a calcium

oxalate inhibitor and can mildly alkalinise the urine.

Commercial vs homemade?
Commercial diets are preferred, especially for struvite dissolution and prevention, as it is not
possible to predict the urinary pH achieved by homemade diets with any precision. Moreover,
homemade diets (especially recipes from books and the internet) can have multiple nutritional
inadequacies.18 If a homemade diet is desired, it is recommended to consult a board-certified
veterinary nutritionist.

Daily allowance and feeding method

Free feeding is not recommended unless the cat is good at self-regulating its intake (which
is uncommon). The daily allowance can be calculated using formulas or following the label
instructions, but both have a high error rate, and adjustments should be made to promote an
ideal body condition score and stable weight. This is best done with a good diet history to figure
out the ideal daily calorie intake.

In overweight patients, a caloric restriction plan is indicated, using a therapeutic weight-loss

diet, if needed, a multifunction obesity + urinary diet, or a weight-loss diet with a secondary
urinary claim; ideally, a wet diet should be chosen (wet diets can also potentially help with
satiety19).

If treats are given (in prevention cases), they can provide a maximum of 10% of the daily caloric
allowance, with 90% from the main balanced diet.

With regard to the feeding method, multiple small meals per day are better than one or two big
meals, to maximise the effect of the diet on the urinary environment, including pH and USG.

Follow-up
Follow-up should include a nutritional assessment (including weight, body condition and
muscle condition score, food intake, etc.), urinalysis and imaging. Measurement of the USG
is especially important to decide whether the strategies need to be adjusted to achieve the
desired urine dilution.

References
1. Queau Y. Nutritional management of urolithiasis. Vet Clin N Am Small Anim Pract 2019; 49(2):
175–186.
2. Freeman L, Becvarova I, Cave N, et al. WSAVA nutritional assessment guidelines. J Small Anim Pract
2011; 52(7): 385–396.
3. Lulich JP, Berent AC, Adams LG, et al. ACVIM small animal consensus recommendations on the
treatment and prevention of uroliths in dogs and cats. J Vet Intern Med 2016; 30(5): 1564–1574.
4. Lekcharoensuk C, Osborne CA, Lulich JP, et al. Association between dietary factors and calcium
oxalate and magnesium ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc 2001;

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219(9): 1228–1237.
5. Buckley CMF, Hawthorne A, Colyer A, et al. Effect of dietary water intake on urinary output, specific
gravity and relative supersaturation for calcium oxalate and struvite in the cat. Br J Nutr 2011;
106(Suppl 1): S128–S130.
6. Queau Y, Bijsmans ES, Feugier A, Biourge VC. Increasing dietary sodium chloride promotes urine
dilution and decreases struvite and calcium oxalate relative supersaturation in healthy dogs and
cats. J Anim Physiol Anim Nutr (Berl) 2020; 104(5): 1524–1530.
7. Bijsmans E, Quéau Y, Biourge V. Increasing dietary potassium chloride promotes urine dilution and
decreases calcium oxalate relative supersaturation in healthy dogs and cats. Animals 2021; 11(6):
1809.
8. Pachel C, Neilson J. Comparison of feline water consumption between still and flowing water
sources: A pilot study. J Vet Behav 2010; 5(3): 130–133.
9. Zanghi BM, Wils-Plotz E, Degeer S, et al. Effects of a nutrient-enriched water with and without poultry
flavoring on water intake, urine specific gravity, and urine output in healthy domestic cats fed a dry
kibble diet. Am J Vet Res 2018; 79(11): 1150–1159.
10. Zanghi BM, Gerheart L, Gardner CL. Effects of a nutrient-enriched water on water intake and indices
of hydration in healthy domestic cats fed a dry kibble diet. Am J Vet Res 2018; 79(7): 733–744.
11. Houston DM, Weese HE, Evason MD, et al. A diet with a struvite relative supersaturation less than 1 is
effective in dissolving struvite stones in vivo. Br J Nutr 2011; 106(Suppl 1): S90–S92.
12. Chiang CF, Villaverde C, Chang WC, et al. Prevalence, risk factors, and disease associations of
overweight and obesity in cats that visited the Veterinary Medical Teaching Hospital at the
University of California, Davis from January 2006 to December 2015. Top Companion Anim Med
2022; 47: 100620.
13. Markwell P, Smith BHE, McCarthy KP. A non-invasive method for assessing the effect of diet on
urinary calcium oxalate and struvite relative supersaturation in the cat. Anim Tech 1999; 50(2):
61–67.
14. Bartges JW, Kirk CA, Cox SK, et al. Influence of acidifying or alkalinizing diets on bone mineral density
and urine relative supersaturation with calcium oxalate and struvite in healthy cats. Am J Vet Res
2013; 74(10): 1347–1352.
15. Dijcker JC, Hagen-Plantinga EA, Thomas DG, et al. The effect of dietary hydroxyproline and dietary
oxalate on urinary oxalate excretion in cats. J Anim Sci 2014; 92(2): 577–584.
16. Mendonça FS, Pedreira RS, Loureiro BA, et al. Hydroxyproline and starch consumption and urinary
supersaturation with calcium oxalate in cats. Anim Feed Sci Technol 2018; 246: 72–81.
17. Bijsmans ES, Quéau Y, Feugier A, et al. The effect of urine acidification on calcium oxalate relative
supersaturation in cats. J Anim Physiol Anim Nutr (Berl) 2021; 105(3): 579–586.
18. Wilson SA, Villaverde C, Fascetti AJ, et al. Evaluation of the nutritional adequacy of recipes for home-
prepared maintenance diets for cats. J Am Vet Med Assoc 2019; 254(10): 1172–1179.
19. Wei A, Fascetti AJ, Villaverde C, et al. Effect of water content in a canned food on voluntary food
intake and body weight in cats. Am J Vet Res 2011; 72(7): 918–923.

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 RENAL & URINARY

FOR LIFELONG CARE

GIVE YOUR CLIENTS THE ESSENTIAL NUTRITION

FOR LIFELONG RENAL AND URINARY CARE
Learning to care for pets with renal and urinary issues
can be challenging. Give your clients the confidence to choose
science-based nutrition with the specific nutrients that work
to help support their pet’s condition and quality of life
 Dublin, 29 June – 2 July

Hypercalcaemia in cats and its role in urolithiasis

Myles McKenna MVB, MVetSci, MVetMed, DACVIM (SAIM), DECVIM-CA
Director of the Global Clinical Consultation Service for Zoetis Diagnostics

Sponsored by
Summary:
Hypercalcaemia is a known a risk factor for developing calcium oxalate
urolithiasis, and 35% of cats diagnosed with calcium oxalate urolithiasis are
hypercalcaemic. Because of the high prevalence of hypercalcaemia in our
feline patients with calcium oxalate uroliths, it is important to routinely screen these patients
for hypercalcaemia and to be confident with the diagnostic and therapeutic approach to the
hypercalcaemic cat.

Calcium homeostasis
Calcium plays a vital role in many physiological processes. including neuromuscular
transmission, muscle contraction, coagulation and intracellular signalling. Calcium
homeostasis is primarily mediated by the effects of three hormones (parathyroid hormone
(PTH), calcitriol and calcitonin) on three organ systems (the kidneys, the gastrointestinal tract
and bone).

PTH is a calcium-increasing hormone, produced by chief cells in the parathyroid glands. It

acts on the nephron to increase calcium reabsorption in the distal convoluted tubule and
to decrease phosphate reabsorption from the proximal convoluted tubule; the end result is
reduced urinary excretion of calcium and increased urinary excretion of phosphate. Its other
main action in the kidneys is to increase the activation of vitamin D. PTH also stimulates bone
resorption by increasing osteoclast numbers in bone, and by increasing osteoclast activity; the
end result is increased release of both calcium and phosphate from bone.

Calcitriol (1,25-dihydroxycholecalciferol) is the active form of vitamin D, activated by the

enzyme 1-α-hydroxylase in the kidneys. It acts on the gastrointestinal tract to increase the
absorption of both calcium and phosphate, and also increases the reabsorption of both
calcium and phosphate in the renal tubules.

Calcitonin is a calcium-lowering hormone, produced by C cells in the thyroid glands. It appears

to play only a minor role in calcium homeostasis in companion animals compared with its role
in humans. Its primary action is to inhibit the osteoclastic resorption of bone.

Measurement of calcium
Approximately 99% of total body calcium exists in the form of hydroxyapatite crystals in bone. In
the blood, calcium exists in three fractions:

Protein-bound calcium: approximately 40% of total calcium is bound to plasma proteins,

especially albumin.

Ionised calcium: makes up approximately 50% of total calcium in normal cats; this is the
biologically active form of calcium that circulates in the form of free calcium ions (not bound to
proteins).
Complexed calcium: makes up less than 10% of total calcium in normal cats; calcium can be

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complexed with anions such as bicarbonate, phosphate or lactate.

Clinical signs of hypercalcaemia

Unfortunately, the clinical signs of feline hypercalcaemia are usually vague and non-specific,
to the extent that they may sometimes not be noted by owners. The four main body systems
affected are the neuromuscular system, the gastrointestinal system, the cardiovascular system
and the urinary system.

NEUROMUSCULAR SYSTEM
Lethargy and/or systemic weakness: hypercalcaemia decreases neuron membrane
permeability to sodium ions, thereby decreasing neuronal excitability and causing muscular
hypotonicity. Muscle tone may be decreased and reflexes may be sluggish. Lethargy may also
result from direct effects of hypercalcaemia on the central nervous system.

GASTROINTESTINAL SYSTEM
Vomiting, anorexia and/or constipation may be noted as a result of decreased contractility of
smooth muscle in the gastrointestinal tract.

CARDIOVASCULAR SYSTEM
Severe hypercalcaemia inhibits myocardial depolarisation, leading to arrhythmias.
Cardiovascular effects may include a prolonged PR interval, a short QT interval, widened QRS
complexes and/or bradycardia.

URINARY SYSTEM
Polyuria and polydipsia (PUPD): the primary mechanism by which hypercalcaemia causes
PUPD is via induction of a reversible nephrogenic diabetes insipidus; hypercalcaemia induces
the degradation of aquaporin 2 channels (the target of antidiuretic hormone) in the collecting
ducts. Hypercalcaemia may also lead to kidney injury by reducing the glomerular filtration rate
(GFR) (by causing direct renal vasoconstriction) and by causing mineralisation of renal tissue
and subsequent tubulointerstitial injury. Finally, hypercalcaemia has been associated with the
formation of calcium oxalate uroliths.

The role of hypercalcaemia in urolithiasis:

In one study of cats with calcium oxalate uroliths, hypercalcaemia was observed in 35% of
cases.1 Hypercalcaemia results in hypercalciuria, which is a significant risk factor for calcium
oxalate urolith formation. It is important to note that hypercalciuria may not always be a
consequence of hypercalcaemia, and it can also be a consequence of the administration of
loop diuretics, glucocorticoids, urinary acidifiers and vitamin D or C.

Differential diagnoses
There is considerable inter-study variation in the reported relative prevalence of the various
causes of feline hypercalcaemia.2–4 This is probably due to the different methodologies used
to define hypercalcaemia (e.g. elevated ionised calcium vs total calcium), differences in the
extent of diagnostic work-ups performed between hospitals, and possibly also geographical
variation. However, in almost all studies there are three causes that are reported as the most
common causes of feline hypercalcaemia:

1. Idiopathic hypercalcaemia
Idiopathic hypercalcaemia is considered one of the most common causes of feline
hypercalcaemia. As the name suggests, the underlying cause is unknown, although a genetic

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cause, and potentially dietary factors, are suspected. It may be seen in cats of any age, and
longhaired cats appear to be overrepresented. The magnitude of hypercalcaemia in affected
cases is usually mild to moderate.

2. Renal disease
Ionised hypercalcaemia is observed in 10–30% of cats with chronic kidney disease. Furthermore,
13% of hypercalcaemic cats in a recent study were found to have acute kidney injury.2 The
relationship between hypercalcaemia and renal dysfunction is complex: renal dysfunction
can cause hypercalcaemia due to reduced urinary excretion of calcium and increased bone
resorption, while hypercalcaemia can cause decreased GFR and tubulointerstitial injury; thus, it
can be difficult to ascertain whether the hypercalcaemia caused the renal dysfunction or vice
versa. Renal diets have also been associated with the development of hypercalcaemia in some
cats. Ionised hypercalcaemia has been found to develop after the introduction of moderate
dietary phosphate restriction in 19% of healthy cats,5 and 13% of cats with chronic kidney disease
developed a new ionised hypercalcaemia when fed a more markedly phosphate-restricted
diet.6 The lower dietary phosphate in renal diets, and the subsequent higher dietary calcium-
to-phosphorus ratio, could lead to enhanced intestinal calcium absorption and subsequent
hypercalcaemia.

3. Malignancy
Malignancy is reportedly found in 10–25% of all hypercalcaemic cats,2,3 where the production of
PTH-related protein and cytokines such as interleukin-1 and TGF-β stimulate bone resorption.
Specific feline neoplasias associated with hypercalcaemia include squamous cell carcinoma,
lymphoma and, less commonly, multiple myeloma, bronchial carcinoma and sarcomas.

UNCOMMON CAUSES OF FELINE HYPERCALCAEMIA

◆  ypervitaminosis D: typically occurs as a result of excessive dietary
H
supplementation of vitamin D, but also can be due to the ingestion of jessamine
(a house plant), certain rodenticides or psoriasis creams.
◆ Granulomatous disease: macrophages can synthesise calcitriol from calcidiol
without negative feedback regulation. Specific causes of granulomatous
inflammation include feline infectious peritonitis, mycobacterial disease, fungal
disease, Toxoplasma gondii and filamentous bacteria (Actinomyces/Nocardia).
◆ Hypoadrenocorticism: very uncommon in cats; may cause increased renal
calcium reabsorption and increased bone resorption.
◆ Primary hyperparathyroidism: due to increased production of PTH by one or more
of the parathyroid glands. This is rare and usually a disease of older cats (median
age 15.5 years).
◆ Iatrogenic: calcium-containing oral phosphate binders, or intravenous
administration of calcium gluconate, could contribute to the development of
hypercalcaemia.

Diagnostic approach to the hypercalcaemic cat

INITIAL STEPS
Step 1: Rule out a spurious result. Ensure there is no EDTA contamination of the sample; EDTA
will chelate calcium and artificially decrease its concentration. Lipaemic serum may result in
spurious calcium elevation.

Step 2: Consider the patient’s age; both total and ionised calcium concentrations are higher

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in kittens than in adult cats and can remain increased until 12 months of age, due to calcium
mobilisation for skeletal growth.

Step 3: Confirm that the hypercalcaemia is persistent. A transient hypercalcaemia may result
from haemoconcentration secondary to dehydration, or from relative increases in intravascular
protein concentrations (especially albumin).

Step 4: Measure ionised calcium. It is not possible to predict ionised calcium concentrations
accurately from total calcium: total calcium is inaccurate in predicting ionised calcium in
cats in 40% of cases. Correction formulae for total calcium have been developed but are
not considered an accurate substitute for ionised calcium measurement. If sending out the
sample to an external laboratory, the sample must be transported on ice to prevent lactic acid
formation (a decrease in pH will falsely increase the ionised calcium concentration). A cat with
an ionised calcium >1.40 mmol/l is generally considered to be hypercalcaemic.

Step 5: Full biochemical analysis is recommended, ensuring that the panel includes phosphate,
albumin and renal values. If available, acid–base analysis should also be performed to assess
for acidosis (which may cause a false increase in ionised calcium) or alkalosis (which may
cause a false decrease in ionised calcium). Concurrent haematology and urinalysis are
recommended in all cases to fully assess the cat’s general health status and renal function.

SUBSEQUENT STEPS
Once ionised hypercalcaemia has been confirmed to be a true and persistent finding,
additional tests are recommended:

1. Measuring PTH and parathyroid hormone-related peptide (PTH-rp), with or without vitamin
D metabolites:
◆ PTH assay: the body’s normal response to hypercalcaemia should be to suppress
PTH production. Documenting a PTH concentration that is increased or even in the
upper two-thirds of the reference interval is abnormal in a hypercalcaemic patient,
and is consistent with primary hyperparathyroidism. Samples must be shipped on
ice to the laboratory as PTH is heat labile.
◆ PTH-rp assay: PTH-rp should be measured if malignancy is suspected, and many
laboratories will run this test concurrently with the PTH assay. It is important to note
that PTH-rp is not always elevated in cats with neoplasia, and therefore a normal
PTH-rp concentration does not rule out neoplasia.
◆ Vitamin D metabolites: typically both calcitriol (1,25-dihydroxycholecalciferol, the
metabolically active form of vitamin D) and calcidiol (the primary circulating form
of vitamin D) are measured. Samples collected for measurement of vitamin D
metabolites must be protected from light, to inhibit degradation.7

2. Diagnostic imaging: thoracic and abdominal imaging should be considered to assess for the
presence of neoplasia or granulomatous disease. Imaging may also detect the consequences
of hypercalcaemia, such as soft tissue mineralisation (especially in the kidneys and gastric
wall) or the presence of calcium oxalate uroliths. Ultrasound examination of the neck is also
recommended in cats with a high clinical suspicion of primary hyperparathyroidism.

Management of hypercalcaemia
The management approach depends on the severity of hypercalcaemia, the rate of
development (acute vs chronic) and the phosphate concentration. Where concurrent

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hyperphosphataemia and hypercalcaemia are present, a high serum calcium-phosphorus

product may result. If the calcium-phosphate product exceeds ~70 mg2/dl2 or ~5.6 mmol2/
l2 there is a high risk of calcium phosphate precipitation occurring in soft tissues, termed
metastatic calcification. This is particularly deleterious to the kidneys, where calcification may
lead to acute kidney injury, and thus emergency intervention is required.

In general, definitive treatment of hypercalcaemia requires that the underlying cause be

addressed (if an underlying cause can be identified). However, until the cause is identified, or in
cases of idiopathic hypercalcaemia, treatment should target the hypercalcaemia directly.

RAPIDLY ACTING TREATMENTS

◆ Intravenous fluid therapy: ideally with a calcium-free fluid such as 0.9% NaCl,
this should be initiated to promote diuresis and to correct any dehydration/
hypovolaemia.
◆ Furosemide: once normal hydration is achieved, furosemide can be administered
to increase renal calcium excretion.
◆ Calcitonin: although calcitonin is rapidly acting, its effects are very short lived,
requiring repeated administration multiple times a day; therefore, it is rarely used
in practice in the management of feline hypercalcaemia.

LESS RAPIDLY ACTING TREATMENTS

◆  lucocorticoids: these reduce bone resorption, decrease intestinal absorption
G
of calcium and increase renal excretion of calcium. As steroids could affect the
results of future diagnostic tests, their administration should be avoided if the
underlying cause of hypercalcaemia has not yet been identified.
◆ Bisphosphonates: these reduce the number of osteoclasts and their activity levels,
resulting in reduced bone resorption. Options include pamidronate (an intravenous
infusion, most suitable for acute settings) or alendronate (administered orally
once a week, most suitable for chronic settings).8 In human medicine, zoledronate
has been shown to be superior to pamidronate in both efficacy and duration of
response, but data on its efficacy in cats are lacking.
◆ Dietary therapy: high-fibre diets bind intestinal calcium, thus reducing its
absorption. Wet diets promote diuresis and generally have a lower calcium
content than dry diets. Diets formulated for the prevention of calcium oxalate
urolithiasis may also be considered, as these are restricted in calcium.

References
1. Midkiff AM, Chew DJ, Randolph JF, et al. Idiopathic hypercalcemia in cats. J Vet Intern Med 2000;
14(6): 619–626. https://doi.org/10.1111/j.1939-1676.2000.tb02286.x
2. Broughton SE, O’Neill DG, Syme HM, et al. Ionized hypercalcemia in 238 cats from a referral hospital
population (2009-2019). J Vet Intern Med 2023; 37(1): 80–91. https://doi.org/10.1111/jvim.16627
3. Coady M, Fletcher DJ, Goggs R. Severity of ionized hypercalcemia and hypocalcemia is associated
with etiology in dogs and cats. Front Vet Sci 2019; 6: 276. https://doi.org/10.3389/fvets.2019.00276
4. Savary KC, Price GS, Vaden SL. Hypercalcemia in cats: a retrospective study of 71 cases (1991–1997).
J Vet Intern Med 2000; 14(2): 184–189. https://doi.org/10.1111/j.1939-1676.2000.tb02234.x
5. Geddes RF, Biourge V, Chang Y, et al. The effect of moderate dietary protein and phosphate
restriction on calcium-phosphate homeostasis in healthy older cats. J Vet Intern Med 2016; 30(5):
1690–1702. https://doi.org/10.1111/jvim.14563
6. Barber PJ, Rawlings JM, Markwell PJ, et al. Effect of dietary phosphate restriction on renal

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secondary hyperparathyroidism in the cat. J Small Anim Pract 1999; 40(2): 62–70. https://doi.
org/10.1111/j.1748-5827.1999.tb03039.x
7. Finch NC. Hypercalcaemia in cats: the complexities of calcium regulation and associated clinical
challenges. J Feline Med Surg 2016; 18(5): 387–399. https://doi.org/10.1177/1098612X16643248
8. Hardy BT, de Brito Galvao JF, Green TA, et al. Treatment of ionized hypercalcemia in 12 cats (2006–
2008) using PO-administered alendronate. J Vet Intern Med 2015; 29(1): 200–206. https://doi.
org/10.1111/jvim.12507

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Diagnosis of feline urolithiasis: those pesky little

rocks, how do I find them?
Serge Chalhoub DVM, Dipl. ACVIM (SAIM)
Søren Boysen DVM, Dipl. ACVECC
Faculty of Veterinary Medicine, University of Calgary

Learning objectives:
◆ Understand how to prioritize diagnostics
◆ Understand all the options in general practice
◆ Discuss more advanced referral techniques to diagnose urolithiasis

Imaging to be covered in detail in other lectures

Introduction
Urolithiasis can be challenging to diagnose: not only in terms of identifying the presence of
stones, but also determining the type of stone. For the purposes of this lecture we will focus on
lower urolithiasis. Upper urinary tract stones (in the kidneys and ureters) tend to be calcium
oxalate (CaOx) in composition, whereas in the lower urinary tract (bladder and urethra) the
most common stone types are struvite and CaOx. In North America, the prevalence of stone
type has switched to more struvite than CaOx, and the cause is unclear.

Urolithiasis refers to bladder stones composed of one or more crystallized minerals and an
organic matrix. These stones may contain a nidus (area of initial growth) and a shell (outer
portion that may have a different composition than the nidus). A urolith is defined by its type
if >70% of one mineral is predominant (<70%: mixed). It is extremely important to note that
crystalluria ≠ urolith (stones are always abnormal but crystals may be clinically unimportant).
Crystals usually form before stones but sometimes are not present. Therefore, a lack of crystals
on urinalysis does not eliminate the possibility of stones. In cats, the majority of stones are
struvite or oxalate. Persians/Himalayans: oxalates. Siamese: urates.

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Diagnosis
Clinical signs may include hematuria, pollakiuria, stranguria, dysuria, incontinence (urge
incontinence, urinary tract infection (UTI)), and visible stones in voided urine. In general, these
clinical signs are grouped into a syndrome known as feline lower urinary tract disease (FLUTD).
Thus, any cat (male or female) with FLUTD symptoms should have a urinalysis and medical
imaging performed. However, many cats with urolithiasis have no clinical signs whatsoever.
In terms of FLUTD, stones represent anywhere from 12% to 22% of causes of FLUTD. 20% of cats
presenting with urethral obstruction will have a stone as its cause. Stones are found either by
accident (medical imaging for another reason, suspicious urinalysis) or when cats develop a
urethral obstruction.

Physical examination changes may include a thickened bladder wall (cystitis), palpable
cystoliths, urethral stones at the tip of the penis (more often when the cat presents for urethral
obstruction), a large bladder (if obstructed especially), and other signs attributed to urethral
obstruction.

Labwork changes are usually non-specific but may give you clues to what type of stones you
have. For instance, for cats with urate stones and portosystemic shunts (PSS) you may see
chemistry panel abnormalities that are consistent with with PSS. However, urate stones are rare
in cats (although they can be seen in Siamese cats). These cats often do not have visible PSS, or
when they do they are not clinical for PSS.

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A complete blood count is usually within normal limits (WNL) (leukocytosis if pyelonephritis and
sometimes UTI), biochemistry is usually WNL (again, look for hints of other diseases such as
hypercalcemia). Cats with idiopathic hypercalcemia are at risk for forming CaOx stones.

Urinalysis: urine pH may sometimes help determine the stone type in cats, but this is not as
reliable as in dogs. In theory, a lower pH occurs with CaOx stones and a higher pH with struvites,
but this is not reliable. In dogs, the most common cause of struvite stones are UTIs whereas in
cats, struvite stones are most often sterile. Therefore, the pH may not be changed. In addition,
an active sediment may be present if the stones cause bladder inflammation. An active
sediment does not always indicate a UTI, which means that not all cats with white blood cells in
the urine need antibiotics!

Imaging: plain film radiographs (radiopaque stones in the bladder or urethra: don’t forget to
include the urethra in abdominal radiographs). Abdominal radiographs are a great place to
start for bladder and urethral stones, especially given that in cats the most common stone
types are radiopaque. However, small stones may be missed, and a colon full of gas, fluid, or
fecal material may make it difficult to find the stones. A double-contrast cystogram may be
useful when urate stones are suspected.

Be careful, as radiographs can miss bladder stones. In a study of cats presenting with urethral
obstruction, many cats that had stones as a cause were missed by radiographs.

Abdominal ultrasound: can be very sensitive for the detection of bladder stones but is poorly
sensitive for urethral stones. However, for bladder stones there are fewer clues as to what the
stone type is vs radiographs. Be careful as the colon can sometimes mimic a bladder stone!
Sometimes small bladder stones may mimic debris in the bladder and thus be difficult to
identify.

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Stone analysis: it is very important to submit stones each time cystotomy is performed or
stones are voided. This will help you guide therapy and prevention, and it also helps identify
trends in stone types.

Struvites
◆ Stone composition: magnesium ammonium phosphate.
◆  ats: NOT associated with UTIs. Risk factors include alkaline urine, highly
C
concentrated urine (dehydration, or just because they are cats and they
don’t drink a lot), and dietary factors. Struvite crystalluria may be normal in
concentrated urine.

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❖ Struvites slightly more prevalent than CaOx

❖ Treatment generally surgery or dietary dissolution
❖ Prevention based on ↑ water consumption (fresh water, more water bowls,
canned diet, wet kibble), urinary management diets, weight loss.

Calcium oxalate
◆  isk factors: stones form due to CaOx crystal supersaturation. Hypercalciuria
R
can occur because of numerous factors – diet, vitamin D, vitamin C, Cushing’s
disease, drugs (glucocorticoids, loop diuretics), hypercalcemia (idiopathic in cats,
hyperparathyroidism), neoplasia (PTHrp). Hyperoxaluria can also be the cause
(leafy vegetables, nuts) but this is debated. Obesity is known to be a predisposing
factor. Breed predispositions also exist.
◆ Diagnosis: urinalysis (acidic pH, CaOx crystals), urine culture (secondary UTI from
the irritation from the stones), radiographs (radiopaque stones).
❖ UTIs are possible with these stones. They are not what causes the stones to form
as struvites.
◆ Treatment: CaOx stones DO NOT dissolve. Treatment requires surgery, voiding ±
retrograde urohydropropulsion, lithotripsy, antibiotics for UTI.
◆ Prevention: ↑ water in diet. Canned food, wet kibble, urinary management diets
(RC Urinary SO, Hill’s C/D, so pH-neutral diets to prevent the pH from swinging to an
acidic pH).
❖ If diet and water fail, you can dd potassium citrate (forms soluble salts with Ca
and ↑ urine pH) or thiazide diuretics (natriuresis in distal tubules promotes Ca
reabsorption).
❖ Monitor via urinalysis and radiographs q3–6 months. Monitor electrolytes if on
thiazide diuretics (hypercalcemia, hypokalemia, dehydration).
❖ There is unfortunately a high rate of recurrence with these stones. It is important
to try your best to prevent them. So initially this means increased water intake,
± special diet, weight loss. If that doesn’t work then consider adding potassium
citrate and then thiazide diuretics.

Urates
◆  isk factors: urates are not usually produced because they are usually converted
R
to allantoin before being excreted into the urine: endogenous + dietary purines →
xanthine → uric acid → allantoin.
❖ Defects in this enzyme pathway in the liver can lead to accumulation of uric

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acid. For instance, with PSS these pathways are not intact, so urates are formed.
❖ Dalmatians have their own reason to produce these stones (defect in hepatic
uric acid transport into hepatocytes, males >>> females). Bulldogs and Siamese
cats also produce more urates.
◆ Diagnosis: clinical signs (lower UTI signs, obstruction in males, and hepatic
encephalopathy). Urate crystalluria. Radiolucent stones (double-contrast
cystogram or ultrasonography needed to see them). Screen for PSS.
◆ Treatment: treat PSS if present. Surgery, hydropropulsion, lithotripsy.

These are the most common stones you will encounter in private practice. There are other
stones that can be formed.

Conclusions
For general practice, a combination of history, clinical findings, and laboratory analysis
including urinalysis will help narrow the differentials. Abdominal ultrasonography and
abdominal radiographs are essential for the diagnosis of urolithiasis (crystals in urine should
not be the only criteria for diagnosis). It is important to know the limitations of each imaging
modality.

References
◆ Labato MA. Lower urinary tract urolithiasis - feline. In: Ettinger S, Feldman E, Cote E (Eds). Textbook of
Veterinary Internal Medicine. 8th ed. eBook. Available from: Elsevier eBooks+. Elsevier - OHCE, 2017.

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SYMPOSIUM

From acute and visible to chronic and hidden: the

benefits of early management for cats’ kidneys
Roswitha Dorsch Dr. med. vet., Dr. habil., Dipl. ECVIM (Internal Medicine)
Thierry Francey Dr. med. vet., DACVIM (SAIM), DECVIM-CA (Internal Medicine)
Teresa Rehme DVM

The Clinic of Small Animal Medicine, LMU Munich, is offering the “Cat’Xpert consultations: a
special healthcare service for cats” in cooperation with Boehringer Ingelheim, and a special
urinary tract consultation for examination, diagnostics and treatment of upper and lower
urinary tract diseases in cats. Special healthcare is essential for our pets’ wellbeing, their quality
of life and, as a result, a long and healthy life.

Regular healthcare appointments can facilitate health maintenance, prevent disease

development and furthermore detect existing health problems at an early stage and lead to a
better quality of life.1 In addition, prevention is generally less costly and more successful than
disease management.1 Nevertheless, owners are often unaware of the importance of regular
preventive healthcare appointments.2 Preventive health care includes primary prevention
(avoiding the development of disease, e.g. vaccination, parasite prophylaxis), secondary
prevention (early detection of disease to avoid the progression of disease, e.g. treatment of
hypertension) and tertiary prevention (reducing the impact of a disease on wellbeing).

Fortunately, over the past few decades, cats’ life expectancy has increased in Europe and the
United States, and this is leading to a bigger population of senior and geriatric cats.3,4 However,
older animals are presented less often for preventive healthcare appointments in comparison
to younger ones, even though age-related chronic diseases occur more commonly with
increasing age2 Studies have shown that physical and biochemical abnormalities are common
in apparently healthy older cats,4,5 which emphasises the importance of regular health checks
to detect and manage chronic diseases at an early stage.6–8

The recommended routine screening of cats is dependent on age:1

◆ <7 years: annual health check including weight check and physical examination
◆ 7–10 years (mature): annual health check including weight check and physical
examination plus blood pressure, complete blood count (CBC), serum chemistry,
urinalysis and thyroxine (T4)
◆ 10–15 years (senior): health check every 6 months including weight check and
physical examination plus blood pressure, CBC, serum chemistry, urinalysis and T4
◆ >15 years (super senior): health check every 4 months including weight check and
physical examination plus blood pressure, CBC, serum chemistry, urinalysis and
T4.

Chronic kidney disease (CKD) is among the most common diseases of cats, and particularly
affects the elderly cat population. Prevalence increases with age, with prevalence rates of 28%

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and 31% in cats older than 12 and 15 years, respectively. Rates were also high in younger cats
when non-azotaemic cats with CKD (CKD IRIS stage 1) were included. Most cats with stage 1
CKD and many cats with stage 2 CKD appear clinically healthy, and can only be diagnosed
with the help of serum chemistry including symmetric dimethylarginine (SDMA), urinalysis and/
or diagnostic imaging. Serum chemistry in CKD stage 1 cats can reveal persistently elevated
SDMA and/or creatinine. Urinalysis adds valuable information, since many cats drink only small
amounts of water and produce concentrated urine with a specific gravity >1.035. Loss of urine-
concentrating ability is one of the first laboratory abnormalities in CKD. In cats with diseases
that do not affect the glomerular filtration rate but affect other functions of the kidney (e.g.
glomerulopathies), proteinuria might be the only laboratory abnormality. Glomerulopathies are
uncommon in cats, but the prevalence increases in areas endemic for vector-borne infectious
diseases, such as those caused by Leishmania infantum or Dirofilaria immitis.

Blood pressure measurement is an important part of preventive health care, particularly in the
mature cat population. Around 20% of cats older than 10 years of age are hypertensive, most
commonly due to CKD or hyperthyroidism. Many cats with hypertension are azotaemic due to
renal disease, but early non-azotaemic CKD can also be associated with hypertension.

Ultrasound examination of the urinary tract adds valuable information and helps to confirm
the diagnosis of CKD. It is routinely indicated in certain breeds of cats that are predisposed to
hereditary diseases such as polycystic kidney disease. Structural abnormalities can precede
loss of kidney function. In some cats, ultrasonographic abnormalities of the kidneys are
incidental findings (e.g. nephrolithiasis, partial unilateral ureteral obstruction, renal infarcts and
poor corticomedullary differentiation) that require further work-up. Serial monitoring of renal
function and/or imaging is indicated to determine whether the disease is stable or progressive
and is leading to loss of functioning nephrons.

References
1. Ray M, Carney HC, Boynton B, et al. 2021 AAFP Feline Senior Care Guidelines. J Feline Med Surg 2021;
23: 613–638.
2. Eschle S, Hartmann K, Bergmann M. Compliance of dog and cat owners in preventive health care.
Tierarztl Prax Ausg K Kleintiere Heimtiere 2020; 48: 349–360.
3. Gunn-Moore D. Considering older cats. J Small Anim Pract 2006; 47: 430–431.
4. Paepe D, Verjans G, Duchateau L, et al. Routine health screening: findings in apparently healthy
middle-aged and old cats. J Feline Med Surg 2013; 15: 8–19.
5. O’Neill DG, Church DB, McGreevy PD, et al. Longevity and mortality of cats attending primary care
veterinary practices in England. J Feline Med Surg 2015; 17: 125–133.
6. Elliott J, Rawlings JM, Markwell PJ, et al. Survival of cats with naturally occurring chronic renal failure:
effect of dietary management. J Small Anim Pract 2000; 41: 235–242.
7. Elliott J and Watson A. Chronic kidney disease: staging and management. In: Bonagura J and Kirk R
(eds). Kirk’s current veterinary therapy XIV. Philadelphia, PA: Elsevier Saunders, 2008, pp 883–892.
8. Syme HM, Markwell PJ, Pfeiffer D, et al. Survival of cats with naturally occurring chronic renal failure is
related to severity of proteinuria. J Vet Intern Med 2006; 20: 528–535.

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 Dublin, 29 June – 2 July

Feline ureteral obstructions – diagnosis and

management
Dr. Allyson Berent DVM, DACVIM (SAIM)
The Animal Medical Center
New York, USA

Introduction
Ureteral disease can create a significant dilemma in our feline patients. The relatively common
incidence of ureteral disease, combined with the invasiveness and morbidity associated with
traditional surgical techniques, makes the investigation of minimally invasive alternatives
appealing. Interventional radiologic (IR) and interventional endoscopic (IE) techniques, such
as ureteropyelography, percutaneous nephrostomy tube placement, ureteral stenting, and the
use of a subcutaneous ureteral bypass (SUB) device, have aided tremendously in the ability
to simultaneously diagnose and treat ureteral obstructions in a minimally invasive manner
with long-term ureteral protection from future obstruction, while concurrently lowering the
morbidity and mortality when compared with traditional surgical techniques (ureterotomy,
neoureterocystostomy, ureteronephrectomy, or renal transplantation). Endourologic procedures
are considered the standard of care in human adult and pediatric surgery and are currently
being applied in veterinary patients regularly. This talk will focus on the diagnosis, management,
and treatment of cats with ureteral obstructions from various causes and will review data from
what has been reported in the past, the more recent interventional modalities, and the future
options on the horizon. Data from over 500 consecutive cases treated interventionally will be
reported and discussed.

Human ureteral intervention

In human urology, the development and improvements in ureteroscopy, ureteral stenting,
extracorporeal shockwave lithotripsy (ESWL), laser lithotripsy, laparoscopy, and percutaneous
nephroureterolithotomy (PCNUL) have nearly eradicated the need for open ureteral surgery
for stone disease, strictures, trauma, and neoplasia. In humans, ureteroliths <5 mm have a
98% chance of spontaneous passage with medical management alone. For larger stones, or
those that do not pass spontaneously, ESWL is effective in 50–81% of cases and ureteroscopy
has a near 100% success rate when Holmium:YAG laser lithotripsy is used. PCNUL has also been
successful for large proximal impacted ureteral stones.

Ureteral stenting was first introduced in 1967 for evaluation of human patients with malignant
ureteral obstructions. Stents are still widely used to treat both benign and malignant obstructive
disease, but are more commonly considered a temporary fixation rather than a permanent
alternative for benign disease. Ureteral stenting for stone disease is typically done after
ureteroscopy for post-scoping spasm and edema, and in children a stent is routinely placed
prior to ureteroscopy to allow passive ureteral dilation in anticipation of immediate ureteral
decompression, spontaneous stone passage, or the ease of ESWL. When stents are used in
humans they typically are either removed within 2 weeks after a permanent fixation procedure
has been employed (i.e. ureteroscopy and laser lithotripsy or ESWL) or left in place long term
with scheduled stent exchanges every 3–6 months to prevent stent encrustation and ureteral
re-occlusion.

The use of a subcutaneous nephrovesicular ureteral bypass device has been reported in

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approximately 50 human patients. The first reports were focused on the use of this device
for malignant neoplasia where reconstructive surgery or ureteral stenting had failed or was
not possible. More recently, this device has been reported for use after renal transplantation-
induced ureteral strictures and in cases where stenting or surgery is not a feasible option due to
patient stability, abnormal anatomy, or irreparable damage. So far, the literature would suggest
that the use of this device has been met with few complications and long-term patency rates
are considered excellent in the human literature.

Feline ureteral obstructions

Feline ureteral obstructions occur most commonly secondary to ureterolithiasis (~70%),
ureteral stenosis (~30%), and trigonal neoplasia (<3%). Additional causes can be accidental
ureteral ligation during surgery, ureteral trauma, ureteral edema following ureteral surgery,
and secondary to purulent material associated with pyelonephritis/pyonephrosis. Obstruction
can result in life-threatening azotemia, particularly when presenting bilaterally (~33%) or in
cats with concurrent pre-existing renal insufficiency/failure (>80–95%). More than 92% of feline
ureteroliths have been documented to be composed of calcium oxalate, which is a trend from
decades prior. In a recent study the presence of dried solidified blood stones was seen in a
small handful of cats as well (~8–10%). This means that these stones will not dissolve medically
and either need to pass spontaneously, remain in place, or be removed.

If medical management fails to encourage stone passage (traditionally: intravenous fluid

therapy, mannitol constant rate infusion, and alpha-adrenergic blockade for 24–48 hours) then
immediate resolution of the obstruction should be considered. The physiologic response the
body has to a ureteral obstruction is very complex. If there is a complete ureteral obstruction,
decompression of the renal pelvis becomes imperative to preserve renal function to the
ipsilateral kidney. Studies in dogs have shown that after a complete ureteral obstruction the
renal blood flow diminishes to 40% of normal over 24 hours, and to 20% of normal by 2 weeks.
This increase in pressure generated by the ureteral obstruction is transmitted to the entire
nephron, resulting in a precipitous decrease in the glomerular filtration rate (GFR). After 7, 14,
and 40 days, the GFR was found to permanently decline by 35%, 54%, and 100%, respectively.
These numbers were in a dog model with no evidence of pre-existing azotemia, chronic
interstitial nephritis, or chronic obstruction/nephroureterolithiasis, so extrapolation of a worse
outcome might be expected in our feline patients. Interestingly, in contrast to the irreversibility
of a complete obstruction, partial obstructions result in less severe/dramatic destruction and
more return to function after the obstruction is relieved, and most cats are partially obstructed.
In one dog model it was found that the GFR returned to normal after a partial obstruction was
present for 4 weeks. Knowing that many of our feline patients are partially obstructed for weeks
to months with concurrent renal compromise (chronic kidney disease [CKD]), aggressive
management and obstruction relief is recommended. Discouraging fixation due to chronicity
is not recommended, as improvement in renal function is routinely documented after fixation,
regardless of chronicity, degree of azotemia, size of the renal pelvis, or the ultrasonographic
appearance of the renal parenchyma. Nearly all kidneys benefit from decompression.

In cases of ureteral obstruction secondary to a ureterolith, some patients can be managed

medically with supportive care until a ureterolith passes. It is important to realize that over
30% of feline ureteral obstructions are reported to be associated with strictures (±stones),
where medical management and traditional surgery are not expected to be highly effective.
If medical management has been attempted then decompression should be considered to
avoid permanent damage. For cases that are oliguric, anuric, hyperkalemic, or overhydrated,
then immediate intervention or intermittent hemodialysis therapy should be considered for

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immediate stabilization. The main interventional options considered in the author’s practice
include nephrostomy tube placement, ureteral stenting, and the placement of a SUB device.
Decompression of the renal pelvis will decrease the hydrostatic pressure and stop the
permanent damage that is occurring to the renal parenchyma, allowing immediate renal
recovery.

Traditional surgery: The PAST

In the past, traditional intervention for ureterolithiasis has been accomplished surgically via
ureterotomy, neoureterocystostomy, ureteronephrectomy, and renal transplantation. A paper in
2005 reported two retrospective studies in a large number of cats. There were high procedure-
associated complications (>30%) and peri-operative mortality rates (21%) documented.
This study was from two universities that have extensive expertise with ureteral surgery. The
morbidity and mortality may be higher in environments where operating microscopes and
microsurgical experience are not as readily available. Many of the associated complications
with surgery are due to site edema, recurrence of obstruction from stones that pass from
the renal pelvis to the surgery site, stricture formation, and ureterotomy-associated or
nephrostomy tube-associated urine leakage. In one study, over 10% of cats that survived their
complications required a second surgical procedure during the same visit, and 30% of those
cats were then subsequently euthanized or died from serial complications associated with their
ureteral stones/surgeries. Of the cats that had long-term imaging follow-up, 40% had evidence
of ureteral stone recurrence, 85% of which had evidence of ipsilateral nephrolithiasis at the time
of the first ureteral surgery. The number of animals that did not have stone recurrence with prior
nephrolithiasis was not evident in that study. Chronic kidney disease was found to be common
at the time of diagnosis (>75% were azotemic with a unilateral obstruction), and persistent
azotemia was commonly seen after a successful surgery (>50–80% of cats). Though, with all
of the surgical concerns, the survival rates were dramatically higher for cats that had surgical
intervention performed when compared with those treated with medical management alone
(33% mortality prior to discharge; 87% failure to improve renal function). Medical management
has been shown to be effective in a minority of cases (7.7–13%) but should be considered prior
to any intervention, particularly for small stones (1–2 mm) in the distal ureter. This large series
was in cats in which surgery was performed or attempted, hence excluding patients that were
not considered good surgical candidates. Over the past 8 years the number of stones found in
the ureter and kidney have been much greater (median of 4 stones per ureter in a 2014 study
of 79 ureters), with over 60% of patients in that study not being considered good traditional
surgical candidates due to the number of stones, location of stones, presence of a proximal
stricture, etc. In the same study, over 86% of cats had evidence of ipsilateral nephrolithiasis,
making the risk of ureteral re-obstruction higher than that of previous studies.

Feline ureteral strictures were reported in 10 cats in 2011, and have since been reported in a
larger series of 79 feline cases of ureteral obstruction and in a series of 22 cats with circumcaval
ureters. Ureteral strictures can occur for various reasons, and are most commonly seen
secondary to a previous surgery of the ureter for stone disease, from a stone getting embedded
in the ureteral mucosa, as a congenital abnormality, associated with idiopathic renal
hematuria, as an idiopathic process, and possibly associated with a circumcaval (retrocaval)
ureter. Most ureteral strictures were found to occur in the very proximal ureter (<2.5 cm from the
renal pelvis), in which traditional surgical approaches were difficult, requiring re-implantation
with renal descensus and psoas cystopexy or a ureteral resection and anastomosis. With a cat
ureter being 0.4 mm in luminal diameter, this can be a very challenging situation, particularly in
a potentially unstable patient.

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Finding an alternative that results in immediate decompression and stabilization of the kidney,
while concurrently allowing patency to be established quickly and effectively, for any cause of
a ureteral obstruction (stone, numerous stones, stricture, debris, blood clots, purulent debris,
blood stones, etc.), which can decrease post-operative complications, mortality, and long-
term re-obstruction would be ideal. The use of IR techniques, either minimally invasively or with
surgical assistance, has aided in circumventing the complications of ureteral surgery (peri-
operative leakage, stricture, re-obstruction, long anesthesia times, worsening renal function,
etc.), particularly in cases that are not considered good surgical candidates. IR techniques have
allowed successful and efficient stabilization of the patient regardless of the cause of ureteral
obstruction, while decreasing renal pelvic pressure and stopping the cycle of pressure-induced
nephron damage and loss.

Percutaneous nephrostomy tube placement

Ureteral obstructions secondary to ureteroliths or malignancy can result in severe
hydronephrosis and/or life-threatening azotemia when presenting bilaterally or in animals
with concurrent renal insufficiency/failure. Fixation procedures used to be relatively prolonged
and complicated in these debilitated patients, especially in facilities where expertise in treating
feline ureteral obstruction is not as vast. One possibility is to place a nephrostomy tube to
quickly relieve the obstruction and determine whether adequate renal function remains before
prolonged anesthesia for ureteral surgery, ureteral stenting or SUB device placement can be
performed. A locking-loop pigtail catheter is recommended (5 or 6 Fr) to decrease the risk of
inadvertent tube removal or urine leakage. Historically, nephrostomy tubes have been met
with much resistance due to the high risk of post-placement complications (>50%). These
complications were usually due to premature removal or dislodgement, urine leakage, or poor
drainage. With the advent of sturdy, multi-fenestrated tubes that form a loop that will lock
the catheter in the renal pelvis, these complications seem to have declined dramatically. One
study in 2012 reported on the use of the locking-loop pigtail catheter in 20 patients. One patient
developed leakage into the subcutaneous space and the remaining catheters worked without
complication. These catheters were deemed to be safe, effective and well tolerated in both
dogs and cats. Catheter placement is typically done percutaneously in dogs using ultrasound
and fluoroscopic guidance, and surgically assisted with fluoroscopy in cats. With the advent of
SUBs and the speed at which they are placed, the speaker no longer places nephrostomy tubes
externalized for the treatment of feline ureteral obstructions.

Ureteral stenting
Ureteral stenting has been performed for a variety of disorders in both dogs and cats (over
400 cases to date). The goal of using a feline double pigtail ureteral stent (Infiniti Medical, LLC)
is to divert urine from the renal pelvis into the urinary bladder during a ureteral obstruction
(ureterolithiasis, obstructive neoplasia, ureteral stricture/stenosis, dried solidified blood clots,
or severe obstructive pyelonephritis or pyonephrosis). Stents also encourage passive ureteral
dilation (for ureteral stenosis/strictures or future ureteroscopy, ESWL, etc.). The double pigtail
stent, which is the stent of choice in cats, is completely intracorporeal, and can remain in place
long term, maintaining ureteral patency and passive ureteral dilation (a 0.4 mm ureter was
documented to dilate to 1.5–2.0 mm within 3–7 days in over 90% of cats). Each loop of the pigtail
is curled (one in the bladder and one in the renal pelvis), allowing direct urinary diversion from
the kidney to the urinary bladder, around the stones, or through the stricture.

In most cats (male and female) the procedure is done using fluoroscopy and surgical
assistance using nephrostomy needle access in an antegrade manner, though it can be
attempted endoscopically in female cats, with a reported 20% success rate (compared with

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over 95% success with antegrade surgical assistance). This procedure requires special training
and experience using wires, catheters, and stents, and is not recommended in all patients
with a ureteral obstruction. The learning curve is very steep and the procedure should not be
performed until the operator is comfortable with the risks that are associated. If the operator
is not comfortable placing a locking-loop pigtail catheter for a nephrostomy tube then this
procedure should not be attempted because if stent placement is not successful the ureter
will experience severe edema and spasm and will be acutely obstructed, requiring another
mechanism of drainage.

A study in 2014 evaluating 69 feline patients (79 ureters) with ureteral obstructions treated
with a ureteral stent had a 96% placement success; 14% were bilaterally obstructed, 28%
were associated with strictures (± concurrent ureteroliths), and 85% of cases had concurrent
nephroliths. The median number of stones in the obstructed ureter was 4. Approximately one-
third of cats had documentation of a urinary tract infection prior to stent placement, and 30% of
cats had at least 1 positive culture in their lifetime post-stent placement. The median creatinine
was 5.3 mg/dL pre-operatively and 2.1 mg/dL post-stent placement. The peri-operative
mortality after surgery was 7.5%, with no death associated with a ureteral obstruction or the
procedure. This compares to a 21% mortality rate with traditional surgery. The most common
long-term (>1 month) complications after ureteral stent placement were dysuria (38%, but
persistent only in 2%), chronic hematuria (18%), stent occlusion (19%), stent migration (6%), and
ureteritis/mucosal proliferation (4%). The dysuria typically resolved with short-term steroid
therapy. A ureteral stent exchange with either a bigger stent or a SUB device was needed in 27%
of cats for either occlusion or migration. This complication was most commonly associated with
ureteral strictures (over 50% of strictured ureters experienced re-occlusion), or an occlusion at
a previous ureterotomy site. Ureters remained patent long-term in most cats, with the longest
stent in place and functional for over 5 years. The median survival time was 498 days. The
median survival time when the cause of death was renal was over 1250 days, with only 21% of
cats dying of suspected CKD. Another study evaluating pre-operative prognostic factors for
short- and long-term survival and renal recovery did not identify any clinical, biochemical, or
imaging findings to suggest overall survival in patients. Due to the high rate of dysuria, since
2010 the author prefers the SUB device to ureteral stenting in cats.

Interventional options: The PRESENT

THE SUBCUTANEOUS URETERAL BYPASS DEVICE (SUB)
The SUB device (Norfolk Vet Products) was initially created for feline patients as an alternative
to ureteral stents when either a stricture was present (higher rate of stent occlusion [>50%]) or
a stent was unable to be successfully placed due to excessive stones, a very narrow lumen, or
patient stability. Over the course of the following 10 years, the long-term outcomes documented
with the SUB device, as far as long-term complications and patient comfort (primarily stent
occlusion and recurrent dysuria), were found to be superior to those of stents. Due to these
findings, the trend has moved toward using the SUB device as a primary treatment option
for feline ureteral obstructions in the author’s practice. It is very important to understand the
risks and benefits of traditional surgery, ureteral stenting, and SUB device placement prior to
deciding the best treatment option for your patient.

The placement of nephrostomy catheters in veterinary medicine was described above, and has
been met with excellent success when the appropriate device is used. The biggest limitation
is the externalized drainage, requiring careful management and hospitalization to prevent
infection and dislodgement. The development of an indwelling SUB device using a combination
locking-loop nephrostomy catheter and cystostomy catheter connected to a subcutaneous

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shunting port has been highly successful for the treatment of feline ureteral obstructions with all
causes (stones, strictures, tumors, and obstructive pyelonephritis). In humans, a similar device
has been shown to reduce complications associated with externalized nephrostomy tubes and
ureteral stents, and to improve quality of life.

The post-operative management of the SUB device is similar to that described below for all
cases of ureteral obstruction. Care should be taken to avoid fluid overload as post-obstructive
diuresis is common. This is accomplished by the use of an esophagostomy tube for nutrition
and enteral hydration post-operatively in all cases. Deep abdominal palpation is discouraged
in these patients. Following discharge, patients are monitored similarly to all feline cases of
ureteral obstructions, including serial ultrasounds and urine cultures. Urine is generally sampled
from the SUB device access port using a special non-coring Huber needle, during which time
the device can be flushed using sterile saline under ultrasound guidance. This is recommended
every 3 months for 2 years and then every 6 months thereafter, to help ensure and maintain
patency. A SUB Flush Kit is utilized (Norfolk Vet Products) as this provides flushing material called
tetra-EDTA which can prevention both mineralization and infection. During a SUB flush this
material is then slowly infused into the device using ultrasound guidance to ensure the renal
pelvis is not overfilled. A cystocentesis should be discouraged in these patients if possible.

The use of the feline SUB device has recently been described in various peer-reviewed formats.
To date, in the author’s practice, over 650 of these devices have been placed over a 14-year
period with excellent short and long-term success. In a recent report of 174 SUB devices placed
in 134 cats, the median creatinine was 6.6 mg/dL pre-operatively and 2.6 mg/dL post-SUB
placement. The peri-operative mortality after surgery was 6.2%. Urinary tract infections were
present in 25% of cats pre-operatively and only 8% chronically. This compares well to traditional
surgery (21% peri-operative mortality) and ureteral stenting (7.5%). Peri-operative complications
include leakage (at the port site) (<5%), kinking of the catheters (or failure of the renal function
to recover; <5%), and blockage of the system with either blood clots, debris, purulent material, or
mineralization (24%; 12.5% needed to be exchanged due to the development of a patent ureter).
Dysuria is uncommonly seen in cats with a SUB device (8%) compared with ureteral stents
(38%). More recently, the SUB device has been modified to a 3.0 version, which removes the
nephrostomy and cystostomy catheters from traversing the body wall, and this has decreased
device kinking dramatically. In addition, these modifications have decreased surgical times to
approximately 35–45 minutes for a unilateral SUB device and 45–55 minutes for a bilateral SUB
device. The SUB device is considered a functional option and is the author’s treatment of choice
in cats with ureteral obstructions of most causes. With the introduction of tetra-EDTA for flushing
of the device the percentage of mineralization and chronic infections has now been shown to
decrease and this lecture will go over these data.

Post-operative management
Feline patients can have substantial post-obstructive diuresis after relieving a ureteral
obstruction, necessitating a large quantity of fluids to maintain hydration. This should be
carefully monitored for and managed. The leading complication post-operatively, regardless
of treatment elected, was the development of congestive heart failure associated with fluid
overload. Most of these patients had a normal echocardiogram prior to their procedure, but
the volume of fluids required to maintain their hydration was overloading their heart. Because
of this finding the author has advocated using a combination of a maintenance rate of enteral
hydration (unflavored electrolyte solution, e.g. Pedialyte) through the use of an esophagostomy
tube (placed at the time of ureteral decompression); a maintenance rate of a low-sodium
maintenance fluid (0.45% NaCl +2.5% dextrose); and the remainder of fluids necessary as a

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replacement fluid. This has been found to lower the sodium load and decrease the risk of fluid
overload in the author’s experience. Once the creatinine level reaches a plateau and the patient
can be discharged, they are monitored at 1 and 4 weeks post-operatively (with blood work and
a urinary tract ultrasound) and then every 3 months thereafter for blood work, focal urinary
tract ultrasound, urinalysis, urine culture, and a SUB flush using tetra-EDTA.

The FUTURE
The SUB device has nearly replaced the use of ureteral stents in cats in the author’s practice
due to the ease of placement, fast anesthesia times (35–60 minutes), lower mortality rates
(6%), and lower short- and long-term complication rates (dysuria 8% versus 38%; re-occlusion
6% versus 27%; chronic infections 8% versus 3%). The issues still experienced with these devices
are the fact that occlusion can still occur, and development of mechanisms to prevent this,
such as serial flushing with tetra-EDTA, redesigning the catheter size and shape, and using
different materials, is underway. As more of these devices are being used, future changes to
perfect the design will occur.

Conclusion
The feline ureter is a frustrating area to gain access to for both diagnosis and treatment
of disease. With the recent advances in veterinary interventional endourologic techniques,
diagnosis and treatment have become less invasive, more effective, and safer. Proper training
and the availability of specialized equipment are needed to help these procedures become
more available in the future. With these new devices in veterinary medicine, we are hoping
to find better alternatives for these problematic conditions, as we have seen in our human
counterparts. These techniques offer an alternative option to traditional surgery, and as the
data are published the veterinary community can decide if, and when, using interventional
techniques will replaced traditional surgery, as is the case in human medicine.

References
Available upon request.

Conflict of Interest statement

The author is a consultant for Infiniti Medical, LLC and Norfolk Vet Products.

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SUBs 101 – Technical aspects and troubleshooting

Laura Owen BVSc(Hons), CertSAS, AFHEA, DipECVS, MRCVS
European and RCVS Specialist in Small Animal Surgery
Associate Professor in Small Animal Surgery, University of Cambridge, UK

Summary
A step-by-step journey through the placement of a subcutaneous ureteral bypass (SUB)
device, to improve understanding of the implant for those medically managing these cases
and giving practical hints and tips on how to avoid/minimise errors for surgeons wishing to
place them.

Surgical procedures involving the placement of an artificial implant are associated with
higher rates of intra- and postoperative complications compared with other clean surgical
procedures. Specialist equipment is required and there is a substantial learning curve to
conquer in order to ensure correct placement of the device and to minimise complication
rates. In this lecture, we will look at the technical aspects of placement of a subcutaneous
ureteral bypass (SUB) device, including specific case challenges, as well as how to troubleshoot
common intra- or postoperative issues.

Preparation
EQUIPMENT:
◆  pacious, sterile operating theatre – additional personnel and equipment are
S
required to perform this procedure and must be able to fit into the operating
theatre. An appropriate surgical table compatible for use with a fluoroscopy unit
must be available.
◆ Fluoroscopy (or ultrasonography + radiography) – placement of a SUB is best
performed using fluoroscopic guidance, which provides direct visualisation of
the position of catheters/wires etc. in real time. Placement of the device has
been reported using ultrasonography and radiography as an alternative,1,2 but
significant ultrasonographic expertise is required to interpret these images
correctly and ensure appropriate placement. Sterile covers should be used for
either machine to maintain asepsis during the procedure. Appropriate health and
safety procedures should be followed for the use of intraoperative fluoroscopy
(gowns/rings/thyroid shield etc.).
◆ SUB kit + spares! – the appropriate-sized SUB kit(s) should be available (cats and
small dogs), as well as a spare kit or parts in case of a problem.
◆ Additional surgical equipment – electrosurgery unit, adhesive incise drape,
sterile cyanoacrylate glue (for internal use), angle-tipped hydrophilic guide wires
(various sizes), abdominal retractors, moistened laparotomy swabs, large cotton
buds, long Debakey forceps.
◆ Personnel (minimum required) – surgical team comprising minimum two
persons, ideally three: anaesthetist, radiographer/radiologist, circulating theatre
nurse.

TRAINING:
Anyone wishing to place a SUB device should undergo a degree of training/personal
preparation for this procedure. Ideally, attendance at a practical course is advised, but if this

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is not possible, review of the Norfolk Vet Products surgical guide and viewing of relevant video
material is recommended prior to proceeding.

A 3D printed model can be purchased from Norfolk Vet Products for practising the nephrostomy
catheter placement prior to attempting this on a live patient.

Tip: Print out the surgical guide instructions for use in theatre or create your
own ‘tick box’ SOP.

SUB placement:
A standard ventral midline coeliotomy is performed, from approximately midway between the
xiphoid and umbilicus to just cranial to the pubis (exact length depending on whether the left
or right ureter is affected). Abdominal retractors (mini Balfour or Gosset) are placed to improve
visualisation.

Tip: The author uses an adhesive incise drape in SUB cases to avoid the use of towel
clamps close to the surgical site that may interfere with fluoroscopic images
(unless digital subtraction is used).

Note: All catheters should be straightened on to the stylets and flushed with sterile
saline before use.

1. NEPHROSTOMY CATHETER
The skill required to place the nephrostomy catheter is highly dependent on the degree of
dilation of the renal pelvis and the position of any calculi. Case selection in the early part of the
learning curve is key to avoiding problems.

◆  ignificantly dilated pelvis: In cats with ureteral obstruction and a significantly

S
dilated renal pelvis, placement of the nephrostomy catheter is usually
straightforward.
❖ Fat is cleared from the caudal pole of the affected kidney.
❖ An 18 G catheter is used to puncture the renal pelvis – aiming from the caudal
pole of the kidney to the centre of the pelvic region. This is performed without
imaging guidance. The ‘stopper’ is removed from the catheter during placement
so that urine can be seen to flow from the hub when correct placement is
achieved. A T-port and three-way tap is attached to the catheter to allow a
urine sample to be obtained for culture and to perform a positive contrast
pyelogram.

Tips:
1. If the urine is haemorrhagic, wait for it to clear before proceeding.
If it is not clearing, alter the position of the catheter inside the
pelvis and continue watching. Blood clots may block the catheter
postoperatively if bleeding is allowed to continue.
2. Dilute contrast agent to a minimum of 50:50 with sterile saline
to enable wires/catheters to be more easily seen during placement.
3. Use different-sized syringes for saline and contrast so the two
do not get mixed up on the instrument trolley.

❖ A modified Seldinger technique is used to place the nephrostomy catheter,

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using fluoroscopic guidance to ensure the catheter is appropriately positioned

and the radiopaque marker is within the renal pelvis. Long Debakey forceps are
needed to hold the catheters/wire in place during the procedure to comply with
UK radiation safety rules.

Note: Ensure the radiopaque marker remains well within the kidney
once the pelvis has decompressed.

❖ T
 he pigtail is tightened using steady traction on the catheter string, and a
haemostat is used to clamp the string (not the tubing) at the desired tension.

Tip: Do NOT overtighten the string, as this will risk kinking the pigtail
and obstructing urine flow.

❖ E
 nsure there is no leakage of urine visible from the catheter insertion site and
the placement is still correct, then advance the Dacron cuff to the kidney
surface and glue it into position. The silicone sleeve on the catheter is also
advanced to make contact with the Dacron cuff.

◆ Minimally dilated renal pelvis: Cases with a small renal pelvis (<8 mm) should be
attempted only once significant experience has been gained with less challenging
patients!
❖ Catheter placement is from the caudolateral aspect of the kidney (5 or 7 o’clock
rather than 6 o’clock). A more accurate aim is required to puncture the pelvis –
ultrasound guidance may be helpful.
❖ An angle-tipped hydrophilic wire is used instead of the J-wire (which is
provided in the kit) and is advanced down the ureter to create more space for
the catheter.
❖ The catheter is advanced over the wire into the ureter. The pigtail is not
tightened – the string can be cut. The radiopaque marker must still be within
the renal pelvis.

◆  alculi in the renal pelvis: In cases with calculi present in the renal pelvis, it may
C
be challenging to obtain the initial renal puncture. Ultrasound guidance may be
needed. Following injection of contrast agent to dilate the pelvis, the nephrostomy
catheter may be placed as normal or into the ureter depending on the space
available.

2. BLADDER CATHETER
The bladder catheter is technically easier to place than the nephrostomy catheter and requires
no extra equipment/imaging.
◆ A purse string suture is placed in the apex of the bladder with 3-0 (2 metric)
monocryl (not tied).
◆ A stab incision is made in the centre of the purse string – take care not to cause
excessive haemorrhage!

Tip: If the bladder wall is thick/inflamed, use of cautery to enter the bladder may
be useful to reduce haemorrhage.

◆ The catheter is placed through the stab incision and the purse string is tightened

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and tied.

Tip: In a small cat, the bladder catheter may need to be shortened to prevent
irritation of the bladder trigone when the bladder is empty.

◆  hree 3-0 monocryl (2 metric) sutures are pre-placed through the Dacron cuff and
T
bladder wall to secure the catheter. Prior to tying the sutures, cyanoacrylate glue is
applied to the underside of the cuff for additional security. The tubing is clamped
to reduce leakage of urine during the remainder of the procedure.

3. CONNECTION OF THE SYSTEM AND SUBCUTANEOUS ACCESS PORT

◆  ssess the length of the catheters and cut to size – do NOT cut too short as the
A
abdomen will change in length/conformation with movement of the cat (e.g.
jumping) when awake.
◆ Place the blue boots on to the catheters – tapered end first.

Tip: If using a pigtail nephrostomy catheter, have an assistant maintain tension

on the string while the haemostat is released and the blue boot is passed on to
the catheter.

◆  onnect the catheters to the ‘Y’ (unilateral SUB) or ‘X’ (bilateral SUB) connector
C
within the abdomen. If the pigtail is to be maintained, the catheter is pushed over
the first ‘barb’ of the connector; the string is then cut sharply at the level of the
catheter with a no. 11 blade and the catheter is pushed entirely on to the connector.

Note: The string MUST NOT be visible at the end of the catheter – this will cause
leakage of urine postoperatively if present.

◆  onnect the actuating tubing (connection to port) to the final arm of the ‘Y’ or ‘X’
C
connector.
◆ The subcutaneous fat is dissected from the body wall on the ipsilateral side to
the affected ureter to create a ‘pocket’ for the port, then the actuating tubing is
passed out through the body wall in a gentle loop. It is shortened as needed to
leave approximately 4 cm of tubing external to the abdomen and connected to
the SwirlPort after application of the final blue boot. The port is secured to the body
wall with four 2-0 (3 metric) Prolene sutures.
◆ The system is visually leak tested and checked for final positioning. All blue boots
are advanced over the connections.
◆ A contrast study is performed under fluoroscopy to confirm the patency of all
catheters (ideally using digital subtraction) and to give an additional check for
leaks/kinks. If all is satisfactory, the abdomen is closed routinely. The subcutaneous
fat is actively closed down around the port to minimise seroma formation and
then the remaining incision is closed routinely.
◆ A lateral radiograph/fluoroscopic study is performed to assess for kinks in the
orthogonal plane.
◆ An oesophageal feeding tube is placed if required.
◆ The cat is warmed and recovered from anaesthesia.

Troubleshooting
Placement of a SUB system is a very technical procedure and hence intraoperative and

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postoperative complications are common,3–5 especially in centres where multiple surgeons are
performing the procedure, when training has been limited or where the procedure is performed
infrequently. The ability to troubleshoot these issues is a necessary part of performing SUB
placement surgery.

INTRAOPERATIVE COMPLICATIONS:
◆  ifficulty placing the nephrostomy catheter into the renal pelvis – more
D
commonly a problem in cases with minimal renal pelvis dilation. Potential solutions
are the use of ultrasound guidance to puncture the renal pelvis, alteration of the
angle of needle puncture, use of a smaller catheter for the initial puncture and use
of an angle-tipped hydrophilic guide wire rather than a J-wire for exchange of the
catheter for the nephrostomy tube (less likely to injure the renal parenchyma and
can be placed into the ureter if necessary).
◆ Haemorrhage from the renal pelvis – this may cease without intervention if only
a small vessel has been injured on entry. If haemorrhage is persistent, the needle/
catheter may need to be repositioned (it may be encroaching on the renal
calyces). If there is concern about blood clots forming within the renal pelvis/
catheter, 1 ml of tissue plasminogen activator (TPA) can be instilled within the
catheter prior to the end of the procedure.
◆ Urine leakage – the most common site of urine leakage is where the nephrostomy
tube joins to the access port, due to the pigtail string allowing wicking of urine
along it. If noted at the time of surgery (or in the immediate perioperative period),
the catheter connection should be redone, making sure the string is not visible
at the end of the catheter or sacrificing the pigtail altogether. Check also for
subcapsular urine leakage from the kidney, indicating that the parenchyma has
been accidentally punctured during the procedure.
◆ Loss of the pigtail string – the string tensioning the pigtail may be cut accidentally
during shortening of the catheter or may retract during attachment of the catheter
to the access port. If this occurs, no remedial action is necessary as the catheter
does not easily migrate from the kidney even without the pigtail.
◆ Catheter is kinked – repositioning of the catheters is performed to ensure they
loop gently around the abdomen. While leaving a 4–5 cm length of catheter in
the subcutaneous space is recommended in the official surgical guidelines, other
authors have suggested placing minimal catheter tubing through the abdominal
wall to prevent kinks. The design of the SUB 3.0 means that kinks outside of the
body wall no longer cause obstruction to urine flow.

POSTOPERATIVE COMPLICATIONS:
◆  lood clot in the renal or bladder catheter – blood clots represent a major
B
complication due to the inability to selectively flush this device. Infusion of TPA
via the port can be attempted.6 If successful, no further action is needed. If
unsuccessful, catheter exchange (revision surgery) will be required.
◆ Catheter kinks – these can occur as a long-term complication due to movement
of the device. This should not be an issue with SUB 3.0 design.
◆ Dysuria (in the absence of infection) – can occur due to the underlying disease
or due to irritation from the bladder catheter. Medical management should be
attempted with analgesia (e.g. gabapentin) ± steroids. If unsuccessful, shortening
of the bladder catheter can be considered.
◆ I nfection – appears to be a more significant long-term complication in the UK
compared with the USA, possibly due to differences in the clinical population or

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the antibiotic choices available.3,7 Use of appropriate antibiotics based on culture

and sensitivity testing results may clear the infection in some cats, but others
may develop multi-resistant infections. Tetra-EDTA infusions can be used to try to
resolve infection. In some cases, removal of the SUB device ± nephrectomy may be
necessary to resolve the issue.
◆ Device mineralisation/obstruction – if the ureter has become patent, no action
is required. If the ureter remains obstructed, dissolution of obstructed material
can be attempted with tetra-EDTA.8,9 If dissolution fails, catheter exchange will be
needed – challenging!
◆ Device migration – migration of the nephrostomy and bladder catheters into
the intestinal tract or into the peritoneal cavity has been reported in a number of
cases long-term.10 Removal/exchange of the device ± intestinal anastomosis and
resection are needed in these cases.

References
1. Livet V, Pillard P, Goy-Thollot I, et al. Placement of subcutaneous ureteral bypasses without
fluoroscopic guidance in cats with ureteral obstruction: 19 cases (2014–2016). J Feline Med Surg
2017: 19(10): 1030–1039.
2. Butty EM, Labato MA. Subcutaneous ureteral bypass device placement with intraoperative
ultrasound guidance, with or without microsurgical ureterotomy, in 24 cats. J Feline Med Surg 2021;
23(12): 1183–1191.
3. Berent AC, Weisse CW, Bagley DH, et al. Use of a subcutaneous ureteral bypass device for treatment
of benign ureteral obstruction in cats: 174 ureters in 134 cats (2009–2015). J Am Vet Med Assoc 2018;
253(10): 1309–1327.
4. Kulendra NJ, Borgeat K, Syme H, et al. Survival and complications in cats treated with subcutaneous
ureteral bypass. J Small Anim Pract 2021; 62(1): 4–11.
5. Dirrig H, Lamb CR, Kulendra N, et al. Diagnostic imaging observations in cats treated with the
subcutaneous ureteral bypass system. J Small Anim Pract 2020; 61(1): 24–31.
6. Dropkin CA, Burdick SK, Berent AC, et al. Use of tissue plasminogen activator to alleviate
postoperative subcutaneous ureteral bypass obstruction secondary to blood clot in seven cats.
J Feline Med Surg 2021; 23(10): 996–1004.
7. Pennington CE, Halfacree Z, Colville-Hyde C, et al. Factors associated with positive urine cultures in
cats with subcutaneous ureteral bypass system implantation. J Feline Med Surg 2021; 23(4): 331–
336.
8. Chik C, Berent AC, Weisse CW, et al. Therapeutic use of tetrasodium ethylenediaminetetraacetic
acid solution for treatment of subcutaneous ureteral bypass device mineralisation in cats. J Vet
Intern Med 2019; 33(5): 2124–2132.
9. Duval V, Dunn M, Vachon C. Use of tetrasodium EDTA for the treatment of intraluminal obstruction of
subcutaneous ureteral bypass devices. J Feline Med Surg 2022; 24(10): e330–e337.
10. Véran E, Vachon C, Bryon J, et al. Multicenter retrospective evaluation of transmural migration of
subcutaneous ureteral bypass devices within the digestive tract in cats. J Vet Intern Med 2022;
36(5): 1677–1685.

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SYMPOSIUM

Use of antimicrobials in the management of urinary

tract infections
Roswitha Dorsch Dr. med. vet., Dr. habil., Dipl. ECVIM (Internal Medicine)

Bacterial urinary tract infections are one of the most common reasons for antimicrobial
treatment in veterinary medicine and contribute to the development of antimicrobial
resistance. While the incidence of bacterial infections is low in younger cats with signs of
lower urinary tract disease, it increases in the elderly cat population with concurrent diseases.
Cats with recurrent bacterial cystitis and cats with subcutaneous ureteral bypass devices are
particularly challenging to treat. Antimicrobial treatment increases the risk of development
of antimicrobial resistance and can be associated with side effects. Adherence to treatment
guidelines1 and confinement to a few first-line antimicrobial agents is imperative to avoid the
development of antimicrobial-resistant bacteria.

Diagnosis of bacterial urinary tract infection

The diagnosis of bacterial urinary tract infection should be established based on the clinical
signs, results of urinalysis and aerobic culture of a cystocentesis-derived urine specimen.
Positive urine cultures are indispensable for a reliable diagnosis. To select an effective
antimicrobial, in vitro susceptibility testing should be performed on all isolates. Diagnostic
imaging can help to assess for complicating conditions (e.g., upper urinary tract involvement).
When possible, urine specimens should be obtained by cystocentesis and before initiating
antimicrobial treatment. Urine can be sampled by catheterization, but the risk of contamination
is higher. Owing to a high risk of contamination, free-catch samples should not be used for
bacterial cultures.

Urine sediment analysis

There is a large overlap of urine sediment findings between cats with bacterial cystitis and
those with other diseases of the lower urinary tract. In feline urine samples, bacteriuria identified
on unstained wet urine sediments is poorly correlated with positive culture results1. In addition,
automated sediment analysis has limited performance, resulting in a high proportion of
specimens with questionable bacteriuria.2 Examination of stained urine sediment improves the
sensitivity and specificity for the detection of bacteria.3 The gold standard remains quantitative
aerobic bacterial culture from a cystocentesis-derived urine sample. The guidelines of
the International Society for Companion Animal Infectious Diseases (ISCAID) recommend
withholding antimicrobial treatment in cats while the results of bacterial culture are pending,
to avoid unnecessary use.

Categorizations of infections and treatment

SPORADIC BACTERIAL CYSTITIS
Bacterial infection of the urinary bladder with compatible lower urinary tract signs (pollakiuria,
dysuria, stranguria, hematuria) with fewer than three episodes in the prevailing 12 months.

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◆ If treatment must be initiated when culture and antimicrobial susceptibility

results are pending, a first-line antibiotic, preferably with a known low local
resistance rate, should be administered, for example, amoxicillin or trimethoprim/
sulfonamide. A treatment duration of 3–5 days is recommended.
◆ If clinical signs disappear within the treatment period and the antimicrobial
was appropriate according to susceptibility testing, additional monitoring and
diagnostic testing is generally not required.
◆ If clinical response to an appropriate antimicrobial within 48 hours is lacking,
initiate further investigations for complicating factors.
◆ In case of poor clinical response, antimicrobials should not be changed
empirically.
◆ If the cat shows clinical improvement but the antimicrobial chosen proves to be of
insufficient effect according to the susceptibility testing, complete the treatment
and repeat urine culture in 3–7 days to ensure that the infection has been cleared.
◆ If clinical improvement is lacking and the chosen antimicrobial proves to
be insufficient according to susceptibility testing, discontinue the original
antimicrobial and adjust according to the susceptibility results.

RECURRENT BACTERIAL CYSTITIS

Three or more bacterial infections in the preceding 12 months, or two or more episodes in the
preceding 6 months. Recurrent urinary tract infection may be defined as reinfection, relapse, or
more or less persistent infections.
◆ Further diagnostics including abdominal ultrasonography, plain radiographs,
contrast studies and urethrocystoscopy to obtain a biopsy of the bladder mucosa
for histologic examination and culture might be indicated.
◆ Identification and treatment of underlying causes (endocrinopathies, micturition
disorders).
◆ Long-term therapy is not automatically warranted.
◆ Reinfection: 3–5 days.
◆ Relapsing infections: 7–14 days.
◆ Urine culture after 5–7 days of treatment if a longer duration of treatment is used.

PYELONEPHRITIS
◆  ost commonly, pyelonephritis is caused by an ascending bacterial infection
M
from the distal urinary tract. If untreated, pyelonephritis can expand to permanent
and progressive kidney damage, retroperitoneal abscesses or septicemia.
◆ Acute pyelonephritis may be associated with distinct clinical signs such as fever
and painful kidneys. More commonly it presents with non-specific signs such as
anorexia, lethargy and vomiting.
◆ Clinical signs should not be used alone for diagnosis, but the presence of clinical
abnormalities indicates that further work-up is needed.
◆ Culture of urine obtained by pyelocentesis is ideal for identifying the bacteria
involved. Otherwise, cystocentesis (repeated cultures may be needed) or blood
cultures may be used depending on the assumed route of infection. Blood
cultures should be considered in immunosuppressed cats and in the presence of
fever and azotemia with negative urine cultures and no abnormalities in the urine
sediment.
◆ Antimicrobial treatment should be immediately started while culture results are
pending.
◆ Fluoroquinolones and intravenous third-generation cephalosporins are

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appropriate choices in acute pyelonephritis.

◆ Treatment duration: 10–14 days.
◆ Follow-up urine culture 10–14 days after cessation of therapy.

URINARY CATHETERS
◆  rophylactic antimicrobial treatment is never warranted, and no evidence
P
supports routine urine cultures after catheter removal. Current guidelines
recommend bacterial cultures only in cats with ongoing clinical signs of lower
urinary tract disease after the catheter has been removed.
◆ Cats with indwelling urinary catheters and clinical signs of urinary tract infection
may be difficult to identify as many were catheterized for signs of lower urinary
tract disease initially. Urine cultures should be performed in the presence of fever,
bacteremia or marked abnormalities in the urine sediment. Because treatment
is more likely to be effective if the catheter is removed prior to treatment, the
catheter should be removed if possible and urine for culture should be collected
by cystocentesis. If the catheter must remain in place, it should be replaced and
urine for culture should be obtained through the new catheter.

SUBCLINICAL BACTERIURIA
Subclinical bacteriuria is defined as the presence of bacteria in the urine as determined
by a positive bacterial culture, in the absence of clinical evidence of urinary tract infection.
Currently, no evidence exists demonstrating a beneficial effect of routine treatment of cats
with subclinical bacteriuria. The decision to treat should not be based on the presence of an
inflammatory urine sediment or identification of a multiresistant isolate.
For feline patients, the following situations can justify antimicrobial treatment:
◆ Suspected pyelonephritis
◆ Patients undergoing surgical procedures of the urinary tract
◆ Patients undergoing endoscopic procedures of the urinary tract with associated
bleeding
◆ If the urinary bladder is thought to be the focus of extraurinary tract infection (e.g.,
discospondylitis)
◆ Diabetic cats if subclinical bacteriuria is thought to be the reason for insulin
antagonism or ketosis
◆ Identification of Corynebacterium urealyticum because of its association with
encrusting cystitis.

Use of critically important antimicrobials

In veterinary medicine, antimicrobials that are critically important in humans should not
be used or be used only in very limited circumstances. Third- and fourth-generation
cephalosporins, such as cefovecin, and fluoroquinolones, such as marbofloxacin and
pradofloxacin, also belong into this group and should be used only if an isolate is resistant
to other antimicrobials or in case of pyelonephritis (fluoroquinolones). Additionally, critically
important antimicrobials should not be used in untreatable infections or in animals with worse
prognoses. In February 2023, an EU regulation prohibiting the use of certain critically important
substances, such as carbapenems and advanced-generation cephalosporins, in animals
became effective.

New treatment strategies

New treatment strategies for recurrent bacterial cystitis that have so far not been evaluated
in clinical studies could be vaccination with autologous vaccines, alteration of the intestinal

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microbiota via fecal microbiota transplantation and the use of bacteriophages. So far, there is
no good evidence for the use of inhibitors of bacterial adhesion to the urothelium (D-mannose,
cranberry extracts) in dogs and cats.

References
1. Weese JS, Blondeau J, Boothe D, et al. International Society for Companion Animal Infectious
Diseases (ISCAID) guidelines for the diagnosis and management of bacterial urinary tract
infections in dogs and cats. Vet J 2019; 247: 8–25.
2. Swenson CL, Boisvert AM, Gibbons-Burgener SN, et al. Evaluation of modified Wright-staining of dried
urinary sediment as a method for accurate detection of bacteriuria in cats. Vet Clin Pathol 2011; 40:
256–264.
3. Neubert E and Weber K. Using the Idexx SediVue Dx to predict the need for urine bacteriologic culture
in cats. J Vet Diagn Invest 2021; 33: 1202–1205.

#ISFMRocksDublin 92
 Always by your side,
you have the best
knowledge database.

Feline bacterial cystitis

in your

www.ceva-gram.com

Easy-to-use Quick access Rich and evolving

with a smartphone to the information content
 Dublin, 29 June – 2 July

SYMPOSIUM
A success story: how to recruit and retain staff as
well as clients through a cat-friendly approach
Cyril Berg DVM
Veterinary Clinic ‘Mon Chat et Moi’ Founder
Marc-Antoine Rappart DVM MSc
Veterinary Clinic ‘Mon Chat et Moi’ Clinic Manager
Clémentine Doucet
Veterinary Clinic ‘Mon Chat et Moi’ Veterinary Nurse

There is a big issue nowadays: how to employ – and how to retain – our staff? To this we can
add another subject, regarding cat-owning clients in particular: how to recruit them and how to
improve their loyalty?

We have been working on these questions for more than 10 years in our clinics. Now, we think it’s
time to share our experience, successes and failures with our colleagues. Miracles don’t exist,
but there are some tips to apply.

What have we implemented in our clinics to focus on these burning topics?

As a matter of fact, patients are the key point in our processes. Therefore, being ‘cat friendly’
was the beginning of our story.

What can being a cat-friendly clinic bring in terms of better management? Why is this
particular way of doing our job a benefit to improve recruitment and loyalty?

Purposes
◆ To share our vets’ and nurses’ experience
◆ To provide tips to make staff, patients and clients happy in order to recruit and
retain them
◆ To develop, explain and contextualize the values of the cat-friendly approach

Plan
1. What are our values and why are they of importance?
2. Being cat friendly: the MCM backbone
3. Recruiting and retaining our clients and patients: creating customer loyalty
4. Employing and retaining our staff
5. The future of MCM

1. What are our values and why are they of importance?

Our work and our choices are guided by these values:
◆ Being avant-gardist
◆ Taking care of cats following the latest scientific guidelines and the highest
standard of care

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◆ Being always available for our clients

◆ Helping our clients to understand their cats
◆ Ensuring cat wellness in our clinics and at home
◆ Transparency and integrity
◆ Being attentive to our staff members’ needs.

2. Being cat friendly: the MCM backbone

Being ‘cat friendly’ is well recognized now. Thanks to ISFM, we know the guidelines. This is a start,
but there is another aspect that is more philosophical. Working with cats, considering their
needs and adapting to them led us to a different practice, which is more attentive not only to
animals but also to human beings.

3. Recruiting and retaining our clients and patients: creating

customer loyalty
This means:
◆ Creating an environment that is suitable for cats, which are easily stressed animals
(outside their homes), and also adapted to the owners, who are also often worried
(at the receptionist desk, in the waiting room, in the consultation room, etc…)
◆ Always focusing on the follow-up of our patients, both at the clinic and at home.
This allows us to ensure excellent quality and continuity of care
◆ Promoting our way of practising online and on social networks = communicating
◆ Working on innovative and ‘making life easier’ services.

4. Employing and retaining our staff

In a nutshell, we want to make our staff happy at work. This doesn’t mean having a pool table in
the clinic but rather giving them a meaningful job.

Of course, having a job that makes sense is crucial. Why am I here? What is the purpose?

A big issue is communication. Belonging to a society means knowing what happens inside it
and where it goes. This gives meaning to the job.

The staff are involved. We aim to give them responsibilities and to let them do extra duties of
their choice, so that they build the clinics with us. Training courses are offered (inside or outside)
regularly.

Management is respected and organised, but everybody is allowed to speak and give their
opinion. This enriches our daily practice.

5. The future of MCM

Our clinic is always improving. We are very attentive to new ideas and to relevant and valuable
insights, and we pay attention to our environment.

The staff are aware of being part of a bigger project: making MCM grow, setting up new clinics
around France.

Working in our clinics means working for our patients, clients and colleagues. The daily question
is: how can we help the others to live a better life?

To sum it up, we are cat friendly but we are also doing our best to be customer and staff
friendly.

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EVERY URINARY
CONDITION DESERVES
TO BE DILUTED
The Lower Urinary Tract Disease encompass
a wide range of issues, manifests in a variety
of symptoms and can be caused by multiple
conditions or comorbidity pathologies.
Thanks to 50 years of science, obsessive
observation and partnerships with veterinarians,
we know that targeted nutrition can play a key role
in urinary patients’ recovery and ongoing health.

This is why we have developed an extensive range

of nutritional solutions tailored to specific urinary
conditions with now improved formulas and
leading edge innovations.

© ROYAL CANIN® SAS 2023. All rights reserved.

URINARY
 Dublin, 29 June – 2 July

Beyond the bladder: urethral obstruction part 1 and 2

Serge Chalhoub DVM, Dipl. ACVIM (SAIM)
Søren Boysen DVM, Dipl. ACVECC
Faculty of Veterinary Medicine, University of Calgary

Key words: Urinary obstruction, lower urinary tract disease, urethral obstruction, cats

Introduction
Urethral obstruction (UO) is a potentially life-threatening consequence of feline lower urinary
tract disease (FLUTD). FLUTD can be defined as any disorder affecting the bladder or urethra
of cats (males and females). It does have multiple other names (e.g. feline urologic syndrome
(FUS), idiopathic lower urinary tract disease, feline idiopathic cystitis, feline interstitial cystitis
(FIC), Pandora syndrome, etc.). There are many causes of FLUTD, all of which can lead to acute
urethral obstruction (Table 1).
Table 1: Causes of feline lower urinary tract disease

Pathophysiology
Complete UO results in increased intravesicular pressure, leading to bladder wall pressure
necrosis and mucosal injury, which may also be transmitted upstream to the ureters and
kidneys. When increased renal pressure exceeds glomerular filtration pressure, renal blood flow
and glomerular filtration rate (GFR) decrease. Tubular concentrating ability is subsequently
affected, leading to impaired sodium and water reabsorption, as well as impaired excretion of
phosphorus, potassium, blood urea nitrogen, creatinine, and hydrogen ions.

Severe metabolic derangements, such as hyperkalemia and metabolic acidosis, can occur.
Hyperkalemia is the most common life-threatening complication and can lead to decreased
depolarization of the heart, with subsequent bradycardia and cardiac arrhythmias. Uremia,
which can cause the clinical signs of depression, vomiting, and anorexia, is seen within 24–48
hours when UO is complete and acute. Ongoing gastrointestinal (GI) losses and decreased fluid

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intake (vomiting, anorexia) can lead to marked dehydration and hypovolemia. If left untreated,
complete UO can result in bladder rupture, uroabdomen, concurrent shock, and death.

Diagnosis:
◆  hysical examination findings/history: Cats often present for vocalizing and
P
unproductive straining in the litterbox. When UO is present for longer than 24 hours,
signs of systemic illness, shock, and bradycardia may be noted.
◆ Clinical findings may include vomiting, anorexia, lethargy, altered mentation,
weakness, stupor, and, if severe, shock and/or lateral recumbency.
◆ Physical examination findings may detect dehydration, tachypnea, bradycardia,
hypothermia, a palpably firm, distended urinary bladder, poor pulses, cool
extremities (signs of shock), and pain on abdominal palpation.
◆ The combination of bradycardia (heart rate <140 bpm) and hypothermia
(<35.5°C) is strongly correlated (>98% predictive value) with potassium
concentrations >8 mmol/L.
◆ Clinical findings may vary further depending on underlying/inciting cause.
◆ Blood work (biochemistry panel) often detects azotemia (≥80% of cats),
hyperkalemia (≥75% of cats), hypoalbuminemia (58% of cats), and varying
degrees of hyponatremia, hyperphosphatemia, hyperglycemia, and
hypocalcemia.
◆ Symmetric dimethylarginine (SDMA) serum assay levels may be increased (≥20
µg/dl).
◆ Urinalysis may detect hematuria, proteinuria, and glucosuria. Examination of the
urine sediment may reveal pyuria, bacteriuria, crystalluria, and/or urinary casts.
Urine specific gravity and pH are neither sensitive nor specific.
◆ Urinary tract infections (UTIs) are uncommon in adult cats (i.e. 1–10 years of age);
however, urine culture may be indicated in some cases (e.g. for detection of
pyuria/bacteriuria).
◆ Abdominal radiographs often identify a distended bladder, but may also detect
underlying causes (e.g. uroliths, urethral stricture). Radiographs are reported to
identify an underlying cause of UO in 30–40% of cats.
◆ Ultrasonography is good at identifying uroliths (particularly if radiolucent) and can
detect bladder or urethral masses.
◆ Electrocardiography (ECG) is recommended, even in the absence of bradycardia.
ECG changes associated with hyperkalemia include prolonged PR interval,
decreased to absent P waves, widened QRS complexes, shortened QT intervals,
and tall T waves. With more severe hyperkalemia, sinoventricular rhythm, atrial
standstill, ventricular fibrillation, and asystole can occur. Although ECG findings
roughly correlate with potassium concentration, there are many factors that
impact cardiac function, and some cats may have potassium concentrations
disproportionate to ECG findings.
◆ Urolith analysis should be performed on any stones removed as analysis can be
helpful in determining long term preventative strategies.

Therapy
◆ IV fluids: Cats with urethral obstruction will often be dehydrated and potentially
hyperkalemic and/or hypovolemic.
◆ There is some debate about the ideal crystalloid fluid to administer, with choices
involving 0.9% saline vs balanced isotonic fluids containing 4–5 mmol/L potassium
(e.g. lactated Ringer’s solution (LRS), Normosol-R). Evidence suggests that

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balanced isotonic crystalloids may be preferred.

❖ Balanced isotonic crystalloids (LRS, Normosol-R) correct acidosis faster than
0.9% saline.
❖ Fluid type has no influence on normalization of serum potassium.
◆ Regardless of the fluid type chosen, cats must be closely monitored for evidence of
volume overload.
◆ Point-of-care ultrasound (POCUS) is extremely helpful in assessing patient volume
status and fluid responsiveness, and for detecting early signs of fluid overload (see
notes on “Hocus POCUS, the role of ultrasound in the critical feline patient”).
◆ Risk factors for fluid overload include fluid boluses, or development of a heart
murmur/gallop rhythm.
◆ Unblock once stabilized (bradycardia corrected if hyperkalemic, improved blood
pressure/perfusion).
❖ Placing urethral catheters in cats is best done under general anesthesia (low
stress, less urethral sphincter tone), therefore make sure the patient can tolerate
anesthesia.
• Correct bradycardia, hypotension, hypovolemia prior to anaesthesia.
◆ Consider decompressive cystocentesis if a urethral catheter cannot be placed
and/or the patient is unstable (risk of bladder rupture). This is controversial but if it
is not possible to unblock the patient and the patient is severely ill from azotemia
and hyperkalemia, it can help.
❖ Pros of decompressive cystocentesis:
• Immediate emptying of the urinary bladder
• Relieve pain
• Facilitate retrohydropulsion of obstructive material
• Passage of a urinary catheter by decreasing intraluminal pressure
• Obtain an uncontaminated sample via cystocentesis for urinalysis and
culture.
❖ Cons of decompressive cystocentesis:
• Potential for iatrogenic trauma to further compromise the urinary bladder
wall resulting in rupture and uroabdomen.
◆ Once the urinary catheter is in place, re-establish normal urine flow. Azotemia
should decrease rapidly if the kidneys are not significantly injured.
◆ Watch for post-obstructive diuresis!!! Also check the abdomen with ultrasound for
any urinary bladder injury if decompressive centesis was performed.

◆ Hyperkalemia:
❖ The mainstay of therapy is IV fluids (fastest way to decrease potassium
concentrations, even if the cat is not yet unblocked).
❖ Calcium gluconate (5 mg/kg of elemental calcium (approximately 0.5 mL/
kg of a 10% solution) given IV over 10–20 minutes) temporarily (approximately
60 minutes) decreases cardiac membrane excitability and may stabilize
patients for long enough to relieve the urethral obstruction and/or allow other
potassium-lowering therapies to take effect. Monitor ECG and/or auscultate the
heart for arrhythmias while administering.
❖ Other therapies to address hyperkalemia are listed in Table 2. In the absence of
ECG monitoring, therapy is generally indicated when the heart rate is below 160
bpm.

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Table 2: Therapies beyond IV fluids to address hyperkalemia

❖ P  ost-obstructive diuresis is not uncommon following relief of urethral

obstruction as waste products are eliminated, drawing fluid with them. There
are also important electrolytes and molecules lost during diuresis that are
important to maintain and monitor (potassium is a big one in cats).
• Therefore, make sure the patient remains hydrated. Monitor closely: hydration
parameters, weight, blood pressure, heart rate, electrolytes.
◆ Sedation/anaesthesia:
❖ Depends how critical patients are: butorphanol 0.2 mg/kg IV ± diazepam 0.2
mg/kg IV. Can supplement with low-dose propofol if deeper sedation is needed.
Ketamine (10 mg/kg) and diazepam (0.5 mg/kg) IV can also be titrated to affect
as needed.
◆ Analgesics
❖ Systemic: buprenorphine, fentanyl patch or continuous rate infusion.
❖ Caudal epidural with bupivacaine or bupivacaine/morphine combination is
often preferred.
❖ The addition of meloxicam has not been shown to have any benefit in cats with
UO and thus is generally not recommended.
◆ Urethral relaxants/antispasmodics
❖ May have some benefit but study results in cats are mixed.
❖ Both phenoxybenzamine (2.5–7.5 mg per cat PO q 8–12 hrs) and prazosin (0.25–
0.5 mg per cat PO q 24 hrs) are α-1 antagonists that cause smooth muscle
relaxation.
❖ Prazosin may be more beneficial than phenoxybenzamine as the latter may
take up to a week to be effective.
❖ Diazepam (2.5–5 mg per cat PO q 8–12 hrs) or alprazolam (0.125–0.25 mg per
cat PO q 12 hrs) are alternative options to α-1 antagonists; however, repeated
oral dosing has been associated with hepatotoxicosis in cats.
❖ Alprazolam may be preferred as it associated with hepatotoxicity.

Hospitalization vs outpatient care

◆  ospitalization and traditional management are still considered the reference
H
standard for management of acute UO in cats. However, if patients are stable,
alternative protocols can work.
◆ Evidence behind these alternative approaches will be discussed in the lecture,
including indications, pros and cons.
◆ Evidence surrounding the catheter type, dwell time, and size will also be discussed.

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Complications:
Complications of UO include bladder damage (possible uroabdomen), urethral damage
(stricture can occur following traumatic urethral catheterization, usually within 3 months),
acute renal failure, UTI secondary to catheterization, persistent lower urinary tract signs, post-
obstructive (osmotic) diuresis (loss of osmotic solute drawing water; may cause dehydration
if this is not monitored and corrected, hence why monitoring hydration and urine output is
important), hypokalemia (post-obstructive diuresis), dehydration, hypoperfusion (adjust
fluid rates to compensate), and detrusor atony (stretching of the bladder so much that
tight junctions are not working). Return of normal detrusor function can be achieved by
preventing excessive detrusor stretch during the days following relief of UO. This can involve
keeping the bladder small via an indwelling catheter. Manual expression of the bladder is an
alternative method for preventing detrusor stretch, but urethral resistance must be minimal
and the bladder must be easy to express. Bethanechol (1.25–5 mg per cat PO q 12 hrs) is a
parasympathomimetic that may be useful for minimizing acute detrusor atony; however, it
should be avoided in patients with ongoing UO and those for whom it is not possible to easily
express the urinary bladder. Consider urine culture and sensitivity testing upon catheter
removal and consider monitoring in hospital for an additional 12–24 hours to ensure that
spontaneous urination occurs following urinary catheter removal.

Prognosis
Reported survival rate to discharge using traditional management protocols is excellent
(91–94%). Long-term survival rate varies with recurrence rates for UO of 11–58% at various time
points, leading to 21% of cats eventually being euthanized. This suggests a guarded long-term
prognosis

Preventive measures
Prescription diets designed to reduce crystalluria and/or dissolve uroliths may be beneficial.
Adequate water intake is important. Ensure that long-term management such as limiting stress
is also instituted. Cats with recurrent episodes of UO may benefit from perineal urethrostomy
surgery. Preventive measures and long-term management of FLUTD will be discussed in more
detail within the presentation.
◆ Surgery
❖ Perineal urethrostomy and its pros and cons will also be briefly discussed in the
presentation.

References
Available upon request

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Minimally invasive management of stone disease

in feline patients
Dr. Allyson Berent DVM, DACVIM
The Animal Medical Center, New York, USA

Introduction
Minimally invasive management of stone disease is currently considered the standard of care
in veterinary medicine according to the American College of Veterinary Internal Medicine
(ACVIM). Urolithiasis is a common problem in veterinary medicine and knowing the stone type
is mandatory in providing the best treatment and prevention for clients and patients. Different
uroliths are treated in different ways: some can be dissolved, others need to be removed, and
some can be cautiously monitored and bypassed when necessary. The invasiveness and
side effects associated with some traditional surgical or medical techniques (i.e. surgery of
the ureter for ureteral obstructions, endoscopic visibility for bladder and urethral stones, etc.)
makes the use of less invasive alternatives using interventional options more appealing.

Kidney and Ureter

Percutaneous nephrolithotomy
Kidney stones can result in progressive renal failure, intractable infections, ureteral pain, and
bleeding. Surgical nephrotomy can be invasive and is associated with significant morbidity. In
people, percutaneous nephrolithotomy (PCNL) is considered the standard of care for kidney
stones too large to be treated with shockwave lithotripsy or retrograde laser lithotripsy. It has
recently been performed successfully in clinical veterinary cases. This minimally invasive
procedure aims to minimize morbidity and preserve as much renal function as possible while
gaining access into the kidney for stone removal. Generally, nephroliths are rarely problematic
in feline patients so this technique is rarely performed in cats.

ESWL for nephro/ureterolithiasis

Extracorporeal shock-wave lithotripsy (ESWL) is another minimally invasive alternative for
the removal of upper urinary tract calculi in the renal pelvis or ureters. ESWL uses external
shockwaves that are passed through a water medium directed under fluoroscopic guidance
in two planes. The stone is shocked and the debris is then left to pass down the ureter into
the urinary bladder over a 1–2-week period. This procedure can be performed safely with
nephroliths smaller than 1 cm and ureteroliths. For stones of larger sizes PCNL is recommended.
This procedure can be problematic in cats and is generally reserved for dogs.

Ureteral stenting and subcutaneous ureteral bypass (SUB) device placement are performed
for a variety of disorders to divert urine from the renal pelvis into the urinary bladder. These
techniques can be useful in patients with ureteral obstruction due to ureteral stones, obstructive
cancer, strictures, etc. In feline patients, SUBs are the author’s treatment of choice and feline
ureteral stenting has not been pursued for the last 10+ years due to the improved morbidity and
mortality rates with SUBs compared with traditional surgery or stents. This topic will be further
expanded upon in the ureteral intervention talk.

Urinary Bladder and Urethra

Laser lithotripsy involves the intracorporeal fragmentation of bladder and urethral stones
(and rarely ureteral or kidney stones), which is assessed using a rigid or flexible cystoscope

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or ureteroscope. The stone is fragmented until the pieces are small enough to be removed
normograde through the urethral orifice, either via voiding urohydropropulsion or with the
assistance of a stone basket. This process is useful for cystic and urethral calculi. All stone types
are able to be fragmented using laser lithotripsy. This is generally not often used in cats due to
their small urethral diameter and sensitivity to any trauma during stone retraction.

Percutaneous cystolithotomy (PCCL) is our preferred minimally invasive technique for lower
urinary tract stone removal, especially in our feline patients. This allows cystic and urethral
stone retrieval in any size, sex, or species, and is very easy to perform in both cats and dogs. This
procedure is performed with a small ventral midline skin incision made over the bladder apex
approximately 1 cm in size. A trocar is advanced into the bladder lumen and a rigid cystoscope
is advanced through the trocar into the urinary bladder for stone removal with an endoscopic
stone basket. The entire mucosal surface of the bladder and entire urethra are visualized and
stones stuck inside the urethra can be removed as well, without the need for urethrotomy.
During this procedure, the bladder can be explored carefully for polyps or masses, which can be
removed with a laser or biopsied if necessary. Once the scope and trocar have been removed,
the incision is closed.

References
Available upon request.

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Urinary tract surgery in general practice – tips and

tricks from a busy referral practice to take back to
your clinic
Laura Owen BVSc(Hons), CertSAS, AFHEA, DipECVS, MRCVS
European and RCVS Specialist in Small Animal Surgery
Associate Professor in Small Animal Surgery, University of Cambridge, UK

Summary
This lecture will look at surgical urinary tract procedures that are readily possible to perform in
first-opinion practice, requiring no or minimal specialist equipment, with the aim of improving
surgical technique and minimising complications.

Cystotomy
The key indication for cystotomy in feline practice is urolithiasis. Other indications include
bladder biopsy or ureteral access.

When cystotomy is planned for removal of uroliths, ensure that radiographs/contrast

radiographic studies have been performed prior to surgery to evaluate the entire urinary tract
for the presence of other stones, particularly within the urethra or ureters.

PROCEDURE
◆  he caudal abdomen and perineum are clipped and aseptically prepared for
T
surgery to facilitate catheterisation/flushing of the urethra. A urethral catheter is
inserted.
◆ Perioperative antibiotics are administered [clean-contaminated or contaminated
procedure].

Note: In a study of dogs undergoing cystotomy, the administration of antibiotics at time
of induction had no effect on subsequent surgical culture results.1

◆  standard caudal midline coeliotomy is performed. Moistened laparotomy swabs

A
are placed on the edges of the incision and abdominal retractors (Gossets or mini
Balfours) are placed to improve visualisation.

Ensure the incision extends to the pubis and is of sufficient length to enable good
visualisation of the bladder neck.

◆  stay suture (2 metric monofilament suture) is placed in the apex of the bladder
A
– a single suture or cruciate pattern depending on the perceived friability of the
bladder wall. This stay suture, if left for long enough, can be anchored around the
arm of the abdominal retractor to retract the bladder cranially without requiring
an assistant.
◆ The bladder is packed off with additional moist swabs to limit contamination of the
abdomen.
◆ Two further stay sutures are placed along either side of the proposed incision site.
◆ A stab incision is made with a no. 11 blade into the ventral surface of the bladder,
on the midline (check the bladder is not rotated), and extended with Metzenbaum

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scissors.

Ensure the incision extends to the caudal aspect of the bladder – this is where
uroliths will collect with gravity and the ureters are very distal in a cat, so the risk
of injury is low provided the incision remains on the ventral midline.

Suction is useful to evacuate the remaining urine but should be used judiciously
near the bladder mucosa (minimising contact) to avoid swelling of the bladder
neck.

◆  Volkmann curette or Debakey forceps are used to remove any visible uroliths
A
and these are placed in two sterile containers.

Uroliths should be submitted for composition analysis and culture (or a bladder
mucosal biopsy specimen can be submitted for culture). In a study of dogs with
urolithiasis and with a negative culture from urine, 18.5% had a positive culture
from the bladder mucosa or a urolith.2

◆  he internal surface of the bladder is palpated and visually examined for any
T
further stones.
◆ The urethral catheter is gradually withdrawn while flushing with saline to ensure
that no uroliths are lodged in the bladder neck or urethra. This is repeated several
times. The bladder itself is rechecked on each occasion for further stones.
◆ Flushing of the urethra can also be performed antegrade if desired.
◆ Once all uroliths have been retrieved, bladder closure is performed in a single-
layer appositional pattern.3 A continuous pattern is usually preferred, but simple
interrupted sutures are also acceptable. Monofilament suture (1.5–2 metric)
should be used.
◆ Leak test?
◆ The abdomen is lavaged and suctioned dry if contamination is suspected.
◆ Omentum is draped over the cystotomy incision.
◆ A swab/sharps count is performed (as per the checklist). Gloves and instruments
are changed if infection is present/suspected.
◆ Coeliotomy closure is performed as standard
◆ Postoperative radiographs are performed to check for residual uroliths.

Tube cystostomy
Placement of a cystostomy tube is performed to achieve either temporary or permanent
urinary diversion for cats with lower urinary tract obstruction, trauma or loss of function. It is a
simple technique to perform, and tubes are generally well tolerated by cats and can be used by
most owners in the home environment to avoid a long hospital stay.

Note: It is a two-person task to empty the cystostomy tube in a cat, so a single owner will very
likely require some assistance with the procedure.

When used as temporary urine diversion, for example, while urethral obstruction is relieved or a
urethral tear heals, a standard long tube is appropriate. Either a Foley catheter or a mushroom-
tipped gastrostomy tube can be used – the mushroom-tipped tube is slightly more challenging
to place, but is more resistant to dislodgement (or deflation of the balloon) than a Foley
catheter. For permanent diversion, these long tubes can be replaced with low-profile tubes that

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sit flush with the skin of the patient.

PLACEMENT VIA A VENTRAL MIDLINE COELIOTOMY

◆  erioperative antibiotics are administered [clean-contaminated or contaminated
P
procedure].
◆ Following a caudal midline coeliotomy, the bladder is located and other organs
are packed off with moistened laparotomy swabs.
◆ A suitable abdominal wall location is chosen for the tube exit site.

This can be on the right or left ventrolateral abdominal wall. The right is more
commonly chosen due to the absence of the colon on this side, but either is
satisfactory.

The relative position of the bladder when full and empty should be considered so
that excessive traction on the cystostomy site by bladder filling/emptying can be
avoided.

◆  large haemostat is pushed through the abdominal wall muscles in the chosen
A
location from internal to external and the overlying skin is tented over the forceps.
A small stab incision is made over the tips of the haemostat and the instrument is
exteriorised. The distal end of the tube (the mushroom or balloon) is grasped and
pulled through the abdominal wall into the abdomen.

Note: In order to make an opening large enough for the tube, the haemostat
is opened within the tunnel to stretch the tract. Stretched tissue will rapidly
contract postoperatively, providing a good seal around the tube and reducing/
preventing urine leakage. An incision that is cut with a blade and is too large
will not heal and urine leakage will continue to be a problem.

REMEMBER to pass the tube through the body wall before placing it into the
bladder, as the other end of the tube will not readily pass through!

Place a Christmas tree adapter and bung on the end of the tube before placing it
into the bladder to avoid getting soaked with urine!

◆  wo stay sutures are placed either side of the proposed cystostomy site in the
T
bladder to enable manipulation of the organ.
◆ A purse-string suture is placed in the craniolateral bladder wall, where the
cystostomy tube is to enter. This is performed with 2 metric monofilament
absorbable suture.

Ensure the purse-string is large enough to facilitate a stab incision and tube
placement without cutting the suture!

◆  stab incision is made through the centre of the purse-string (ensure this is full
A
thickness by using a haemostat to check or visualising urine leakage) and the tube
is placed through this incision into the bladder lumen, using the stay sutures for
counter-traction if needed. The purse-string is tightened and tied securely.
◆ Four ‘pexy’ sutures are placed between the bladder (partial thickness) and the
transversus abdominis muscle to encircle the tube site.

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❖ The order of suture placement is dorsal, caudal, cranial, then ventral to facilitate
visualisation.
❖ 2 metric monofilament suture is suitable
❖ Simple interrupted sutures or horizontal mattress sutures are appropriate.

◆  raction is applied to the tube to ensure the mushroom/Foley is flush against the
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bladder wall and the tube is secured to the skin with a finger trap suture.

Note: Ensure a correct technique for finger trap suture placement is used.4

◆ Omentum can be placed around the pexy site if desired.

◆  wab and sharp counts are completed. Gloves and instruments are changed if
S
infection is suspected.
◆ The coeliotomy incision is closed routinely.
◆ A medical pet shirt is used to prevent patient interference with the tube. A buster
collar is also applied if needed.

Postoperatively, the tube is emptied 3–4 times daily or is connected to a closed collection
system. Gloves should be worn at all times when handling the tube.

The cystostomy tube should remain in situ for 10–14 days to allow a secure fibrous adhesion to
form between the bladder and the body wall, to prevent uroabdomen occurring when the tube
is removed. When this time has passed and the tube is no longer required, the tube is removed
either by deflating the balloon (Foley) or applying traction (mushroom-tipped) with or without
the use of a stylet, after cutting the finger trap suture to release it from the skin.

Sedation is required to remove a mushroom-tipped cystostomy tube. A Foley catheter can be

removed while the patient is conscious in the vast majority of cats.

Antimicrobial therapy should be avoided while the tube is in place, unless clinically indicated.
Urine culture should be performed at time of tube removal – urinary tract infection is very
commonly associated with this procedure – and appropriate treatment given based on the
results of culture and sensitivity testing.

Ureteronephrectomy

Ureteronephrectomy may be indicated in cats with renal or ureteral trauma, ureteral

obstruction resulting in hydronephrosis, renal neoplasia or occasionally cats with ureteral
ectopia where resolution of the primary problem is not feasible.

Note: As far as possible, the contralateral kidney should be assessed for normality prior to
ureteronephrectomy and the owner should be warned that renal failure could be induced by
removing 50% of the total nephrons.

Cats with renal or ureteral trauma or ureteral obstruction (and ureteral ectopia) are likely to
have a relatively normally shaped kidney, with renal blood vessels in a normal anatomical
position, which makes these cases suitable for the less experienced surgeon. Where renal
neoplasia is the underlying reason for nephrectomy, this may have resulted in distortion of the
normal anatomy and significant neovascularisation, making for a more challenging surgery.

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Note: In cats with suspected renal neoplasia, fine-needle aspirates should be taken to rule out
lymphoma prior to performing ureteronephrectomy.

PROCEDURE

Note: An assistant is essential for this surgery

◆  dministration of antimicrobials is not usually required [clean surgery], unless

A
surgical time is anticipated to be >90 minutes.
◆ A standard ventral midline coeliotomy is performed.
❖ The falciform fat should be removed if it is impeding visibility.
◆ Moistened laparotomy swabs are placed on the edges of the incision and an
abdominal retractor is inserted.
◆ The entire abdomen is explored, looking in particular for evidence of metastasis if
renal neoplasia is suspected/diagnosed.
❖ Biopsy liver nodules if present – for histopathology.
◆ A duodenal or colonic manoeuvre is performed to expose the right or left kidney,
respectively. The intestine can be held in this position by the assistant, or malleable
retractors can be used by them to retract the organs.
◆ An incision is made through the peritoneum lateral to the kidney using
Metzenbaum scissors and Debakey forceps. This incision is extended cranially
and caudally using electrosurgery as needed (or consider use of a vessel-sealing
device in the case of neoplasia).
◆ Digital dissection or a large cotton bud is used to peel the retroperitoneal fat from
the kidney surface and to allow the kidney to be retracted medially.
◆ The hilar region of the kidney is palpated to identify the renal artery.

Note: 10% of cats have more than one renal artery –more commonly on
the left side

❖ Mixter forceps or mosquito haemostats are used to dissect around the artery.
❖ An encircling ligature is placed closest to the aorta with 2–3 metric multi- or
monofilament suture.
❖ A transfixing ligature is placed just distal to the first ligature with the same
material.
❖ A gap of approximately 0.5 cm is left and a further encircling ligature is placed
distal to the first two ligatures.
❖ The artery is cut between the second and third ligatures (leaving two ligatures
in the cat).
◆ The renal vein should now be visible – noted by its bluish colour.
❖ Mixter forceps or mosquito haemostats are used to dissect around the vein –
more cautiously than around the artery!
❖ Two encircling ligatures are placed approximately 0.5 cm apart.
❖ The vein is sectioned between the two ligatures.

Beware the position of the left ovarian vein emptying into the left renal vein in an
intact male/female cat – either neuter, or preserve this vessel. Multiple renal veins
may also be present – more commonly on the right side.
◆ Any remaining peritoneal attachments are peeled or dissected away, leaving the

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ureter still attached.

◆ The kidney is left in situ and the dissection is moved to the bladder.
◆ The ureter is located at its point of entry to the bladder wall.
❖ Dissection around the ureter close to the bladder is performed with Mixter
forceps.
❖ Two encircling ligatures are placed and the ureter is sectioned between them.
◆ The kidney is grasped and gentle traction is applied to remove the ureter from the
retroperitoneal space and out of the patient.
◆ The renal fossa is checked for haemorrhage.

Note: Haemostatic agents (e.g. Lyostypt or Vetigel) can be used to stop minor ooze.

◆  he abdomen is lavaged with warm saline, a swab and sharps count is completed,
T
gloves and instruments are changed if neoplasia is suspected, and routine
coeliotomy closure is performed.

Perineal urethrostomy
Perineal urethrostomy (PU) is the most commonly performed urethral surgery in the cat. It is
indicated for recurrent or unresolvable urethral obstruction, urethral stricture (in the penile
urethra) or distal urethral trauma. Amputation of the penile urethra and suturing of the pelvic
urethral mucosa to the skin of the perineum provides a much wider urethral opening, removing
the risk of future obstruction (or removing the area of injury).

Note: A positive contrast retrograde urethrogram should always be performed before

performing a PU to ensure there is no urethral pathology present cranial to the PU site.

PROCEDURE (WILSON AND HARRISON TECHNIQUE)

Note: An assistant is very useful for this surgery.

◆  he (male) cat is positioned in sternal recumbency at the end of the operating

T
table, with its hindlimbs extended over a sand or beanbag support and the tail
elevated over its back (secured with ties).

Ensure the sandbag is not excessively compressing the caudal abdomen during
surgery.

◆  purse-string suture is placed in the anus to prevent faecal contamination.

A
◆ A urinary catheter is placed to aid dissection and sutured in place.
◆ An elliptical incision is made around the prepuce and scrotum with a no. 15 blade.
◆ Metzenbaum scissors are used to dissect the subcutaneous fat ventral and lateral
to the penis. Allis tissue forceps can be placed on the penis/prepuce to aid with
manipulation, and the assistant can move this to facilitate dissection.
◆ Once the level of the ischium is reached, the ischiocavernosus muscles MUST be
cut to free the penile body sufficiently and avoid tension on the urethrostomy site
postoperatively. These can be identified by passing a curved haemostat beneath
them on either side. Electrosurgery is useful here to reduce haemorrhage. The
ventral penile ligament is also sectioned.

Failure to cut the ischiocavernosus muscles is the most common cause of PU

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failure/stricture.

◆  nce ventral dissection is complete, a digit can be readily passed between the
O
penile body and the ischium to palpate the pubis.
◆ Dorsal dissection is then performed to the level of the bulbourethral glands,
including sectioning of the retractor penis muscle.

In male cats neutered at a young age, the bulbourethral glands are unlikely to be
visible. In these cases, the level of dissection is a few centimetres cranial to the
caudal ischium.

◆  n incision is made in the more distal penile urethra, using the catheter as a
A
guide. This incision is then extended cranially with iris scissors to the proposed
urethrostomy site.

At the level of the urethrostomy site, an 8 Fr urinary catheter should easily pass
into the urethra and Kelly haemostats will pass up to the box lock.

◆  eginning dorsally, the urethral mucosa is sutured to the skin edges (no
B
subcutaneous tissue is included in these sutures). These sutures should be
performed with 1 or 1.5 metric monofilament suture in a simple interrupted or
continuous suture pattern.5 This should be performed meticulously – failure
to achieve primary healing will result in stricture formation. Magnification with
surgical loupes can be helpful.

Either absorbable or non-absorbable monofilament suture is suitable for

urethrostomy sites.5,6 If non-absorbable suture is used, these sutures are
removed after 10–14 days, under sedation.

◆ Suturing is continued laterally to form a suitably sized stoma (approximately

2 cm). When the stoma size is judged adequate, the remaining penis is ligated
with 2 metric monofilament suture and amputated. The subcutaneous fat and
remaining skin are sutured to complete the PU.

Postoperatively, a rigid buster collar is essential to prevent patient interference; ripped

newspaper is preferred to cat litter; urethral catheters and use of a rectal thermometer are
avoided. No cleaning of the stoma is performed until suture removal (if required).

References
1. Buote NJ, Kovak-McClaran JR, Loar AS, et al. The effect of preoperative antimicrobial administration
on culture results in dogs undergoing cystotomy. J Am Vet Med Assoc 2012; 241(9): 1185–1189.
2. Hammaide AJ, Martinez SA, Hauptman J. et al. Prospective comparison of four sampling methods
(cystocentesis, bladder mucosal swab, bladder mucosal biopsy, and urolith culture) to identify
urinary tract infections in dogs with urolithiasis. J Am Anim Hosp Assoc 1998; 34(5): 423–430.
3. Thieman-Mankin KM, Ellison GW, Jeyapaul CJ, et al. Comparison of short-term complication rates
between dogs and cats undergoing appositional single-layer or inverting double-layer cystotomy
closure: 144 cases (1993–2010). J Am Vet Med Assoc 2012; 240(1): 65–68.
4. Earley NF, Meakin LB, Parsons KJ, et al. Mechanical properties of 6 finger-trap suture techniques. Vet
Surg 2017; 46(6): 765–772.

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5. Agrodnia MD, Hauptman JG, Stanley BJ, et al. A simple continuous pattern using absorbable suture
for perineal urethrostomy in the cat: 18 cases (2000–2002). J Am Anim Hosp Assoc 2004; 40(6):
479–483.
6. Frem DL, Hottinger HA, Hunter SL, et al. Use of poliglecaprone 25 for perineal urethrostomy in cats: 61
cases (2007–2013). J Am Vet Med Assoc 2017; 251(8): 935–940.

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SYMPOSIUM

Drugs and cats – are they small dogs?

Jill E. Maddison BVSc, DipVetClinStud, PhD, FACVSc, SFHEA, MRCVS

Although cats and dogs are physiologically similar in many respects, and dosing regimens
recommended for dogs can frequently be extrapolated to cats, there are some important
differences in drug disposition between the two species that can have a profound influence
on dosing recommendations for cats in comparison to dogs. The majority of differences relate
to pharmacokinetic differences in drug metabolism. However, differences in haemoglobin
structure, receptors and behavioural differences may also account for differences in drug
disposition between the two species.

Giving the cat a drug

This can be challenging! There are fewer drug formulations developed specifically for cats,
medications may need to be split or crushed, and medications may not mix with food. As cats
do not drink much water, solid dose forms can become trapped in the oesophagus. This is
particularly an issue with doxycycline and clindamycin due to the risk of ulceration.

The taste preferences of cats can differ from those of dogs and this impacts the palatability
of a drug. For example, cats may like sucrose but not saccharin, and they prefer amino acids.
Dogs like salt but cats do not. Dogs avoid hot spices. Cats avoid medium-chain triglycerides
and caprylic acid.

Absorption and distribution

The feline small intestine is shorter than that of the dog; cats may compensate for this by a
slower transit time and increased intestinal permeability. Cats have a higher bacterial load in
their small intestine. They also have a smaller stomach and easily vomit if it is overloaded.

Because cats often graze (i.e. eat intermittently), tablets may not dissolve. They have a more
alkaline intestinal pH than dogs, which can potentially alter the absorption of some drugs.
For example, itraconazole needs an acidic environment to dissolve, and the oral solution is
absorbed much better than tablets in cats.

The kinetics of drug absorption appear to be similar in dogs and cats regardless of the route of
administration. There are minor differences in factors that influence drug distribution between
dogs and cats. For example, cats have a smaller blood volume per kg body weight (66–70 ml/
kg) than dogs (90 ml/kg) and therefore plasma drug concentrations may differ between the
two species for drugs that are confined to the plasma compartment.

Metabolism
Cats are deficient in some glucuronyl transferases, which are important for glucuronidation
of drugs, a Phase II metabolic process. There have only 2 isoforms, vs 10 in dogs and 9 in
humans. However, they are not deficient in all glucuronyl transferase families. In addition, a drug
normally metabolised by glucuronidation may have a wide safety margin or the drug may be

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metabolised by a different route in cats (although this can result in toxicity for some drugs). For
example, sulphation is well developed in cats compared with dogs, and acetylation, which is
deficient in dogs, appears to be well developed in cats. Acetylation is poor in the dog and good
in the cat. Drugs metabolised by this route will have a shorter duration of action in the cat, e.g.
hydralazine, diltiazem and sulphonamides.

Haemoglobin
Another species difference, which may increase the risk of adverse reactions in cats compared
with dogs, is the increased susceptibility of feline haemoglobin to oxidation and therefore
methaemoglobinaemia. There are a number of proposed mechanisms postulated to explain
this, including the different structure of feline haemoglobin, lower concentrations or activities or
intracellular repair enzymes and differences in the intracellular concentrations of glutathione-
conjugating enzymes. Drugs affecting oxidative processes include some the sulphonamides,
nitrofurans and sulphones.

Receptors
Differences between dogs and cats with respect to drug receptor distribution and affinity
have been described, with morphine representing the archetypal example. In addition to a
slower rate of biotransformation due to the deficiency of glucuronidation in the cat, differences
observed in the pharmacodynamic effects of morphine in the cat compared with the dog
include central nervous system (CNS) stimulation (CNS depression in the dog), centrally
mediated emesis at much reduced sensitivity compared with the dog (the dog requires a dose
1/740 of that of the cat), and pupillary dilation (miosis in the dog). However, at a dose of 0.1
mg/kg subcutaneously (compared with 0.1–2 mg/kg in the dog), morphine provides effective
analgesia.

Other drug effects

Other examples of drugs which have different effects in cats compared with dogs include
xylazine and febantel (which induce emesis much more readily in cats than in dogs) and
digitalis glycosides (the cat is less tolerant than the dog, presumably because of increased
sensitivity of feline cardiac Na+,K+-ATPase to inhibition).

Behavioural differences
The grooming behaviour of cats increases the likelihood that topically applied medications
will be ingested. Advantage can be taken of this behaviour by applying medications intended
for ingestion to accessible parts of the cat’s body (e.g. anthelmintic or antibiotic paste
preparations). However, cats are at greater risk of exposure to purposefully or adventitiously
applied topical toxicants such as disinfectants (particularly phenolics that are principally
candidates for glucuronidation) or pesticides. Indeed, concentrated preparations of permethrin
applied topically to cats can be lethal when ingested.

Other physiological factors that influence drug disposition

Other physiological factors that may influence drug disposition are similar in dogs and cats.

AGE
Age-related differences should always be considered. Paediatric and geriatric animals are
potentially more susceptible to adverse drug effects due to:
◆ Alterations in drug distribution (greater volume of distribution in paediatric
animals, reduced lean body mass and total body water in geriatric animals)
◆ Lower plasma protein (in young and old animals)
◆ Drug metabolism (reduced hepatic metabolism in neonates, and reduced hepatic

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blood flow and reduced hepatocyte mass and function in geriatric animals)
◆ Drug elimination (glomerular and tubular function is reduced in neonates and old
animals).

PATHOLOGY
Febrile state, dysfunction of the organs of metabolism and excretion, cardiovascular and renal
dysfunction affecting water balance and drug distribution, and gastrointestinal disorders
affecting drug absorption can all account for significant within-species differences in drug
disposition. Adjustment of dosage regimens or avoidance of the use of particular drugs may be
necessary in patients with particular disease states. Such disease factors that influence drug
disposition have a similar importance in cats and dogs.

It should be noted that there are no satisfactory laboratory indices of liver dysfunction to allow
prediction of the degree to which drug metabolism or disposition will be affected by liver
disease. Metabolising enzymes vary in how they change as liver function decreases – some
decline early, some decline proportionally to loss of function and some hang in there until right
at the end. It is impossible to predict!

In general, when administering drugs that are extensively metabolised by the liver to patients
with liver disease the dose interval should be prolonged. Examples of drugs where this should
be considered are benzodiazepines, NSAIDs and opioids.

The effect of inappetence in diseased cats is important as dietary protein is an important

source of sulphate and other compounds used in Phase II drug metabolism in cats. Taurine
may also be important. Anorexic cats therefore may be more susceptible to adverse drug
reactions because of reduced drug metabolism.

Table 1: Drugs not recommended for use in cats

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Table 2: Drugs that are therapeutically useful in cats but may have different dosing/toxicity/activity profiles than in
dogs

#ISFMRocksDublin 115
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 Dublin, 29 June – 2 July

Hocus pocus: the role of ultrasound in the critical

feline patient
Serge Chalhoub DVM, Dipl. ACVIM (SAIM)
Søren Boysen DVM, Dipl. ACVECC
Faculty of Veterinary Medicine, University of Calgary

General introduction to veterinary point-of-care ultrasound (POCUS)

In 2004, publication of the abdominal focused assessment with sonography for trauma (FAST)
exam in dogs that had suffered motor vehicular injury was the first work in small animals to
become more broadly known as point-of-care ultrasound (POCUS). Although the terms POCUS
and FAST are often used interchangeably, they are not synonymous. FAST exams, in both
human and veterinary medicine, were developed to – and still primarily focus on the search
for free fluid in body cavities and pneumothorax. By contrast, POCUS is broader in scope; it
incorporates all clinically driven real-time assessments that can be answered within minutes
using ultrasonography. More specifically, POCUS is defined as the acquisition, interpretation,
and immediate clinical integration of ultrasonographic imaging performed patient-side by an
attending clinician (not by a radiologist or cardiologist), with the goal of answering a focused
question or series of questions rather than assessing all structures of an organ(s).

General applications of POCUS

The application of POCUS exams varies depending on the clinical setting (Fig. 1), as follows:

1.  riage POCUS uses the minimum number of views possible to identify the most
T
immediate life-threatening and critical conditions;
2. Serial POCUS is applied to monitor the progression or resolution of pathology and
response to therapy;
3. Systemic or multi-organ POCUS is performed in more stable patients (with
or without specialist assistance) to detect asymptomatic conditions, new
developments, and/or to ensure sonographically detectable problems have not
arisen before undertaking procedures, anesthesia, or discharge/service transfer;
and
4. Interventional POCUS is used to reduce complications of procedures where
applicable (Fig. 1).

Which POCUS examination(s) to choose will also depend on the pre-test probability of a
problem being present. The nice thing about POCUS is that it is often limited to very specific
binary responses: for example, is fluid present yes/no? This is arguably one of the easiest
POCUS skills to learn and apply in veterinary patients, including cats. POCUS is easily applied to
rapidly search for free fluid in the pericardial, pleural, and abdominal spaces with a high degree
of accuracy. Furthermore, air in the pleural space (pneumothorax) can also be assessed,
although this does take more skill to master. Going one step beyond the search for free fluid
and/or pneumothorax, a quick assessment of the lungs and the left atrial:aortic ratio (LA:Ao)
of cats allows additional clinically driven and relevant questions to be answered with POCUS.
Most importantly, with minimal training the clinically driven question “is it cardiac, pulmonary,
or pleural space disease” can rapidly be answered in less than 1–2 minutes by adding the lung
and very simple/basic cardiac views to the POCUS examination.

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Figure 1: Point-of-care ultrasound (POCUS) exams

are patient centered and targeted. They are also
integrative and have 4 general applications, which
vary depending on the targeted objectives of the
scan, the pre-test probability of a problem being
present (based on history, initial clinical exam,
and other diagnostic findings), and the clinical
setting encountered: (1) triage POCUS uses the
minimum number of windows possible to identify
the most immediate life-threatening and critical
conditions; (2) serial POCUS is applied to monitor
the progression or resolution of any pathology and
response to therapy; (3) systemic or multi-organ
POCUS uses multiple windows in more stable patients
(with or without specialist assistance) to detect
asymptomatic conditions, new developments, and/
or to ensure sonographically detectable problems
have not arisen prior to undertaking procedures,
anesthesia, or discharge/service transfer; and (4)
therapeutic POCUS is used to reduce complications
of interventions where applicable. Source: Dr. Søren
Boysen, with permission.

POCUS exams are not meant to replace comprehensive sonographic exams, which are
traditionally consultative in nature, being performed and interpreted by radiologists,
cardiologists, or other board-certified specialists. Consultative sonography is intended to
comprehensively evaluate extensive anatomy and physiology, often being performed with
numerous open differential diagnoses in mind. POCUS applies specific goal-directed questions
to well-defined clinical scenarios or problems to interpret a limited number of conditions with
the goal of expediting patient care (e.g., presence of free fluid yes/no; pulmonary edema
(B-lines) yes/no, etc.). POCUS therefore follows a different standard of practice compared with
consultative sonography (see Table 1). For example, one may initially perform an abdominal
POCUS exam in the cardiovascularly unstable feline patient that presents in shock with a
history of protracted
Table 1 Comparison of formal and POCUS exams vomiting, bradycardia,
hypothermia, weakness,
lethargy, and not
eating. The initial
focused objective of
the scan, considering
the history and clinical
findings, would be to
rapidly identify the
presence or absence
of free abdominal
fluid, which if present
can be aspirated and
evaluated. In contrast, a
radiologist-performed,
consultative ultrasound
of the cat’s abdomen

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(when the cat is more stable) would describe the entire anatomy of the abdomen, including
a systematic, detailed description of the solid and hollow viscus organs. By keeping POCUS
focused to specific goal-directed questions, within the context of defined clinical scenarios, the
chance of errors is decreased, the most important clinically relevant questions are prioritized,
and user confidence is increased.

General indications to perform POCUS

There is really no limit to the indications for POCUS, with new applications being developed
as research grows; however, the applications will vary depending on the clinical scenario
encountered and the sonographer’s comfort and skill level. The easiest way to start, particularly
in cats, which are less prone to pneumothorax in comparison to dogs, is to look for free fluid
in the various body cavities (pericardial, pleural, and abdominal), along with a quick scan of
the lungs to look for increased B-lines and the LA:Ao to rapidly help differentiate pulmonary
parenchymal from heart failure as a cause of respiratory distress in cats.

Specific indications of POCUS exams in cats include trauma patients, any unstable cat, any cat
as part of the initial triage exam, post-surgery cats not recovering as expected, routine daily
assessment of hospitalized cats, and any time free abdominal fluid might be suspected.

Serial POCUS
Serial POCUS exams are recommended to:

1.  onitor the progression/resolution of patients with positive findings (e.g., resolution

M
or progression of cavitary fluid volumes) and
2. To detect new developments in patients over time, particularly those that become
unstable in the absence of an identifiable cause, and/or have received significant
quantities of intravascular fluids or other therapeutic interventions.
The frequency of serial exams depends on the patient and may vary from several minutes to
hours. The exam should be repeated as often as required to identify the reason a patient is
unstable if no identifiable cause is evident on ancillary diagnostic tests, or to determine why a
patient changes from stable to unstable. If the patient is stable and the goal is to simply follow
the resolution or progression of underlying pathology, the exam can be repeated every 2–4
hours.

Limitations
In most cases POCUS is better at ruling in pathology than ruling it out; a negative POCUS
result does not exclude pathology. In humans, abdominal POCUS exams have low sensitivity
for penetrating abdominal injury and retroperitoneal injury, and this is also likely in cats.
However, it is still worth evaluating cats with penetrating injury and suspected retroperitoneal
injury, as a positive result may dictate further diagnostics and therapy. Initial hypovolemia
or severe dehydration may limit the detection of effusion, making it important to use serial
exams during and following adequate resuscitation. There is a learning curve to POCUS
exams and sonographers should know their limitations; some skills are easier to acquire than
others (e.g., fluid detection vs pneumothorax). Finally, although POCUS aims to answer point-
of-care binary-driven answers to specific questions, the clinical interpretation of POCUS is
highly dependent on concurrent clinical findings such as signalment, history and physical
examination, as well as other binary POCUS questions (e.g., a cat presenting for collapse with
the POCUS finding of a thick left ventricular wall and a small left atrium would be suggestive
of pseudohypertrophy secondary to hypovolemia, while a thick left ventricular wall associated
with an enlarged left atrium and increased B-lines would be suggestive of hypertrophic
cardiomyopathy). As mentioned above, POCUS is part of the holistic approach to patient care.

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Abdominal POCUS
PATIENT POSITIONING AND MACHINE SETTINGS

◆  ring the ultrasound machine to the patient! Do not discontinue stabilization

B
efforts or compromise patient safety to perform any POCUS exam!
◆ A designated portable ultrasound unit is recommended for busy clinics to ensure
ultrasound is available at the time of patient presentation and can be transported
to the patient as needed. Handheld ultrasound units are a relatively low-cost
option that makes applications of POCUS more readily available across the
veterinary profession.
◆ Given that concurrent injuries can preclude placing patients in a particular
position (e.g., respiratory distress, spinal cord injury, etc.), sonographers should
become familiar with performing POCUS exams with patients in ALL positions
(lateral, sternal, standing). Most importantly in cats, given the evidence to support
the benefits of low-stress handlings, patients should be scanned in the position in
which they are most comfortable whenever possible.
◆ To maximize success, the scanner must consider gravitational effects and patient
positioning for different pathologies and make minor protocol adjustments
accordingly; fluid falls while air rises, which changes based on patient positioning.
◆ Dorsal recumbency is contraindicated in unstable patients (respiratory and
cardiovascular), and the authors never scan patients in dorsal recumbency.
◆ Patients initially placed in lateral recumbency can be gently repositioned into
sternal recumbency to assess the gravity-dependent paralumbar region if
necessary, following evaluation of the other sites.
◆ A microconvex/curvilinear probe is used for all feline POCUS scanning, with a
frequency generally between 5 mHz (patients >15 kg) and 7.5 mHz (patients
<15kg). A linear array probe is sometimes helpful in cats when assessing
superficial abdominal structures but all POCUS questions can be answered with a
microconvex probe.
◆ Although ultrasound consoles have many functions, the key machine functions for
POCUS are frequency, gain, depth and focal position.
❖ Frequency is adjusted to highlight structures of interest, typically 5–7.5 mHz (see
individual sections to follow). As for any sonographic exam, higher-frequency
settings are indicated for more superficial structures, while lower-frequency
settings are required for evaluate deeper structures.
❖ Gain: The received ultrasound signal can be modified by adjusting the gain.
Decreasing the gain yields a darker (black) image with a loss of detail, while
increasing the gain yields a brighter (whiter) image. Gain is adjusted to user
preference and the structures of interest, depending on the binary question to
be answered (see individual sections).
❖ Gain can be set to maximize thr detection of anechoic fluid by using either bile
in the gall bladder or urine in the urinary bladder as a reference echogenicity
for fluid.
❖ Depth is adjusted to visualize the region of interest. Begin with a somewhat
higher depth setting in order to obtain a “big picture” assessment to find the
structure of interest, and then gradually decrease the depth to visualize the
desired structures in more detail.
❖ Extending the depth at the subxiphoid location allows evaluation of the pleural
and pericardial spaces (see below).
❖ Focal position is adjusted to the area of interest.

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◆  lcohol is often used as the coupling agent; part the fur so the skin is visible before
A
applying alcohol.

NOTE: Ultrasound gel can also be used alone or in combination with alcohol and appears to be
easier to use with some cats, particularly those placed in a pediatric incubator or equivalent,
where hypothermia may become more of an issue due to the evaporative cooling of liquid
alcohol.

◆  lcohol can create artifact on subsequent radiographs and should be replaced

A
with gel if electrocautery or defibrillation is a possibility due to the risk of fire.
◆ Sedation is rarely required as POCUS is non-invasive and requires minimal
restraint. In some situations, sedation may decrease anxiety and facilitate POCUS.
◆ If image resolution is questionable, clipping of the fur and the addition of
ultrasound gel may improve image quality but this is very rarely, if ever, needed in
cats.
◆ It is essential that all key organs at each site be thoroughly evaluated to ensure
the specific question to interpret is confidently answered. The 5 sites currently
evaluated during feline abdominal POCUS are 1) the subxiphoid window, 2) the
umbilical window 3) the urinary bladder window, 4) the right paralumbar window,
and 5) the left paralumbar window (Fig. 2).
◆ Fanning and rocking the probe through 45° angles in both longitudinal and
transverse axes to the organ of interest at all sites maximizes the chance of
detecting pathology while minimizing false-negative and false-positive results.

Figure 2: All 5 sites of abdominal POCUS (1. subxiphoid, 2. umbilical, 3. urinary bladder, 4. right paralumbar, and
with the patient rolled into sternal recumbency for the remaining gravity-dependent 5) left paralumbar) are
evaluated in all patients regardless of patient positioning; however, the area scanned should be modified slightly
depending on the pathology to rule in/rule out and considering how patient positioning will affect where pathology
accumulates. For example, if the patient is in a standing position and the goal is to detect free peritoneal fluid,
the probe is placed directly on the midline over the umbilical and urinary bladder regions with the ultrasound
beam directed towards the spine (vs towards the tabletop when the patient is in a lateral position). Each location
is evaluated in longitudinal and transverse planes, with rocking and fanning of the probe to maximize the area
evaluated and to ensure all target structures/sites are thoroughly evaluated. At the urinary bladder and umbilical
sites, with the patient in lateral recumbency as shown, the probe should be directed from the non-gravity-
dependent side of the patient towards the gravity-dependent body wall, where fluid is most likely to accumulate.

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Subxiphoid (Fig. 2): the diaphragm, liver, gall bladder, stomach, and the areas between these
structures are evaluated.
◆ To find the correct subxiphoid site, palpate the ribs and follow them cranioventrally
until the “V” at the xiphoid region is identified.
◆ To begin with, place the probe in the point of the “V” in longitudinal axis to the
body.
◆ Rock the probe cranially and adjust the depth until the liver and diaphragm are
visible within the ultrasound image.
◆ Fan the probe through all planes of the liver and rock the probe to assess all
parts of the liver (small fluid accumulations often collect between the liver and
diaphragm and/or between liver lobes).
◆ The gall bladder is visualized to the right of midline – cats often have bilobed gall
bladders, which is a normal finding. The common bile duct of cats is often more
tortuous as well.
◆ By placing the probe directly perpendicular to the spine at the subxiphoid region
and slowly fanning left and right, the proximal stomach wall is identified and can
be assessed for motility (see below).
◆ Following longitudinal plane scanning, the probe is rotated into the transverse axis
and again fanned and rocked through all planes.
◆ The caudal vena cava, pleural space, and pericardial space can also be
evaluated at the subxiphoid site by extending the depth of the probe beyond the
diaphragm.
◆ NOTE that in cats the heart will often not be visible at the subxiphoid view if the
apex of the heart fails to contact the diaphragm, which is normal in many cats. If
the heart is, however, enlarged (due to cardiomyopathy, pericardial effusion, or
both) then it can often be visualized via the subxiphoid view. The most common
cause of pericardial effusion in cats is hypertrophic cardiomyopathy, and the
effusion is often insufficient in quantity to be clinical or require pericardiocentesis.

Umbilical (Fig. 2): the gravity-dependent body wall, intestines, spleen, and the regions between
these structures are evaluated.
◆ To find the correct site, the probe is placed over the umbilical region and directed
towards the tabletop with the patient in lateral recumbency. The protocol is
modified slightly if the patient is in sternal recumbency or standing.
◆ The probe is then rocked and fanned through all longitudinal and transverse
planes looking for specific pathology, typically free peritoneal fluid, although other
pathology can sometimes be detected at the umbilical site depending on the
specific clinical question asked.
❖ Failure to assess the umbilical site may result in displacement of gravity-
dependent pathology as the probe is slid under the patient to assess the
gravity-dependent paralumbar site.

Urinary bladder (Fig 2): the urinary bladder, gravity-dependent and non-gravity-dependent
body walls, and the areas between these structures are evaluated.
◆ To find the urinary bladder, the probe is initially placed in the longitudinal axis to
the body, between the pelvic limbs.
◆ Avoid applying too much pressure to the probe as this tends to compress and
displace the urinary bladder.
◆ Adjust the depth settings to allow both the dorsal and ventral walls of the urinary
bladder to be visualized.

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◆ If the patient is in lateral recumbency, slide the probe to the non-gravity-
dependent side of the patient and angle the ultrasound beam through the urinary
bladder, while fanning, to identify fluid that might accumulate in the deeper
gravity-dependent sites along the body wall.
◆ Slide the probe cranially to locate the apex of the bladder and fan the probe
through all planes at the bladder apex.
◆ Slide the probe caudally to evaluate the trigone and urethral areas.
◆ Following thorough longitudinal scanning, rotate the probe to a transverse axis
and repeat the scan.
◆ If the patient is standing or in sternal recumbency, the probe is placed on the
midline with the ultrasound beam directed towards the spine to ensure the most
gravity-dependent areas between the abdominal wall and ventral urinary bladder
wall are assessed.

Left paralumbar (Fig. 2): the spleen, left kidney, intestines, body wall, and the areas between
these structures are evaluated.
◆ To find the left paralumbar region, start by finding the left kidney: Use your index
finger to trace the last rib from the mid-abdominal region caudally and dorsally
until the last rib contacts the hypaxial/lumbar muscles.
◆ NOTE: the kidney is usually located at this site. In cats is it common to find both
kidneys from either paralumbar location.
◆ The probe is fanned and rocked through all longitudinal and transverse axes to
assess the left kidney. Depending on operator experience the renal pelvis may be
assessed at this site (see below).
◆ It may be easier to find the spleen and slide the probe caudally until the left kidney
is located.
◆ The spleen is fairly mobile and the tip may sometimes be seen contacting the left
kidney.
◆ If the spleen is not encountered when scanning the left kidney, it can often be
located cranial and often lateral to the left kidney.

Right paralumbar (Fig, 2): the right caudal liver lobe, right kidney, body wall, duodenum, and
the areas between these structures are evaluated.
◆ To find the right paralumbar region in cats, trace the last rib dorsally with
your finger until the hypaxial/lumbar muscles are encountered. The probe is
then placed caudal to the last rib, just below the hypaxial/lumbar muscles, in
longitudinal axis to the body. Increase the depth setting and then fan and rock
the probe at this location until the kidney is visualized. Once found, decrease the
depth until the kidney fills the proximal half of the ultrasound image.
◆ NOTE: In cats, unlike dogs, it is not always necessary to place the probe between
the most caudal ribs (e.g., 11th or 12th intercostal spaces) to locate the kidneys.
◆ When the correct site is identified, the probe is fanned and rocked in both
the longitudinal and transverse axis to assess the kidney and its surrounding
structures. Depending on the skill of the operator, the renal pelvis can also be
assessed (see below).

◆  bdominal effusion: Uncontained free abdominal fluid appears black (anechoic

A
or hypoechoic) and forms sharp angles and triangles between organs and
structures. To make sure fluid is free and not contained within a structure (e.g.,
stomach, urinary bladder, gall bladder?) be sure to thoroughly evaluate all key

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organs at all sites, fanning through all planes in both the longitudinal and the
transverse axis. Decrease the depth to highlight suspected areas if needed.
❖ If free fluid is identified it is imperative that fluid samples be collected for in-
house analysis (total solids, cell count, cytology, and more specific analyses
such as glucose, lactate, creatinine, triglycerides, and bilirubin) which may
assist with the diagnosis, guide other diagnostics, and dictate immediate
interventions. Ultrasound guidance is very helpful as it allows the aspiration
needle to be visualized, ensuring that fluid can be collected with confidence
and with fewer complications. Consider sample submission to a reference
laboratory for cytology and culture.
❖ N OTE: Compared with dogs, a higher proportion of healthy adult cats and
kittens may have a small degree of ultrasonographically detectable free
abdominal fluid visible on abdominal POCUS. However, the total quantity is
quite small, with pockets of <2–3 mm of free fluid, and should be interpreted in
light of the history and clinical findings.

PITFALLS OF ABDOMINAL POCUS AND FREE ABDOMINAL FLUID

Hepatic vessels can sometimes be mistaken for fluid. It is important to remember that
ultrasound is a dynamic imaging modality and therefore by fanning, rocking, sweeping, sliding,
changing the depth, and rotating the probe (longitudinal to transverse and vice versa) it is
easier to confirm the presence of free abdominal fluid vs contained fluid (blood) within vessels.

Edge shadowing is where the ultrasound beams create dark shadows on the edges of an
organ, which can be mistaken for fluid. It can cause the wall of a structure to partially disappear,
which should not be confused for rupture of an organ (e.g., do not confuse edge artifact for
rupture of the urinary bladder or other organ rupture). Edge shadowing from structures such as
the gall bladder, stomach wall, urinary bladder, etc. should not be mistaken for free fluid. Edge
shadowing will disappear depending on the angle at which the ultrasound beam strikes the
structures of interest; changing the angle of insonation by manipulating the probe to change
this angle is helpful.

Intestinal and stomach wall and content? can also be mistaken for abnormal fluid or
structures, particularly when intestinal wall edema is present. By moving the probe and
assessing multiple planes (longitudinal and transverse) it will be easier to determine whether
the structure is intestine or stomach.

Mirror image artifact of the gall bladder, or hepatic vessels, which are often distorted, can be
confused for pleural effusion, or even sometimes misinterpreted as signs of diaphragmatic
hernia.

Acute hemorrhage or very cellular effusions can sometime mimic soft tissue structures
or stomach content, making it more difficult to identify as free abdominal fluid. Probe
manipulations (e.g., applying pressure to the probe to displace underlying free abdominal fluid)
can sometime create “swirling”, which may help differentiate cellular effusion from tissues.
Fanning and rocking the probe will also often identify “structures” within the fluid (e.g., floating
omentum or intestines, etc.) and may allow sharp angles/triangles to be visualized.

Pleura and lung ultrasound (PLUS)

Pleural space and lung pathology are common causes of respiratory distress in cats. The
diagnosis of underlying pleural space and lung disease in cats is enhanced with the application

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of pleural and lung ultrasound (PLUS) (Fig. 3). In life-threatening situations of respiratory
distress, it is important for the practitioner to consider the most likely cause of dyspnea as
suggested by the signalment, emergency triage, history and/or clinical examination. The
practitioner should similarly understand where lesions are suspected to accumulate depending
on patient position (e.g., air rises and fluid falls; in sternal recumbency with pneumothorax
air accumulates dorsally, pleural effusion ventrally; in lateral recumbency air accumulates
at the widest gravity-independent point and fluid at the widest gravity-dependent point of
the thorax). Finally, the practitioner should recognize the hallmarks of normal and pathologic
artifacts, as well as the sonographically scannable PLUS borders to decrease the chance of
false-negative and false-positive results.

Using binary questions with PLUS (pleural fluid yes/no, B lines yes/no, etc.) ensures specific
pathologies are considered and systematically ruled in or ruled out on the list of differential
diagnoses. This approach helps to keep these exams standardized, as well as answering
important clinical questions (hence why we do these exams). The binary question approach
allows the clinician to expand their ultrasound skills as they become more comfortable with
sonography and allows newer techniques to be incorporated without drastically changing the
techniques used.

It is important to understand that PLUS involves an understanding of how to interpret artifacts,

as healthy lungs contain air which impedes ultrasound transmission, rendering it impossible to
visualize the lung itself. Fortunately, the normal findings of PLUS change because of underlying
pleura and lung pathology, which allows pathology to be identified via artifact interpretation
with relatively high sensitivity and specificity.

Figure 3: Pleural and lung ultrasound (PLUS) of the cat. Depending on the clinical presentation and triage findings,
different clinically relevant questions may need to be ruled out with greater urgency than others. There are 3
general conditions to assess with PLUS: 1) pneumothorax (2a; not covered in this talk) 2) alveolar interstitial disease
or lung consolidations (2b; consolidations will not be covered in detail in this talk); and 3) pleural effusion (2c).
The cat should be scanned in the position in which it is most comfortable. In dyspneic cats this is often standing
or in sternal recumbency. Standing is shown in the image. 2a) To ensure lung is identified and to standardize the

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PLUS exam, begin by placing the probe just caudal to the thoracic limb at the level of the middle to upper two-
thirds of the thorax (red asterisk). This allows identification of the pulmonary parenchyma and avoids confusing
other structures for lung (the probe should be over only the ribs and lung to start). 2b) Protocol to assess for
pneumothorax, which will not be covered in this talk. 2c) To assess for lung pathology, multiple lung regions should
be assessed. The sliding PLUS protocol scans between sonographically defined lung borders to ensure multiple lung
regions are assessed in a systematic “S”-shaped fashion (red arrow). Pulling the skin towards the starting location
(similar to when placing a chest tube) will significantly reduce the quantity of alcohol required to scan the lung sites
as the probe and skin can be moved together. 2d) To assess pleural effusion, the ventral pleural borders should be
scanned. To identify the most ventral pleural borders, the probe can be slid ventrally in a parallel orientation to the
ribs until the sternal muscles are identified. To help differentiate pleural and pericardial effusion, the pericardio-
diaphragmatic window should be identified. To find the pericardio-diaphragmatic window, slide the probe caudally
from the mid-thoracic region until the curtain sign is identified, and then ventrally along the curtain sign until the
heart becomes visible or the costochondral junctions are reached (red arrow). Moderate to large volumes of pleural
effusion can be identified at this location. 2e) For scant to small volumes of pleural effusion, the probe is turned
parallel to the ribs and slid ventrally until the pectoral/sternal muscles fill one-third of the sonographic image. Each
intercostal space is then assessed by sliding the probe cranial a rib space at a time, while also scanning dorsally to
identify ventral lung at the cardiac notch in addition to the ventral pleural space borders. Figure courtesy of Søren
Boysen, 2021, with permission.
https://www.dropbox.com/s/mz7ligov4ilcdc6/1b%20PLUS%20trimmed%20cat.mp4?dl=0

PLEURAL EFFUSION
Lung ultrasound is less sensitive and specific for the identification of pleural effusion in cats
than has been reported in humans. Fluid appears as hypoechoic/black accumulations forming
sharp angles between the thoracic wall and lungs. It can be differentiated from pericardial
effusion at the pericardio-diaphragmatic window (Fig. 2d). Mild quantities of pleural effusion
accumulate at the ventral borders in sternally recumbent patients and the widest gravity-
dependent locations in laterally restrained patients. Turning the probe parallel to the ribs and
scanning the most ventral regions of patients in sternal recumbency increases the sensitivity of
finding fluid (Fig 2e).

ALVEOLAR INTERSTITIAL SYNDROME

The sliding PLUS protocol scans between sonographically defined lung borders to ensure
multiple lung regions are assessed in a systematic “S”-shaped fashion (Fig. 2c). The presence
of >3 B-lines, or coalescing B-lines, is diagnostic of alveolar interstitial syndrome (AIS). Only
pathology reaching the lung surface is detected via ultrasound; however, most diseases
causing AIS (non-cardiogenic and cardiogenic pulmonary edema, contusions, pneumonia,
etc.) reach the lung surface, at least in humans. POCUS has been described to successfully
diagnose and monitor cardiogenic pulmonary edema and aspiration pneumonia in cats.
Although lung consolidation can also be detected with PLUS, this is beyond the scope of this talk.

POCUS AND PATIENT POSITION FOR THE DYSPNEIC CAT

Cats are easily stressed and can decompensate when dyspneic: sternal recumbency is the
preferred position for dyspneic cats (some prefer standing). Shaving is not required; the fur is
parted and alcohol is used as the coupling agent for all POCUS exams.

Cardiac POCUS
Cardiac POCUS is a quick subjective evaluation of cardiac function and rapidly identifies
pericardial effusion, tamponade, cardiomyopathy, left-sided congestive heart disease, left
ventricular (pseudo)hypertrophy, right-sided cardiac enlargement, and interventricular septal
deviation, all of which should be assessed in the feline patient presenting for respiratory
distress. However, for novice sonographers the goal of cardiac POCUS in cats is to look for
pericardial effusion and to subjectively assess (eyeball technique) the LA:Ao, as these are
arguably two of the easier cardiac ultrasound skills to learn (Fig. 4). Evidence suggests that
novice sonographers can obtain the windows necessary to assess these structures in cats with
minimal training.

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Figure 4: Schematic and still images of

the different right parasternal short-
axis views, starting at the level of the
papillary muscles and moving towards
the heart base through the mitral valve
until reaching the left atrial to aortic
root. a) The initial view obtained is
often the midventricular region of the
right parasternal short-axis window
at the level of the papillary muscles,
referred to as the “mushroom” view. b)
After obtaining the “mushroom” view
with the probe in the right parasternal
short-axis plane, fan the probe dorsally,
directing the ultrasound beams towards
the base of the heart until the mitral
valve becomes apparent within the
left ventricular lumen. This is the “fish
mouth view”. c) Fanning the probe more
dorsally from the mitral valve towards
the base of the heart will identify the “Mercedes and the whale”, which is used to evaluate the left atrial:aortic root
ratio (LA:Ao). Figure courtesy of Søren Boysen, 2021, with permission.
https://www.dropbox.com/s/m2wkfp4p9t6ivdr/1a%20Feline%20cardiac.mp4?dl=0

NORMAL CARDIAC VIEWS ASSESSED ON CARDIAC POCUS

◆  here are many views that can be obtained on short-axis right parasternal
T
imaging of the heart (Fig. 4).
◆ However, there are only 3 key windows to learn with cardiac POCUS that will
identify the majority of pathologies we are worried about: 1) the 4-chamber long-
axis right parasternal view, 2) the “mushroom”, and 3) the left atrial aortic view
of the right parasternal short-axis view. This talk will focus on the last window
mentioned, which is most helpful in determining whether respiratory stress in cats
with identifiable B-lines on ultrasound is due to left-sided congestive heart failure
or not. The other windows and clinically relevant questions of cardiac POCUS in
cats will not be covered in this lecture.

TECHNIQUE
Cardiac POCUS in cats with dyspnea is often performed with the patient standing or in sternal
recumbency and starts with palpation of the chest, identifying the apical beat of the heart,
which is the site at which the probe should be placed (1–2 cm above the sternum; 4th–5th
intercostal space).

CARDIAC CHAMBERS (LA:AO)

◆  he goal is to determine if a patient presenting with respiratory distress has signs
T
related to congestive heart failure, primary pulmonary disease, pleural effusion, or
a combination of these three.
◆ Obtain the “Mercedes and a whale” view of the heart (right parasternal short-axis
view).
◆ The chambers observed will be the left atrium (whale), aorta (Mercedes symbol),
right ventricle and right atrium above, and the pulmonary artery beside the aorta
◆ From this view, one can subjectively estimate the size of the left atrium relative to
the aorta.
◆ To do this, freeze the image on your machine. You can play with your cine loop
function to help return to the most ideal image. The subjective estimate of left
atrial size should be made when the aortic valves close, and the atrium is at its

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largest during systole.

◆ A normal LA:Ao is less than 1.5 in cats. There is a gray zone regarding left atrial
enlargement but values above 2 should prompt serious consideration of left atrial
enlargement and likely indicates significant cardiac disease.
◆ Another subjective way to determine whether the left atrium is enlarged is to
estimate how many aortas could fit in the left atrium. If it is 4 or more, then the left
atrium is likely very enlarged.

References
Available upon request

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 Dublin, 29 June – 2 July

CLINICAL PRACTICE STREAM

Fluids and CRIs for felines – making the maths easy

Laura Jones
BSc (Hons), DipAVN (Small Animal), ISFMDipFN, VTS(SAIM), RVN

Introduction
The administration of both intravenous fluid therapy and medications via constant-rate
infusion (CRI) are important skills for the veterinary nurse. In order to do this successfully, the
team must understand where fluid losses originate from and how they differ, as well as how to
quantify fluid losses and calculate their replacement.

This session will provide an overview of fluid therapy, including fluid losses, calculations and
fluid types commonly used in cats. Lastly, we will discuss options for CRI administration, and
how to calculate and administer these.

Fluid losses
The first steps in providing fluid therapy are determining if fluid losses are present, how severe
those losses are and where those losses have originated from. This is achieved by reviewing the
patient’s clinical history and performing a thorough clinical examination in order to determine
the type of fluids lost and whether any hydration or perfusion deficits are present:1,2,3
◆ Hypotonic fluid (fluid with a lower concentration than plasma) losses occur when
there is a primary water depletion, for example, if a patient is not drinking or has
increased water losses through polyuria (such as with chronic kidney disease,
diabetes mellitus or diabetes insipidus) and is not drinking sufficient amounts to
keep up with increased losses.4 Where hypotonic losses occur, water moves from
the intracellular space to equilibrate fluid levels. This results in dehydration.4
◆ Isotonic fluid (fluid the same concentration as plasma) losses occur when water
and electrolytes are lost, for example, through haemorrhage or extracellular fluid
losses such as vomiting and diarrhoea.2,4 With isotonic losses, fluid does not move
to compensate for any losses, leading to intravascular volume reduction and
hypovolaemia.2,4
◆ Hypertonic fluid (fluid with a higher concentration than plasma) losses are
seen less commonly, but include third-space fluid losses (e.g., pleural effusion
or ascites). When hypertonic fluid is lost, the extracellular fluid becomes less
concentrated than the intracellular fluid, causing water to move into cells to
equilibrate the two compartments. This worsens any hypovolaemia present, as
the intravascular volume reduces further.2,4

Identifying dehydration and hypovolaemia

Dehydration and hypovolaemia are not interchangeable terms and are specific to the
body compartments from which fluid is lost. Dehydration occurs when fluid is lost from the
intracellular and interstitial fluid compartments, unlike hypovolaemia, where fluid is lost from
the intravascular space. Intravascular fluid losses cause a reduction in tissue perfusion (blood,
and therefore oxygen, delivery). The two conditions have different clinical signs and are
managed in different ways.4

Patients with hypovolaemia have changes in heart rate, pulse quality, respiratory rate,

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mucous membrane colour, capillary refill time, mentation, and the temperature and colour
of their extremities; these are termed ‘forward perfusion parameters’.3 Specifically, signs of
hypovolaemia include:5
◆ Bradycardia (heart rate >160 bpm) (*Note – this differs from dogs, which become
tachycardic during hypovolaemia)
◆ Hypotension (systolic arterial pressure <100 mmHg)
◆ Pale mucous membranes
◆ Progressively weak dorsal pedal and femoral pulses
◆ Hypothermia (temperature <38.0oC)
◆ Plasma lactate level >2.5 mmol/l4.5.

Patients with hydration deficits have changes in skin turgor (elasticity), moistness of mucous
membranes and globe position.3,4 The severity of these signs can be used to estimate the
patient’s percentage dehydration, which can be used to calculate replacement fluid volumes
(Table 1). Patients with severe dehydration can also have changes to their forward perfusion
parameters.3
Table 1: Assessment of hydration deficits4

Fluid selection
The main types of fluid therapy used in practice are crystalloids and colloids (including blood
products); the exact fluid type used will depend on the fluid deficit present and the patient’s
underlying disease process.4

Crystalloids are solutions that can easily leave the intravascular space and move into
other fluid compartments, particularly the intracellular compartment.3,4 They contain water,
electrolytes and other solutes in varying concentrations, and are typically used to treat
dehydration and electrolyte abnormalities and to correct free water deficits.3 Crystalloids can
be categorised into the following:
◆ Free water: These include 5% dextrose in sterile water, 4% dextrose in 0.18% saline,
and 0.45% saline. Free-water solutions are hypotonic, and after administration
the dextrose is rapidly metabolised, leaving water behind.3,4 These fluids replenish
the interstitial and intracellular fluid compartments, but are not suitable for the
replenishment of intravascular volume or the correction of perfusion deficits.3,4
◆ Replacement solutions: These include lactated Ringer’s (Hartmann’s) solution,

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0.9% saline and Ringer’s solution. Replacement solutions are balanced, isotonic
crystalloids that can be used to replenish both the extracellular and intracellular
fluid compartments.3,4 These solutions are versatile and used frequently in practice
to correct both hypovolaemia and dehydration, as well as to compensate for any
ongoing fluid losses.3 When used to replenish the intravascular space, these fluids
will equilibrate with the surrounding interstitial fluid, leaving only 25% of the fluid
volume present within the vascular space after an hour.3
◆ Replacement fluids have relatively low concentrations of potassium as they are
similar in composition to extracellular fluid, and so with long-term use patients can
become hypokalaemic, particularly if they have concurrent anorexia.3
◆ Maintenance solutions: Maintenance solutions are used rarely and include fluids
such as Plasmalyte-M. They are balanced, isotonic solutions with higher potassium
concentrations and lower sodium concentrations than replacement fluids.3 These
solutions may be used after fluid deficits and any electrolyte derangements have
been corrected.3 These solutions are typically used in combination with 0.9% saline,
and can be administered only slowly.3,4
◆ Hypertonic solutions: 7.2% saline is a hypertonic crystalloid commonly used in
practice. Hypertonic crystalloids have a higher osmolarity than plasma; when
administered, they create an osmotic gradient that pulls water from the interstitial
space into the circulation.3,4 Because they draw water from the interstitial space,
they should never be used in a dehydrated patient.
Typically, a 2–4ml/kg bolus is used in cats, given over 2–5 minutes;4 as the fluids
will be redistributed over time, any hypertonic fluids should be followed with an
appropriate replacement solution.4

Colloids are large molecules that increase the colloidal pressure of plasma, holding fluid
within the intravascular space after administration and subsequently increasing intravascular
volume.3,4 They can be natural or synthetic:
◆ Synthetic colloids include gelatins and hydroxyethyl starches. Gelatins are created
from mammalian collagen and contain relatively small molecules, so they have
a shorter duration of effect than other colloids; after 90 minutes of administration,
only 24% remains in the circulation.4 Hydroxyethyl starches are derived from plant
starches and are typically administered as a bolus of 1–5ml/kg in cats.4,6
◆ Natural colloids include blood products such as whole blood, plasma, packed red
blood cells and albumin.3

Calculating fluid requirements

The rate and method of fluid administration will depend on the type of fluid deficit present.

Patients with perfusion deficits or hypovolaemia will require urgent, rapid volume resuscitation
as a life-saving procedure;4 this is given as larger fluid boluses (Table 2) over shorter periods
of time (typically 15–60 minutes), with regular monitoring of forward perfusion parameters and
fluid rates adjusted based on these results.4
Table 2: Bolus fluid rates in the hypovolaemic cat4

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Hydration deficits are calculated based on the patient’s estimated percentage dehydration.

Fluid deficit can be calculated using the formula

body weight (kg) x % dehydration/100 = volume to correct (in litres)2,6 or
body weight (kg) x % dehydration x 10 = volume to correct (in ml).

Hydration deficits are typically corrected over 24–48 hours, depending on the severity of
dehydration and the individual patient or disease process.4 Following the correction of any
dehydration, fluid rates should be reassessed and adjusted to meet the patient’s maintenance
fluid requirements.

Maintenance fluid requirements in cats can be calculated using the formula

body weight (kg)0.75 x 80 = volume required per day (in ml).3,6

Patients with ongoing fluid losses should receive appropriate fluid volumes to account for these
losses. These can be estimated by weighing litter trays or bedding to quantify urinary losses (if
the patient does not have a urinary catheter placed) or losses via vomiting or diarrhoea, and
recording fluid volumes retrieved from thoracic, abdominal, or wound drains.

Constant-rate infusions
CRIs are used commonly in hospitalised cats, particularly those that are critically unwell. They
allow the administration of a steady flow of analgesic drugs, for example, eliminating the peaks
and troughs associated with bolus dosing.7

There are two main methods of CRI administration: via the patient’s fluid therapy/via a fluid
bag, or via a syringe driver. The method used for each individual patient depends on the
equipment available, the size of the patient, the anticipated duration of the CRI and the
patient’s fluid therapy requirements.7

In cats, the author prefers to use a syringe driver for CRIs wherever possible, since they allow the
administration of small, precise volumes and are ideal for patients at risk of volume overload.
Additionally, the administration of a CRI separate from the patient’s intravenous fluid therapy
allows both the CRI and the fluid rate to be adjusted independently.

Converting units
CRI doses may be in mg/kg/day, μg/kg/hour or μg/kg/minute, rather than in mg/kg/hour. If
the dose does not match the concentration of the CRI (e.g., the dose is in μg/kg/hour but the
medication is in mg/ml), the units will need to be converted before calculating the CRI.8
• To convert doses from /day to /hour, divide by 24.
• To convert doses from /minute to /hour, multiply by 60.
• To convert doses from g/kg to mg/kg, multiply by 1000.
• To convert doses from μg/kg to mg/kg, divide by 1000.

Calculating CRIs administered via a fluid bag

When administering CRIs via the patient’s fluid therapy, both the patient’s drug dose and the
fluid therapy rate need to be considered, since they will determine how much drug needs to be
added to the bag.8

To calculate the volume of the drug to add to the patient’s fluid bag:
1. Calculate the rate of the drug needed in ml/hour (dose x weight / concentration)

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2. Calculate the number of hours the patient’s fluid bag will last (total volume of fluid
in bag / fluid rate per hour = number of hours)
3. Multiply the drug rate (ml/hour) by the number of hours the bag will last. This will
equal the volume of the drug (in ml) needed to add to the fluid bag.

Calculating CRIs administered via a syringe driver

To administer a CRI via a syringe driver, take the patient’s dose (in mg/kg/hour) and multiply it
by their body weight (in kg). Then divide this value by the drug concentration (in mg/ml) to get
the rate in ml/hour.8

Conclusion
Fluid therapy is a key aspect of treatment in many hospitalised cats. In order to successfully
administer fluids appropriately, the veterinary team must identify where the patient’s
fluid losses have originated from, calculate the patient’s fluid deficit and correct it over an
appropriate duration. In addition, maintenance fluid requirements and any ongoing losses must
be replaced, with careful monitoring throughout fluid administration for complications such as
volume overload.

CRIs are useful tools for the administration of analgesia, as well as other medications, at a
steady rate. These can be administered either via the patient’s fluid therapy or via a syringe
driver. Understanding how to calculate and administer CRIs, as well as which route is most
appropriate for the individual patient, is an important skill for the veterinary nurse.

References
1. Wellman ML, DiBartola, SP and Kohn CW. Applied physiology of body fluids in dogs and cats. In:
DiBartola SP (ed). Fluid, electrolyte and acid-base disorders in small animal practice. 4th ed. St. Louis:
Elsevier Saunders, 2006, pp 2–25.
2. Lyons BM and Waddell LS. Fluid therapy in hospitalized patients, part 1: patient assessment and
fluid choices. https://todaysveterinarypractice.com/fluid-therapy-part-1fluid-therapy-hospitalized-
patients-patient-assessment-fluid-choices/ (2018, accessed 4 April 2020).
3. Hughston L. Go with the flow: the basics of fluid therapy for small animal veterinary technicians.
https://todaysveterinarynurse.com/articles/go-with-the-flow-the-basics-of-fluid-therapy-for-
small-animal-veterinary-technicians/ (2016, accessed 4 April 2020).
4. Aldridge P and O’Dwyer L. Practical emergency and critical care veterinary nursing. Chichester: Wiley-
Blackwell; 2013.
5. Walden LA. Recognizing and treating shock in cats. https://www.dvm360.com/view/recognizing-
and-treating-shock-cats (2019, accessed 4 April 2020).
6. Davis H, Jensen T, Johnson A, et al. 2013 AAHA/AAFP fluid therapy guidelines for dogs and cats. J Am
Anim Hosp Assoc 2013; 49: 149–159.
7. Ortel S. Back to basics: constant rate infusions. https://www.vetfolio.com/learn/article/back-to-
basics-constant-rate-infusions (undated, accessed 23 April 2023).
8. Jones L. The ultimate guide to calculations: how to do medical maths easily. https://www.
veterinaryinternalmedicinenursing.com/blog/the-ultimate-guide-to-calculations (2020, accessed
23 April 2023).

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CLINICAL PRACTICE STREAM

Behavioural considerations to reduce the risk of

urinary disease
Gonçalo da Graça Pereira DVM, MSc, PhD, Dip ECAWBM (BM), Dip ECAWBM
(AWSEL)
Egas Moniz School of Health and Science, 2829-511 Caparica, Portugal

Many cats are now living in a restricted environment inside our houses with partial or
complete deprivation of access to the outdoor environment. The outdoor environment is itself
a coveted resource that, when limited, can lead to physical and behavioural disturbances.
When monotonous, unchanging and unchallenging environments provide insufficient mental
stimulation, animals show signs of boredom, often manifesting as abnormal behaviour
patterns.1 The absence of activity and environmental management are major causes of
stress. Furthermore, cats living in a restricted environment may not have enough physical
space to allow an acceptable flight distance, thereby reducing the cat’s opportunity to retreat.
This situation is exacerbated by an increased density of cats living in the same home. Group
housing of cats is seen both in shelter situations and in people’s homes. Usually these cats
are not related, are neutered and cannot migrate.2 Wolfle (2000) suggested that for some
social species (such as some rodents, dogs and non-human primates) companionship is
often considered the most important need to achieve well-being.3 But, in the wild, cats are
solitary hunters,4 depending on themselves to survive. In general, the presence of other cats in
a cat’s territory is not well tolerated, and the cat uses displays of aggression to keep the others
away.5 The owner can also create social relations incompatible with feline specific behavioural
biology, by not ensuring, in most cases, environmental conditions that address many of cats’
basic instincts.5 Cats organise their territory in a way that allows them to hunt, feed, rest and
eliminate far from other cats.6 The existence of safe resting and toileting areas is crucial.4 Space
availability affects each individual cat in different ways, according to their respective comfort
with proximity to other cats. The environment’s balance can be disturbed by a poor distribution
of required areas and resources (food, water, litter trays).6 The increase of interactions between
cats can cause an increase in agonistic encounters and unwanted behaviours (e.g. spraying,
scratching, aggression).7

When living and interacting together, cats and humans create a bond.7 The number of
interactions is, on average, low, but there is a variability in this and also in the types of
interactions presented.8 Owners’ expectations of their cats can cause an increase in pressures,
both behavioural and evolutionary, that can cause welfare issues. Inadequate contact with
people and uncontrolled access to other cats have been mentioned as stressors for this
species.9

All stressors can predispose the body to many different diseases, and several pathologies can
be directly linked with stress. Others, with a more subtle connection, can be risk factors (or at
least co-risk factors) that can lead to a specific pathology. Urinary diseases can be related to,
apart from many other risk factors, not only the water input but also the urination. The more
water the cat drinks, the less concentrated the urine is. The more the cat urinates, the less
possibility there is for precipitation.

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We want to decrease stressors, to achieve better physical, emotional and cognitive health.
Stimulating and creating a safe environment that ensures the cat’s behavioural needs are met
will be fundamental both to increase physical (and cognitive) activity and also to decrease
environmental stressors. Thus, environmental optimisation is required to guarantee that
animals are in a good state of physical and emotional welfare.10,11 The goal of environmental
optimisation is to decrease the perception of possible threats present in the household, and
consequently decrease the activation of the stress response.11 After identifying the major
stressors that influence cats’ welfare, one could think that owners are terrible. But a possible
reason is totally different: owners simply do not know their cat’s behavioural needs. Da Graça
Pereira and colleagues (2014) showed that owners had a lack of information about their cats’
behavioural needs.8 But, sadly, another conclusion from the same study was that, when owners
were compared with veterinarians in relation to certain categories of cats’ behavioural needs,
veterinarians and owners were at the same level of knowledge.8 So, there is a long way to go
to change the lifestyle of cats, as we need to improve veterinary education as well as provide
educational/informative training for owners.8

Additionally, we want to increase cats’ water intake as well as providing adequate conditions
for them to urinate. One of the major stressors identified in cats is their toilets, and there are
many details that make a difference from a cat’s perspective. Some of the characteristics of a
good litter tray are presented here, and during the lecture the author will describe some signs to
identify whether a cat is comfortable with its toilet or not. The available litter tray should be of a
size sufficient to allow the cat to turn around inside, and to get in and out without any problem.6
Usually it is recommended to be at least one and a half times the cat’s body length. The
majority of cats prefer a fine (sand-like) litter9 and it is recommended to have at least one litter
tray per cat plus one extra, or another possible rule is: “a cleaned toilet for each cat, in enough
number to give the chance for all cats to use one, if they need it, at the same time”. Several
litter trays should be dispersed around the house and not all concentrated in the same room.
They should be located in a place that is easy to access and quiet, if possible with two different
access points to avoid the feeling of being enclosed,6 and far from noisy equipment such as
washing machines. Cats usually have a preference for open litter trays with a simple litter
without any odour, but a preference test can be performed, such as giving the cat the option to
choose what they prefer. Hygiene is very important and is determined by the frequency of use
of the litter tray, but the tray must be as clean as practically possible.

What are the needs in terms of the water (and feeding) stations that lead to a higher water
intake? Provision of water and feeding stations should assure that all cats from the same
household have access at all times, with an individual bowl being available ad libitum.6 Cats in
the wild hunt between 100 and 150 times per day, during a period of 6 to 8 hours.5 This behaviour
is shown in the typical feeding pattern of 10 to 20 small meals during 24 hours that cats usually
present.9 Having one food bowl per cat in different places helps avoid conflict between cats.
The existence of multiple feeding stations, at different heights and in quiet locations, allows
cats to eat in a calm way without stress.9 For this reason, the number of food and water bowls
should be at least the same as the number of cats. Both food and water bowls should be
spread around different rooms in the household, in order to assure access to these essential
resources. In the wild, the majority of water that cats take in comes from the blood of their prey
and drinking water from sources that they encounter in their territory. The idea of eating and
drinking during the same meal is something that comes from a human perspective. For this
reason, the food and water bowls should not be side by side, and they should never be close to
the litter tray! Good placement will increase the chance of cats drinking more water during their
daily activity.

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Wet food is another way to increase the water intake, as well as the use of an electric fountain
so that the animal can have access to running water (however, some cats can be scared by
the noise produced by the fountain). The water bowl should be wide and shallow rather than
deep11, and regularly filled with fresh water. Aromatised water (an ice cube of fish stock, for
example) can be useful to increase the intake of water, but should be used with care as it can
produce frustration in some cats. Cats should be given the option to choose between dry and
wet food in separate bowls, instead of substituting the usual diet by a new one, allowing the
animal to express its preferences. If the cat refuses (or the owner’s decision is not to provide)
wet food, other ways to increase water intake should be searched for according to the animal’s
characteristics (e.g. fountains, drop-by-drop taps, or changing the type of water bowl or even
the material of the water bowl).

If we decrease the surrounding stress and improve quality of life and animal welfare10 through
the implementation of strategies that decrease noradrenergic activation,11 we will surely
decrease the risk and manifestation of pathologies (including problem behaviour, urinary
disease and many others).11

References
1. Wemelsfelder, F. (1990). Boredom and laboratory animal welfare. In: Rollin, B.E., Kesel, M.L. (eds), The
experimental animal in biomedical research. Boca Raton, FL: CRC Press: 243–272.
2. Price, G. (2005). The sociability of cats: how their group structure affects our lives. In: Proceedings of
the North American Veterinary Conference, Orlando, Florida.
3. Wolfle, T.L. (2000). Understanding the role of stress in animal welfare: practical considerations.
In: Moberg, G., Mench, J.A. (eds), The biology of animal stress: Basic principles and implications for
animal welfare. Wallingford, CABI: 355–368.
4. Beata, C. (2005). Territoriality, sociality: Updating cat’s behavior. In: Proceedings of the 30th WSAVA
Congress, Mexico City.
5. Heath, S. (2009). Minimizing stress for cats living in a domestic environment. In: [electronic version]
Proceedings of the Southern European Veterinary Conference & Congreso Nacional AVEPA, Barcelona,
Spain.
6. Colin, M. (2010). Manejo e Prevenção da Ansiedade no gato. Focus Auxiliar, 4–11.
7. Landsberg, G., Hunthausen, W, Ackerman, L (2002). Handbook of behaviour problems of the dog and
cat. Oxford: Butterworth and Heinemann.
8. Da Graça Pereira, G., Fragoso, S., Morais, D., Brito, M.T.V., De Sousa, L. (2014). Comparison of
interpretation of cat’s behavioral needs between veterinarians, veterinary nurses, and cat owners.
J Vet Behav 9, 324–238.
9. American Association of Feline Practitioners (2004). Feline behaviour guidelines. https://catvets.
com/public/PDFs/PracticeGuidelines/FelineBehaviorGLS.pdf.
10. Da Graça Pereira, G. (2011). Eliminação inadequada em gatos: é comportamental? Veterinary
Medicine (Portuguese edition), 13(75): 41–45.
11. Westropp, J.L., Buffington, C.A.T. (2004). Feline idiopathic cystitis: current understanding of
pathophysiology and management. Veterinary Clinics of North America: Small Animal Practice 34:
1043–1055.

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CLINICAL PRACTICE STREAM

Post discharge: at-home management

of complex cases
Laura Jones
BSc (Hons), DipAVN (Small Animal), ISFMDipFN, VTS(SAIM), RVN

Introduction
Our responsibility to our patients does not end when they leave the clinic; the veterinary team
plays a vital role in the successful at-home management of feline patients, particularly those
with complex needs. Renal and urinary patients are a great example of this as they have many
at-home nursing considerations, from behavioural and environmental considerations for
urinary tract disease patients to administering subcutaneous fluids to patients with chronic
kidney disease.

Part of our care of these patients, then, should include an assessment of the patient’s
environment and at-home needs, and a discussion with the client on how to successfully
manage the patient at home.

This session will look at the at-home care requirements of renal and urinary patients, as well as
the behavioural considerations for these patients.

Post-treatment challenges
Renal and urinary patients can present many challenges following in-hospital treatment. These
include behavioural and environmental considerations, nutrition, hydration, administration of
medications and pain assessment.

Behaviour
Any period of significant change from a cat’s normal routine will undoubtedly cause stress,
and hospitalisation and returning home from the clinic is no exception. Inability to escape from
a carrier, travel, lack of control over the environment, and the patient’s own illness, pain and
discomfort will all be stressors for the patient.1

In multi-cat households, non-recognition aggression is common. This is generally seen after a

period of separation, for example, when reintroducing a cat after a veterinary visit. The cause of
this aggression is not fully understood, but is thought to include:
◆ Unfamiliar smells causing the returning cat to be unrecognizable and perceived
as a threat.
◆ Abnormal behaviour or illness as the returning cat settles back in at home, which
the other cat perceives as threatening.
◆ Particular smells on the returning cat, for example, surgical spirit or disinfectant,
reminding the other cat of its own negative experience at the vet.
◆ Stress or alarm pheromones emitted by the returning cat signalling danger to the
other cat, causing it to act aggressively.2

Cats should be able to recover from hospitalisation and settle at home in a quiet environment,
initially with minimal contact with humans or other household pets, and away from other
household cats. Separating them for anything from a few hours to 1–2 days may be necessary,

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with gradual supervised reintroduction.1 Any bedding from the cat’s carrier should be washed
as soon as possible (to remove veterinary scents) and bedding from shared resting areas
should be given to the returning cat, to help re-establish familiar scents.1 Synthetic pheromones
can also be used in any shared areas of the home, and additional resting and hiding areas
should be provided to allow cats to take time away from each other where needed.

Environment
Providing an appropriate environment for recovery is also important, particularly in cases of
urinary tract disease or in multi-cat households. In addition to providing the recovering cat
with a quiet, warm resting area where it can be non-invasively supervised, sufficient resources
should be present for all cats in the home.

Each cat should have access to separate food and water sources, toileting facilities, hiding and
sleeping/resting facilities. These should be distributed throughout the home and away from
busy areas, or areas in view of other cats (e.g., by doors or windows).

Depending on the reason for hospitalisation, cats may need either indoor-only rest or cage rest.
This can be frustrating for cats, limiting their ability to express normal behaviour and causing
boredom; to minimise this, ensure the cat receives stimulation regularly. Puzzle feeders, placing
the crate near to a window where the cat can watch birds (as long as this does not frustrate it),
hiding places and elevated resting places (where appropriate) are all good ways to enrich the
cat’s environment during recovery.

Nutrition
Before the patient leaves the clinic, the client should understand which diets are suitable for the
patient, how much of these to feed and how often, and what time to offer food (based on the
timing of the cat’s last meal in hospital).

Initially, most cats can be tempted to eat with a wide variety of foods, and the patient’s food
intake should be monitored closely at home as it recovers from hospitalisation.

If a long-term dietary change is recommended, this should not be introduced until the patient
has settled at home and recovered from the acute aspect of the illness/surgery. By avoiding the
introduction of a new permanent diet until the cat is feeling well, we minimise the risk of food
aversion and non-acceptance of the new diet.

A gradual transition to the new food is needed, with most cats coping well with a diet transition
over 1–2 weeks. In some cases, clients may need to persevere with a longer transition, switching
a few kibbles at a time in severe cases.

In some cases, patients may be discharged with enteral feeding tubes in situ. Where
appropriate, the veterinary team should provide advice on how to manage these tubes at
home, including how to care for and re-dress the tube, as well as how to administer food and
medications.

Hydration
Patients with renal and urinary disease often require adjustments to their water intake. In such
cases, clients should be advised how to monitor water intake at home, and how to increase it,
using methods such as:
◆ Increased availability of water sources
◆ Using different receptacles of varying material, width, and height to encourage

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cats to drink
◆ Using running water (from water fountains or dripping taps)
◆ Using the poaching liquid from boiled chicken or fish to flavour water
◆ Using hydration support products.

Subcutaneous fluids may also be required to support these patients at home; if this is the case,
the veterinary nurse is ideally placed to educate and support clients with doing this.

Medication
Advice on the administration of oral (and parenteral, if applicable) medications should be
provided. Where possible, a non-invasive or less stressful way of administering medications
should be identified, such as the use of tablet ‘putty’ and treats, as well as liquid treats to hide
liquid medications in, or providing gelatine capsules so that multiple oral tablets can be given
simultaneously. If clients are struggling with giving tablets, it may be possible to identify (or
reformulate via a ‘specials’ manufacturer) a suitable liquid alternative.

Monitoring
At-home monitoring provides the veterinary team with vital information on disease
management, as well as indicating any potential changes in the patient’s condition. Clients
should be advised to note any changes in demeanour, appetite, thirst, urination, defecation,
activity levels and any other comments or concerns, alongside the timings and doses of any
medications given.

Clients should be given advice on how to assess pain at home, since pain in cats can be
challenging to spot. Assessment tools such as the Feline Grimace Scale can be used by clients
with appropriate training, and good reliability has been noted when this system is used by
clients.3

The client should also be given information on ‘call parameters’ where, if these signs are seen
at home, they should contact the clinic for re-evaluation. The exact signs to monitor for will
depend on the individual disease process and the severity of the patient’s signs. This advice
may include how to spot a urinary tract obstruction in a patient with lower urinary tract disease,
for example.

Conclusion
The care our complex feline cases need does not end in the hospital, and the veterinary team
has a responsibility to educate and support clients in carrying out this care at home. Areas
for clients to monitor in particular include nutrition, hydration, pain, signs of deterioration or
emergency complications. In addition, behavioural and environmental support should be
provided, and advice given on administering medications in a stress-free way. Veterinary
nurses are ideally placed to help with this, increasing the support the client receives and
maintaining the wellbeing of our patients after discharge.

References
1. International Cat Care. Taking your cat to the vet. https://icatcare.org/advice/taking-your-cat-to-
the-vet/ (2022, accessed 23 April 2023).
2. Vetstreet. Nonrecognition aggression in cats. https://www.vetstreet.com/care/nonrecognition-
aggression-in-cats (2011, accessed 23 April 2023).
3. Monteiro BP, Lee NHY, Steagall PV, et al. Can cat caregivers reliably assess acute pain in cats using
the Feline Grimace Scale? A large bilingual global survey. J Feline Med Surg. Epub ahead of print 17
January 2023. DOI: 10.1177/1098612X221145499.

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CLINICAL PRACTICE STREAM

Hospitalisation and post discharge: behavioural

considerations for cats
Gonçalo da Graça Pereira DVM, MSc, PhD, Dip ECAWBM (BM), Dip ECAWBM (AWSEL)
Egas Moniz School of Health and Science, 2829-511 Caparica, Portugal

When there is a strong reason to hospitalize a cat it is important that the decision is made very
carefully, as being away from its territory and safe environment can be detrimental, potentially
delaying its recovery. However, there is also a strong belief that it is better for their health to
hospitalize cats, as it increases the chance of better diagnosis and treatment. Nevertheless, we
must consider the emotional and cognitive health of the cat as part of the hospitalization plan.
Many times we are so focused on physical health that when the animal leaves the hospital it
is cured but it can take away an emotional and cognitive (due to the learning that happened
during the hospitalisation) problem, and this can take a long time and effort to resolve.

If these animals are fearful and uncertain about the outcome of their experience, is it realistic
to expect them to be calm, quiet and cooperative with us as veterinary practitioners simply
because we are working for their health and welfare? In a busy practice it is not unusual to have
a ‘houseful’ of patients and feel under pressure to speed up our procedures and do our ‘good’
work quickly, even if that results in us holding these animals in uncomfortable positions and
using techniques that are motivated by the desire to get the job done. Some will say that cat-
friendly techniques take too long, but in reality respecting the emotional needs of our patients
will lead to cooperation from the patient and make the process much faster in the future. The
memory of a ‘bad experience’ can lead an animal to anticipate that it will be ‘threatened’ the
next time it comes to the practice, resulting in protective behavioural manifestations that can
result in more time required to finish the procedure and practice staff using more forceful
handling techniques – leading to more problems.

So, let me ask you: have you ever been hospitalised? If your answer was yes (otherwise you
can ask another person you know who had had this undesirable experience), what are the
memories you carry with you? When you were almost asleep, did a nurse come to give you an
injection, a pill or to take your blood pressure? What about the lights? And noises? In fact, for
the majority of people who have gone through this experience, one of the things that is easily
remembered is the sleep deprivation. Could we say that something similar is occuring during
the hospitalisation of our animals? Yes, we can! This is the reason why the same concerns
and recommendations related to the waiting room or consultation room should be taken
into account if the cat has to be hospitalized at the practice. So, let’s review some of these
recommendations.

Physical considerations
If it is not a cat-only practice, the hospitalisation ward should have a specific area for cats
and another area for dogs. If it is not possible to have separate wards, at the very least visual
barriers should be created so that the cats can feel more secure (also think about placing
visual barriers between cages). A blanket, especially if it has the cat’s household’s scent, could
be used to cover the cage (at least partially, as some cats like to see the outside as well – and
this way the cat can choose what it prefers), giving extra protection to the cat that is inside.

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LIGHT: If the lights need to be turned on the whole night, the blanket covering the front of the
cage can also be very important to increase darkness in the cage, which is very important to
improve the quality of sleep.

TEMPERATURE: Another important reason to have separate wards for dogs and cats is related to
the room temperature. This is very important for cats, as they feel more comfortable in higher
temperatures compared with dogs.

SOUNDS: It is important to be aware of potentially ‘scary’ noises that exist in the hospital setting.
Apart from obvious sounds, there are many others that must be considered. Water running or
a disinfectant spray can be misinterpreted by the fearful cat as another cat hissing, and the
sounds of the motors in vacuum cleaners or clippers can be so stressful that the cat reacts with
an immediate protective response. Background sounds, such as the sounds of nature (although
note that the sounds of birds can frustrate some cats!) or white noise, can hide some of these
scary noises.

SMELLS AND PHEROMONES: Between treatments/examinations, make sure that the room is
properly cleaned, as many alarm or attack pheromones could be present in the air. Ideally, the
room should be ventilated, cleaned and then synthetic feline facial pheromones sprayed on the
table before the next cat is examined. Synthetic pheromone diffusers should also be plugged in
(in a multi-species practice, there can be one for dogs and one for cats, as they are specific for
each species). Remember the importance of smells (in addition to pheromones) from the cat’s
perspective; practising good hygiene and using products with neutral odours is fundamental.

Interactions
It is important for the veterinary staff to be seen as the cat’s best friends during the
hospitalisation! So, let’s give the cats what they like most. Ask the caregivers to bring the cat’s
favourite treats, favourite toys and blankets with the scent of home, to be used by the clinic
team whenever this is possible. Cats’ favourite treats are often things like tuna, wet food or
liquid treats (e.g. Lick-e-lix), but there are many possibilities because each cat has its own
preference. Some behaviourists recommend that food treats should be avoided when the
animal is already fearful, due to conflict between the emotional motivations of desire/seeking
and fear, so passive offering of treats, to allow the cat choice, should be used. Apart from this,
also think about the negative association that can be made between the treats being offered
and the treatment during the hospitalization. This is also the reason why a new food should not
be started during hospitalization. When this is not possible because there is a specific need for
a new diet, provide different brands or a different flavour to take home.

Unpleasant situations should always be minimised. Usually, in our busy days, we approach the
hospitalised cat only to examine or treat it, forgetting about the importance (if the cat likes it)
of being petted and played with to create a positive interaction. Take it as a major rule, with
exceptions dependent on the case and the physical limitations of the clinic, that treatments
and examinations should not be done with the cat inside the cage. The cage in which the cat is
hospitalised should be its safe area. The cat’s carrier, brought from home, can be used for these
procedures. If the cat is in a negative (protective) emotional state, such as fear or anxiety, lifting
the upper half of the carrier so that it is slighty open will enable you to slide a towel in over the
bottom half so that the cat is totally covered by the towel. The majority of cats will hide below
the towel, where they feel more secure, and allow a complete examination/treatment without
the need for restraint.

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Towels can be the veterinarian’s best friend when handling cats. A clean towel should be used
for each cat when they are anxious or require handling. The towel can be lightly heated in a
microwave as cats often respond more to warmth. The examination/treatment should always
start with the less invasive aspects before the more invasive ones, and the same should be
true for the handling used. Always start with minimal handling. For example, avoiding the
use of restraint before and/or after an injection will help to prevent the cat from anticipating
negative interactions in the future (which would happen if restraint is seen as a sign that
something painful is coming). Always use a new needle for the injection and never forget to
lubricate the thermometer! Refrigerated medication should be taken from the fridge so that it
is close to environmental temperature before being injected. The necessary equipment (cotton
wool, needles, syringes, etc.) should always be prepared and positioned in an easily accesible
location before the starting the treatment so that it can be easily reached and used.

A cat that is sick and impaired will be more sensitive to the surrounding environment. Each
cat should have access to a space for elimination that is separate from the resting or hiding
locations. If this separation of resources is not achieved, the cat will be distressed and may
display unusual or unwanted behaviours such as hiding in the litter tray or eliminating in the dry
food bowl. Environmental optimisation in a way that leads to cognitive stimulation is also a way
to decrease stress and anxiety.

Post discharge
Finally, once the animal is better it will be returning home, and once again, it is important to
prepare for this event. If there are any other cats in the household, a reintroduction plan should
be given to the client.
◆ Contact between the cats should never be forced.
◆ The other cat(s) should be given time to get used to the scent of the arriving cat,
before moving on to visual contact and finally direct contact.
◆ The returning cat should not be simply taken out from the carrier to go and greet
the other(s); it can help for the cat to stay inside the carrier, covered with a towel/
blanket that has the scent of the household group of cats on it for a while (the
duration will depend on the individual and will vary from case to case), giving time
to see the reaction of the other cat(s) to the arrival.

This process, as well as instructions for giving medications, should be written in the discharge
advice the cat is sent home with. There must be a clear and concise plan for the process and
treatment. Otherwise, no matter how good your knowledge and advice, there will be little to no
chance of success.

References:
◆ Yin, S. Low stress handling, restraint and behavior modification of dogs and cats. CattleDog Publishing, 2009.
◆ Landsberg, G, Hunthausen, W, Ackerman, L. Behavior problems of the dog and cat. 3rd ed. Elsevier, 2013.
◆ Bowen, J, Heath, S. Behaviour problems in small animals – practical advice for the veterinary team. Elsevier,
2005.
◆ Shephard, K. Behavioural medicine as an integral part of veterinary practice.
In: Horwitz, D, Mills, D. (eds). BSAVA manual of canine and feline behavioural medicine. Gloucester: British
Small Animal Veterinary Association, 2009; pp 195–216.

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CLINICAL PRACTICE STREAM

What tube and when? Feeding tube management

and care
Cecilia Villaverde
BVSc, PhD, DACVIM (Nutrition), DECVCN

Sam Taylor
BVetMed(Hons), CertSAM, DipECVIM-CA, MANZCVS, FRCVS

Summary:
Feeding tubes are an excellent tool to manage cats that cannot or will not eat enough, and,
depending on the case, can be used both in hospital and at home. This lecture will discuss
important aspects to decide in which cases they should be used, when to place them, and how
to develop a feeding plan.

There is a close relationship between illness and malnutrition. An inadequate nutritional status
can predispose to illness via several mechanisms, such as effects on the immune system
and damage to the intestinal barrier function. On the other hand, ill animals are more prone
to malnutrition due to either reduced food intake and/or increased nutrient and energy
requirements. Several studies in veterinary medicine support that patients not meeting their
energy requirements can have poorer outcomes1–3 and that nutritional support can help in
these situations. Therefore, efforts should be made to ensure that ill cats receive adequate
nutritional support.

Patient selection
Performing a complete nutritional assessment4 is important for several reasons, such as
deciding on the best feeding plan (diet, allowance, feeding method) and best route of feeding,
and also to identify the patients that will benefit from nutritional support and when to start it. For
hospitalized patients, Table 1 shows some of the risk factors that will indicate that the patient
requires nutritional support.

Table 1: Malnutrition risk factors in hospitalised patients

◆  ge: younger and older animals are more prone to malnutrition than young adults.
A
◆ Chronic losses (e.g. vomiting, diarrhoea, polyuria, or hypermetabolic state) will
accelerate the rate of development of malnutrition.
◆ Involuntary weight loss is one of the clearer markers of malnutrition, but also

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denotes that the process is quite advanced.

◆ Length of anorexia/hyporexia correlates tightly with malnutrition risk, and it
precedes weight loss; therefore, this risk factor alone can be enough to start
assisted feeding.
◆ Low body condition (BCS) is related to inadequate energy intake of some duration,
as loss of at least 10% of body weight is needed to note a low BCS. While patients
that present with low BCS require more urgent support, high BCS is not a reason
to not provide nutritional support if other risk factors are present. Overweight cats
that do not eat are at high risk of hepatic lipidosis,5 and it is important to provide
assisted feeding in a timely manner to prevent this serious condition.
◆ Low muscle condition score (MCS) is a nutritional risk factor but is not specific,
meaning that low protein and energy intake can contribute to a low MCS, but
many other factors do as well, such as sarcopenia, cachexia, or intestinal disease.
◆ The skin is the largest organ in the body and has a high turnover rate; as such,
nutritional deficiencies can show there.6
◆ Some laboratory findings can be representative of malnutrition; however, these
measurements are late (i.e. the malnutrition is already advanced) and are also not
specific or sensitive, so they should be interpreted together with the other factors.

When to start?
The sooner the better, as suggested from most studies from human and veterinary medicine.1,7,8
It is important to stabilize the patient (well hydrated, haemodynamically stable, no acid–base
or electrolyte abnormalities) before feeding.

Route of feeding
Oral voluntary intake is the preferred feeding method, and there are a variety of strategies
that can be used to promote this. If oral intake is not sufficient, and the patient is still anorectic
or hyporectic, and losing weight, assisted feeding is required. This can be via the enteral or
parenteral route; enteral is preferred9,10 as it is safer, cheaper, easier, and more adequate
nutritionally. Parenteral feeding (central or peripheral) is not nutritionally complete, therefore it
can be used only for the short term.11,12

Forced feeding is not recommended, as it can result in food aversions, aspiration pneumonia or
injuries, and is also stressful for the patient. It is also unlikely to meet feeding requirements.

Feeding tubes
Feeding tubes may be placed to provide fluids and nutrition but also to facilitate long-term
medication (e.g. for mycobacteriosis). They can be placed quickly and should be considered
proactively, for example, if a patient is being anaesthetised for diagnostic tests but is
consuming less than the resting energy requirement (RER) or is predicted to be inappetent after
surgery.

Type of feeding tube

The type of feeding tube chosen will depend on the patient, its underlying illness, its
temperament and the likely duration of the inappetence. The most commonly placed are naso-
oesophageal (NO), nasogastric (NG) and oesophagostomy (O) tubes. Each has advantages
and disadvantages.
◆ NO or NG tubes can provide nutrition for generally 5 days or less and are also
useful when a cat is not a candidate for anaesthesia. The narrow diameter
reduces diet choice to liquid diets and the tube can become obstructed. Crushed

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medications may also obstruct the tube but liquid medications usually pass
easily.
◆ O tubes are well tolerated, and larger bore so facilitate the use of many diets and
the administration of crushed or liquid medications. However, placement requires
anaesthesia. Common complications are dislodgement, obstruction and stoma
site infection.

Other types of feeding tube, such as gastrostomy (G) tubes, are less commonly placed but are
indicated in cases of oesophageal disease/dysmotility.

Placement of feeding tubes

Step-by-step guides to the placement of NO/
NG and O tubes are available via these QR
codes. Placement of an NO/NG tube can be
facilitated by mild sedation/anxiolysis (e.g.
gabapentin, butorphanol) and placement
should be confirmed with radiography and/
or capnography and checking for a vacuum
or aspiration of acidic stomach content in the
case of an NG tube.

Placement of O tubes can be assessed by radiography, endoscopy or fluoroscopy, and should

be checked before each use by checking for negative pressure and injection of 2 ml sterile
saline to monitor for coughing or respiratory noise that could suggest endotracheal intubation.
G tubes are placed surgically or with endoscopic guidance and can be used long term.

Complications
Complications are unusual and usually minor with both NO/NG and O tubes. Patient
interference can be minimised with cat-friendly interactions and environment and using soft
collars, for example.

Serious complications include endotracheal intubation and, for O tubes, damage to

neurovascular structures in the neck resulting in haemorrhage or transient Horner’s syndrome
(both rare). Stoma site infection can occur with O and G tubes and is usually managed
with antimicrobial dressings and increased cleaning of the area, and avoided with aseptic
placement. Cats on chemotherapy or corticosteroids may be more likely to suffer stoma
site infections. Complications of G tubes can include injury to abdominal viscera, peritonitis,
cellulitis, vomiting and metabolic derangements.

Tube removal
Cats should be offered food, under supervision, while the NO/NG feeding tube is in place.
Removing Elizabethan collars, or using soft fabric versions, may help to encourage voluntary
intake. If cats are still not eating adequately voluntarily when the NO or NG tube has been in
place for 5 days, consideration should be given to placing a more medium-term tube such as
an O tube. Some cats may be deterred from eating by the presence of the tube; hence, tube
removal and ‘testing’ of appetite may be needed, with the tube replaced if voluntary intake
remains inadequate. With O tubes, cats should be able to eat normally (fabric collars, rather
than hard plastic Elizabethan collars, can help) and appetite and food intake can be monitored.
Sometimes O tubes can be left in place to facilitate medicating the cat even when its appetite
has returned. G tubes cannot be removed for 10–14 days post-placement to allow a seal to form

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at the gastrostomy site. NO/NG and O tubes can be removed with the cat conscious; G tube
removal is dictated by the type, with some requiring endoscopic removal.

Developing a feeding plan

Every cat with a feeding tube should be given a customised feeding plan, which includes diet,
allowance, and feeding method.

1. DIET CHOICE
The diet choice must cover the nutritional requirements of the patient (which depend on its life
stage), be well tolerated, and include any necessary modifications if the cat has a nutrient-
sensitive disease. Other factors that will affect diet choice include availability and cost,
palatability (which does not matter with the feeding tube, but can help when stimulating food
intake), energy density (the higher the better) and texture (some diets will not be able to fit
through certain feeding tubes).

If possible, choosing a convalescence-type diet is indicated, as these have a high energy

density, are palatable, and are made specifically to be easy to fit through feeding tubes. Some
are liquid and some have a slurry consistency. Moreover, these diets are highly digestible, high
in protein of good quality, high in fat (which helps with texture, palatability, and energy density)
and low in carbohydrates and fibre (as these cats can have insulin resistance and fibre can
clog the feeding tube).

2. AMOUNT TO FEED (ALLOWANCE)

For hospitalized patients, the goal is to feed RER (70 x body weight (kg)0.75, kcal/day). Once RER is
reached, and well tolerated, the amount can be increased if needed: for example, if the patient
is losing weight, a kitten is not growing, or an underweight patient is not gaining weight. The RER
should be calculated using the current weight of the cat, to avoid both over- and underfeeding
issues, and afterwards adjustments in 10% intervals can be made to achieve the weight goals of
each case.

When the RER is calculated, the daily allowance can be calculated by dividing the RER (kcal/
day) by the energy content of the diet (kcal/g or ml) to give the g or ml per day. Using ml is
easier as the feedings through the tube are usually done with a syringe. The manufacturer of
the diet might need to be contacted for the energy content, or this can be found in product
guides in the case of veterinary diets.

3. FEEDING METHOD
Once the feeding tube is in place and the cat has recovered from the anaesthetic or sedation,
we need to test the tube with a small amount of water (the author uses 3–5 ml/kg body weight,
a couple of times) to test that water flows with no obstacles. After that, feedings can be started.
It is recommended to start with one-quarter or one-third of the RER, divided over 3–6 meals
per day. The longer the period of inappetence and the more severe the disease, the slowest the
transition should be to prevent refeeding issues.

The food should be warmed to body temperature and placed in the syringe. Before feeding,
the tube should be flushed with 5 ml of warm water to ensure there are no obstacles. The meal
should be given slowly (at least 10–15 mins per meal). Afterwards, the tube should be flushed
with 5–10 ml of warm water to make sure all the food has gone into the cat and to prevent
obstruction.

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Follow up
It is important to monitor body weight to adjust the food allowance and achieve weight goals:
weight stability in patients with good or high BCS, and weight gain (after weight stability is
achieved) in growing kittens, underweight cats, or in all cats losing weight with RER. Overweight
cats should be kept well stable, and a weight loss plan should be developed and implemented
once the patient is fully recovered from the present disease and eating on its own.

Food can be offered orally once the cat feels better, and the feeding
tube can be removed once the cat has been consuming its RER
voluntarily for 3–4 days. If the feeding tube can be in place for only a
few days (such as for NO/NG tubes) and the patient is still not eating
enough, a more permanent tube (e.g. O tube) should be placed.

More details on feeding tubes/placement/management

and appetite stimulants can be found in the 2022 Inappetent
Hospitalised cat Guidelines here: https://journals.sagepub.com/doi/
full/10.1177/1098612X221106353, including videos of the techniques,
nutritional history forms and tube feeding records to download.

References
1. Molina J, Hervera M, Manzanilla EG, et al. Evaluation of the prevalence and risk factors for
undernutrition in hospitalized dogs. Frontiers in Veterinary Science 2018; 5: 205.
2. Brunetto MA, Gomes MOS, Andre MR, et al. Effects of nutritional support on hospital outcome in dogs
and cats. J Vet Emerg Crit Care 2010; 20(2): 224–231.
3. Remillard RL, Darden DE, Michel KE, et al. An investigation of the relationship between caloric intake
and outcome in hospitalized dogs. Vet Ther 2001; 2(4): 301–310.
4. Freeman L, Becvarova I, Cave N, et al. WSAVA Nutritional Assessment Guidelines. J Small Anim Pract
2011; 52(7): 385–396.
5. Armstrong PJ, Blanchard G. Hepatic lipidosis in cats. Vet Clin North Am Small Anim Pract 2009;
39(3): 599–616.
6. Hensel P. Nutrition and skin diseases in veterinary medicine. Clin Dermatol 2010; 28(6): 686–693.
7. Will K, Nolte I, Zentek J. Early enteral nutrition in young dogs suffering from haemorrhagic
gastroenteritis. J Vet Med A Physiol Pathol Clin 2005; 52(7): 371–376.
8. Mohr AJ, Leisewitz AL, Jacobson LS, et al. Effect of early enteral nutrition on intestinal permeability,
intestinal protein loss, and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med 2003;
17(6): 791–798.
9. Eirmann L, Michel KE. Enteral nutrition. In: Silverstein DC, Hopper K (eds). Small Animal Critical Care
Medicine. 2nd ed. St. Louis: Elsevier Saunders, 2014, pp 687–690.
10. Chan DL. Nutritional support of the critically ill small animal patient. Vet Clin North Am Small Anim
Pract 2020; 50(6): 1411–1422.
11. Chan DL, Freeman LM. Parenteral nutrition in small animals. In: Chan D (ed). Nutritional Management
of Hospitalized Small Animals. Chichester: Wiley, 2015, pp 100–116.
12. Pyle SC, Marks SL, Kass PH. Evaluation of complications and prognostic factors associated with
administration of total parenteral nutrition in cats: 75 cases (1994–2001). J Am Vet Med Assoc 2004;
225(2): 242–250.

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CLINICAL PRACTICE STREAM

Critical care aspects of managing an acute renal

injury
Laura Jones
BSc (Hons), DipAVN (Small Animal), ISFMDipFN, VTS(SAIM), RVN

Introduction
Acute kidney injury (AKI) is an often severe, life-threatening emergency requiring intensive
treatment and nursing care. Patients often present with severe acid–base, electrolyte and fluid
balance abnormalities that require careful correction, alongside correcting the underlying
cause of the AKI (where possible) and providing supportive care.

This session provides an overview of AKI in cats and discusses the diagnosis and management
of the condition, alongside advanced nursing care requirements such as renal replacement
therapies and advanced vascular access options.

Acute kidney injury

AKI is defined as an abrupt and sustained decrease in kidney function, leading to an abnormal
glomerular filtration rate (GFR), a decrease in renal tubular function and a drop in urine output.1
Cases can vary and range from mild renal injury without azotaemia or many clinical signs to
patients with sudden and severe disease where marked renal injury is present (leading to acute
renal failure).2,3

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

In addition to azotaemia, AKI patients often present with:

◆ Marked dehydration and/or hypovolaemia
◆ Marked acid–base abnormalities (metabolic acidosis)
◆ Marked electrolyte abnormalities (classically hyperkalaemia)

Treatment is aimed at managing the underlying cause, correcting fluid, acid–base and
electrolyte derangements and providing supportive care.3

Stages of AKI
There are four stages of AKI: initiation, extension, maintenance, and recovery. Initiation is the
stage where the insult to renal function is actively taking place. Here, patients may show
clinical signs but will not always do so, and biochemical changes are usually not present.
During extension, the damage to the kidney has occurred, and obvious clinical signs and
biochemical/imaging abnormalities are present. In the maintenance phase, the kidneys
reach their maximum level of damage and renal function begins to regenerate. In recovery,
an improvement in clinical signs and examination findings is noted, alongside biochemical
improvement.2,3

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

Causes of AKI
Several factors can cause AKI, including toxin ingestion, infectious disease and urinary tract
obstruction, it can also develop following the administration of certain medications. These
causes can broadly be categorised into pre-renal, intrinsic renal or post-renal causes, since
different causes result in injury to different areas of the urinary tract1.

Pre-renal azotaemia is defined as a decreased GFR secondary to hypoperfusion in a structurally

normal kidney. It can be caused by any disease resulting in insufficient perfusion of the kidneys,
such as hypovolaemia or hypotension. It can also be hospital acquired (e.g., due to prolonged
hypotension under general anaesthesia) and, if left untreated, can lead to intrinsic renal AKI (as
the renal hypoperfusion causes injury to the nephrons).2,3

Intrinsic renal azotaemia occurs due to injury to the nephrons causing dysfunction. There are a
variety of causes, including toxin ingestion, internal toxic damage and infection.2,3

Post-renal azotaemia occurs where urine cannot leave the body or if the flow is redirected.
It is a common cause of AKI, especially in cats, and can be caused by urethral or ureteral
obstruction, or trauma or rupture of the urinary bladder or urethra. Like pre-renal azotaemia,
post-renal azotaemia can lead to intrinsic renal AKI if it is not resolved promptly.2,3

Clinical signs
Clinical signs of AKI are varied and include:2,3
◆ Polyuria
◆ Polydipsia
◆ Lethargy
◆ Depressed mentation
◆ Hyporexia
◆ Anorexia
◆ Vomiting
◆ Oliguria (urine output <0.5 ml/kg/hour) (in cases of urinary tract obstruction or
severe loss of renal function)
◆ Anuria (in cases of urinary tract obstruction or severe loss of renal function)
◆ Stranguria (in cases of urinary tract obstruction)
◆ Bradycardia or bradyarrhythmias (in cases of hyperkalaemia)
◆ Neurological signs (in cases of toxin ingestion).

Diagnosis of AKI
A variety of diagnostic tests are performed in patients with AKI, including biochemistry,
haematology, venous blood gas analysis, urinalysis and diagnostic imaging.

Biochemistry typically reveals acute, severe azotaemia with marked increases in blood
urea nitrogen (BUN) and creatinine. Phosphate levels are also increased, and hypo- or
hypercalcaemia may be seen. Hypocalcaemia is usually seen due to calcium binding (e.g., due
to ethylene glycol toxicity) whereas hypercalcaemia is usually seen with certain toxins (e.g.,
vitamin D toxicity). Hyperkalaemia is also common, as the kidneys cannot excrete potassium;

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this is a life-threatening emergency that can result in bradycardia and cardiac arrhythmias.

On blood gas analysis, a metabolic acidosis is seen. This is a combination of a low pH, low
bicarbonate and low base excess. Other acid–base parameters, such as the anion gap (the
difference between the positively and negatively charged ions within the blood) can be used to
tell us more about the cause of the patient’s acidosis – that is, whether it is due to the presence
of additional acidic compounds being present or not. The anion gap is increased when there is
extra acid present, for example, in patients with ethylene glycol toxicity (because it is converted
to oxalic acid).

Haematology is often unremarkable in AKI patients, but changes associated with specific
underlying causes may be seen, for example, haemoconcentration in patients that are
dehydrated.

Urinalysis is used to assess the patient’s urine-concentrating ability, alongside determining

whether abnormal cells, crystals or infection are present, which could help identify an
underlying cause of the patient’s AKI.

Finally, diagnostic imaging such as abdominal ultrasonography or contrast radiography may

also be performed in AKI patients. Ultrasonography can be used to identify stones, strictures or
masses causing post-renal AKI, and detects free fluid. Radiographic studies can be enhanced
with contrast to identify post-renal abnormalities.

Treating and nursing the AKI patient

The treatment options for AKI patients will vary depending on the underlying cause of the
disease. They include:2,3
◆ Pre-renal AKI: Correct hypoperfusion, manage underlying disease (sepsis, systemic
inflammatory response syndrome (SIRS), cardiac disease, etc.)
◆ Intrinsic renal AKI: Supportive care, antidotes to specific toxins, treatment of
infectious diseases/infection
◆ Post-renal AKI: Relieve urethral obstruction, place subcutaneous ureteral bypass
(SUB) for ureteral obstruction, surgically repair ruptured/herniated bladder.

In addition, supportive treatment, including analgesia, appropriate intravenous (IV) fluid

therapy and anti-emetics, is provided as necessary.

Fluid therapy
Fluid therapy support is a vital part of treating AKI. The administration of IV fluids restores
hydration and perfusion status in dehydrated and hypovolaemic patients, corrects acid–
base disturbances, and can correct electrolyte imbalances as well as reduce azotaemia and
hyperkalaemia.

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

Signs of fluid overload include:

◆ Serous nasal discharge
◆ Conjunctival oedema
◆ Hypothermia

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◆ Tissue oedema
◆ Tachypnoea
◆ Increased respiratory effort
◆ Acute weight gain.

Fluid rates should be calculated and administered based on a careful assessment of the
patient’s hydration and perfusion status and reassessed regularly throughout hospitalisation.

If the patient becomes fluid intolerant during treatment, we need to change our approach to
focus on trying to get the kidneys to form urine again, rather than continuing to administer
potentially high rates of fluid therapy.

We achieve this first by administering diuretics such as mannitol or furosemide and measuring
the patient’s response (seeing whether their urine output increases)4. If this does not work, we
are left with the option of renal replacement therapies, also known as dialysis.

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

Haemodialysis is not performed outside of very specialist settings. A large dialysis catheter is
placed into the jugular vein and connected to an extracorporeal circuit containing a specialised
filter and dialysate fluid. The filter and dialysate fluid can draw waste products and toxins from
the bloodstream into the dialysate/filter, leaving the ‘clean’ blood to be returned to the patient.

Peritoneal dialysis is a more accessible but less effective method of dialysis. Like haemodialysis,
it is very nursing intensive, and patients require 1:1 intensive nursing care and treatment. With
peritoneal dialysis, a peritoneal catheter is surgically placed into the abdomen, through which
dialysate is infused via a closed system. The fluid sits in the abdomen for a specified ‘dwell time’
before it is drained into a collection bag. During the dwell time, solutes and waste products
cross the capillary walls and peritoneal membrane and enter the dialysate, which is then
removed.1,3

Managing hyperkalaemia
Patients with AKI are frequently hyperkalaemic and require correction of this to prevent life-
threatening consequences. Potassium levels may be managed or reduced by administering:1
◆ Calcium gluconate, which protects the heart from the effects of hyperkalaemia
but does not lower the potassium level itself.
◆ Glucose, which reduces blood potassium levels by stimulating the body to release
insulin, driving potassium from the bloodstream into the cells.
◆ Neutral insulin, which reduces blood potassium levels by driving it into the cells. As
hypoglycaemia can result from insulin administration, glucose is typically given at
the same time.

Nursing care
Nursing considerations for the AKI patient are extensive, and include:
◆ Monitoring renal function
◆ Repeat assessments and examinations
◆ Urinary catheter management

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◆ Nutrition
◆ Monitoring fluid balance
◆ Vascular access
◆ Monitoring cardiovascular function.

Nutrition
AKI patients are frequently anorexic and nutritional support forms a large part of their nursing
care.

Patients should be weighed regularly, and their resting energy requirement (RER) calculated
each day based on their current or admitted weight. The percentage of the RER consumed each
day should be recorded. Enteral feeding support is given where hyporexia or anorexia persists
for 3 or more days.

Naso-oesophageal tubes can be beneficial in these patients; they are quick and simple
to place, can be placed in the conscious patient, and can be placed by veterinary nurses.
Alternatively, if the patient is being anaesthetised for other procedures, an oesophagostomy
tube may be placed at the same time.

The best food we can give to an AKI patient is the one the patient will eat – rather than focusing
specifically on a particular diet type.

Vascular access
Vascular access is another important consideration when nursing the AKI patient. In addition to
requiring regular blood sampling to check electrolyte, BUN and creatinine levels and acid–base
balance, these patients also need multiple IV fluids, constant-rate infusions and IV medications.

In most cases, a single peripheral IV catheter will not be sufficient, so further options such as
central venous catheter (CVC) placement will be required.

CVCs are placed in the jugular vein via a guide wire and end in the cranial vena cava. They
include multiple, separate lines within the large catheter, so can be used to administer multiple
fluids and medications simultaneously and can be used for repeated blood sampling without
venepuncture.

They require careful aseptic handling and management to prevent infection:

◆ Sterile placement and handling of the insertion site is indicated
◆ Site inspections, cleaning and re-dressing should be performed twice a day
◆ Unused ports should be flushed with sterile saline every 4–6 hours.

To sample from a CVC, the push–pull method is used. To do this:5

◆ Flush with a volume of saline equal to the catheter’s priming volume (usually
0.3–0.5 ml)
◆ Draw back 3 x this volume into the same syringe
◆ Reinfuse this into the CVC
◆ Repeat 3 times.
◆ Switch to a clean syringe and collect your sample
◆ Flush the CVC with saline.

When collecting samples from a CVC, especially in patients that are having regular sampling,

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it can be easy to inadvertently cause anaemia. To minimise this risk, take care with sample
volumes, collecting only what is needed for each test. It is also advisable to assess a baseline
packed cell volume when the patient has its initial diagnostics.

Renal function
Monitoring renal function is a vital part of nursing the AKI patient. In addition to performing
regular bloods to check renal parameters, an easy way to do this is by measuring urine output.
This is best achieved by placing an indwelling urinary catheter, but if this isn’t possible, then it
can be performed by weighing bedding and litter trays before and after use.

Urinary catheter management

Patients with indwelling urinary catheters are at high risk of developing a hospital-acquired
urinary tract infection. To minimise this risk, aseptic placement and management of the
catheter is an important nursing consideration. This can be achieved by:3,4
◆ Always using a collection system
◆ Storing bags in a clean tray/off the floor
◆ Wearing gloves when handling the catheter, bag and line
◆ Cleaning the prepuce/vulva, catheter and lines every 4 hours
◆ Performing regular sediment examinations to check for infection.
◆ Avoiding prophylactic antibiotics.

In addition, every 4–6 hours (as indicated based on the individual patient), the bag should be
emptied and the volume collected recorded. The specific gravity can also be measured at this
time, as well as the patient’s urine output, calculated using the following formula:

Total ml emptied / hours since last emptied / body weight = urine output (ml/kg/hour)

Repeat assessments/examinations
Regular clinical examinations are required in these often severely ill patients. These should
include a full clinical examination with thoracic auscultation, pain assessment and (where
appropriate) abdominal palpation, in addition to collection of vital parameters. Body weight
should also be checked every 6–12 hours in these patients because most acute weight changes
are associated with changes in fluid balance. These assessments should also include carefully
monitoring fluid balance, checking for signs of volume overload and monitoring for signs of
nausea.

Where hyperkalaemia is present, the heart rate and rhythm should be regularly checked, and
the patient placed on a continuous ECG if possible.

Conclusion
AKI is a common cause of azotaemia in cats, often presenting as an emergency, with advanced
treatment and nursing care requirements. Diagnosis is made based on clinical examination
and history findings alongside biochemical, haematological, and venous blood gas results
and diagnostic imaging. Treatment options are varied depending on the underlying cause of
the AKI, and include administering antidotes for specific toxins (e.g., ethylene glycol), relieving
urinary tract obstructions and correcting hypotension or hypovolaemia, in addition to providing
supportive care.

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References

1. Cole L. Management of acute kidney injury in the dog and cat. https://www.veterinaryirelandjournal.
com/images/pdf/small/sa_dec_2017.pdf (2017, accessed 23 April 2023).
2. Palm C. Acute azotaemia. In: Drobatz KJ, Hopper K, Rozanski E and Silverstein DC. (eds). Textbook of
small animal emergency medicine. Ames: Wiley-Blackwell, 2019, pp 595–601.
3. Steele AM. Urogenital emergencies. In: Norkus CL (ed). Veterinary technician’s manual for small
animal emergency and critical care. 2nd ed. Ames: Wiley-Blackwell, 2019, pp 159–196.
4. Francey T. Acute kidney injury: Diagnosis and management. https://www.vin.com/apputil/content/
defaultadv1.aspx?pId=14365&catId=73691&id=7259355 (2015, accessed 23 April 2023).
5. Barr CA, Giannotti G, Graffeo CE, et al. Effect of blood collection by the push-pull technique from
an indwelling catheter versus direct venepuncture on venous blood gas values before and after
administration of alfaxalone or propofol in dogs. J Am Vet Med Assoc 2017; 251: 1166–1174.

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CLINICAL PRACTICE STREAM

Wake up to inappetence: practical solutions for the

cat that won’t eat both in the clinic and at home
Sam Taylor Sponsored by
BVetMed(Hons), CertSAM, DipECVIM-CA, MANZCVS, FRCVS

Summary:
Inappetence is a very common clinical sign in cats, and has multiple medical causes.
However, food intake is more complex and is influenced by stress, pain, medications and
many other factors. Addressing these factors can potentially ameliorate the damaging
effects of reduced food intake on recovery from illness, wound healing, the immune system
and ultimately long-term survival.

Inappetence is a common clinical sign of multiple physical diseases, but is also influenced by
mental wellbeing. When we think about inappetence in cats, we need to consider the effect
on both the cat and the caregiver. For many owners, feeding their cat provides them pleasure.
This can lead to overfeeding and obesity, but it can also lead to anxiety for owners when their
cat does not eat. Therefore, inappetence has effects on the cat and the owner – and this
combination can even influence treatment decisions.

Effects of inappetence on caregivers

◆ Increased anxiety and ‘caregiver burden’
◆ Increased difficulty giving medications
◆ Concerns over costs of treatment
◆ Misperceptions of recovery/improvement from illness (the cat’s condition may be
improving but this is not perceived by the caregiver if the cat still refuses food)
◆ Frustration with the veterinary clinic
◆ Declining further investigation and treatment, which can ultimately result in
accelerated euthanasia

Effects of inappetence on cats

◆ Compromised immune system
◆ Increased intestinal permeability and dysbiosis
◆ Slower wound healing
◆ Proteolysis and loss of muscle (weakness, increased pain from arthritis)
◆ Onset of ‘frailty’ with negative prognosis (particularly in older cats)
◆ Reduced quality of life
◆ Longer hospitalisation
◆ Risk of hepatic lipidosis
◆ Dehydration (hence constipation)
◆ Electrolyte abnormalities (e.g. hypokalaemia)

Reduced appetite is likely to result in loss of body condition, and there is evidence in many
illnesses that reduced body condition score is associated with a poorer prognosis (e.g. in
conditions such as chronic kidney disease (CKD), lymphoma or hyperthyroidism).

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Effect of stress on appetite

We know that stress can reduce appetite, and inappetence can be a ‘sickness behaviour’ – that
is, like feline idiopathic cystitis, it is reported in susceptible cats without underlying illness. Within
a clinic environment, becoming a Cat Friendly Clinic, hence reducing the stress due to the
environment and handling of the cat, can itself help increase food intake. At home, sadly many
cats are suffering the effects of stress, and there is a species misunderstanding from caregivers
– e.g. that having more cats benefits them, feeding in busy areas with double bowls. Hence,
environmental and management techniques can improve food intake in general and improve
health.

Appetite stimulants
Appetite stimulants can be very useful in the management of inappetence; however, they
should not be considered alone for inappetent cats. This is because in the presence of
underlying disease their effect may be reduced without other treatments (for pain, nausea,
reducing stress) and they are not a substitute for investigating the cause of the reduced
appetite. However, there are many circumstances where they can be used to the patient’s
benefit:
◆  uring investigation of disease to avoid further negative effects of reduced food
D
intake (e.g. when waiting for blood test results)
◆ To assist transition to preferred diets (e.g. with novel flavours or textures)
◆ Supportive care during chronic disease management (e.g. CKD, lymphoma,
pancreatitis)
◆ In cats that are eating, but less than their resting energy requirement (RER)
◆ To encourage fluid intake (e.g. constipated cats, polyuric cats), as many cats get
the majority of their water from food
◆ To overcome food aversion (cats that have been syringe fed or had severe
nausea)
◆ To assist in medicating cats in food
◆ When placing a feeding tube is not an option.

There are few contraindications to appetite stimulants but, as mentioned, they would not be
recommended in cats with, for example, ileus, active vomiting and nausea, pain, critically ill cats
or those with oral/pharyngeal/oesophageal disease affecting prehension and swallowing.

The most commonly used appetite stimulant in cats is mirtazapine, which is available as
Mirataz (Dechra) transdermal in the USA, Canada and Europe. Capromorelin (Elura; Elanco) is
licensed in the USA and can be obtained by import to other countries. Transdermal mirtazapine
has been shown to result in weight gain in cats with various illnesses and be efficacious in
cats with CKD (when it can be used daily). The transdermal formulation has a flatter drug
concentration curve than the oral formulation and hence fewer side effects tend to be seen.

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CLINICAL PRACTICE STREAM

Nutritional intervention case studies: when food

makes a big difference
Cecilia Villaverde
BVSc, PhD, DACVIM (Nutrition), DECVCN

Summary:
All cats, healthy or not, require nutrition, and should receive a feeding plan from the veterinary
team, both to prevent nutritional pathology (associated with inadequate diets) and to
manage any nutrient-sensitive diseases that might be present. This lecture will discuss
several cases to highlight the importance of adequate nutrition to prevent and manage
disease.

Introduction
There is a close relationship between nutrition and health. Cats require nutrients and energy,
both provided by food, to perform physiological functions for growth, and for overall function.1
Therefore, inadequate nutrition can and will result in disease associated with deficiencies or
excess of nutrients or calorie imbalances. These problems, associated with incorrect nutritional
management, are called nutritional pathologies. Nutritional pathologies are much less common
than before thanks to the advent of commercial complete products; however, we can still see
them when the patient is fed an imbalanced home-prepared diet or the wrong commercial
diet. Nutritional pathologies include nutritional secondary hyperparathyroidism and taurine
deficiency. That said, commercial diets that are improperly formulated or that have other issues
can also be imbalanced and should not always be discarded as the cause of the problem.
On the other hand, there are some situations where feeding is not the cause of the problem
but it can be used as part of the therapy of specific diseases, such as urolithiasis, chronic
renal disease and hepatic disease. The diets used in this situation are called “veterinary” or
“therapeutic” diets.2

All cats, therefore, should receive a tailor-made feeding plan, including diet choice (with or
without treats and supplements), daily allowance, and feeding method, to minimize the risk of
nutritional pathology and to provide the best care if they have any nutrient-sensitive diseases.
In order to devise the feeding plan, cats need to undergo a nutritional assessment.3

Nutritional assessment
There is no simple way to assess the nutritional status of a patient. There are around 40
essential nutrients and there are no good status markers for the majority of them. Moreover,
marginal deficiencies or excesses can take years to manifest, so a normal physical examination
and lab work does not guarantee that the current feeding plan is safe. For these reasons,
risk factors are identified via a nutritional assessment that evaluates the animal, food, and
environment, and actions are taken if any are identified. The WSAVA website4 has a document
that provides guidelines plus a variety of tools to help the whole veterinary team do the
assessment. The goal is to perform a screening assessment with most of the information from
a routine visit (most of the additional effort would go to obtaining a diet history), including
signalment, history and nutritional assessment.

Risk factors identifiable in the history and physical examination are listed in Table 1.

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Table 1: Risk factors identifiable in the history and physical examination

The signalment does not identify risks per se but can help identify animals more susceptible
to nutritional problems, such as those with extreme energy needs, either very high (lactating
queens) or very low (very inactive neutered pets), or extreme ages (very young and seniors).
Other information from the history might represent a risk factor only in some cases (e.g., free
feeding is more of a concern in a mature, indoor, neutered adult cat than in a young, outdoor,
intact cat).

If any factors are identified on the screening, an advanced nutritional assessment is indicated.
This will vary depending on the specific risk factors found, but can require diagnostics,
more detailed skin examination, or a closer look into the diet or feeding method. After that,
the veterinary team will provide new recommendations to address those potential issues.
Nutritional and calorie information on commercial products can be hard to find, as the label is
very limited, so I recommend contacting the manufacturers directly when more information is
needed.

To convert as-fed values to energy basis (units of nutrient per 1000 kcal), the calculations are
as follows:
1. From % as fed (g of nutrient per 100 g of food): divide the % of nutrient by kcal of
metabolizable energy per 100 g, and then multiply by 1000.
Example: A diet with 9% protein and an energy density of 120 kcal/100 g:
(9/120) x 1000 = 75 g protein/1000 kcal

2. From ppm (mg or IU per kg of food): divide the amount of nutrient by the kcal of
metabolisable energy per kg, and then multiply by 1000.
Example: A diet with 20 IU of vitamin E and an energy density of 1200 kcal/kg:
(20/1200) x 1000 = 16.7 IU vitamin E/1000 kcal

(Some people prefer to calculate per 100 kcal; to do this you can divide the result of the
above calculations by 10.)

The energy content is rarely reported on the label; to obtain it you need to check the
manufacturer’s website, the product guide, or call the company. You can also estimate it from
the label analysis, but this is cumbersome and can result in errors.

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Developing a feeding plan

The feeding plan includes the food choice (with or without treats and/or supplements), daily
allowance and feeding method.

DIET CHOICE
For patients with nutrient-sensitive diseases, it is important to list the nutritional goals to help
find a diet that will meet them. For veterinary diets, I recommend obtaining product guides
from the available reputable brands, as they provide much more nutritional information (and
often in the right units to enable comparison) than the label. These guides also commonly
provide a rationale/explanation of the nutritional characteristics of each product, as well as
citing research. It is important to consider diets for the same condition as different, to better
customize the choice. For example, different diets for chronic kidney disease contain different
amounts of protein, phosphorus, potassium, and so on, which will make some diets more
appropriate than others for the individual case, depending on staging, muscle condition score,
appetite, etc. Veterinary diets are regulated in Europe under PARNUTs (foods with a particular
nutritional purpose: https://eur-lex.europa.eu/legal-content/EN/TXT/?uri=uriserv:OJ.L_.2020.067.
01.0001.01.ENG&toc=OJ:L:2020:067:TOC).

Homemade diets can be a good choice in some cases where no commercial options are
suitable, but they have pros and cons, reviewed elsewhere.5

Treats can be very positive, but it is important to provide guidanceto try to ensure that treats
are tolerated, do not affect the balance of the main diet, and do not negatively affect the
therapeutic effect of the main diet. Treats should not provide more than 10% of the daily calories
and should be chosen following the same strategies as the main diet.

Supplements need to be assessed on a case-by-case basis. Supplements for “overall health”

are rarely useful, and I recommend only using supplements with specific goals in mind, for
example, oral vitamin B12 in cases of chronic enteropathy, omega-3 fatty acids in some
inflammatory diseases, or taurine in dilated cardiomyopathy cases. Some supplements can
provide calories (e.g., oils); therefore, they should be included in the 10% of calories allowed for
treats and imbalanced items.

DAILY ALLOWANCE
While diet choice is more dependent on the nutritional needs of the patient, the daily allowance
is dependent on the patient’s energy requirements. Diet history is the best way to estimate the
patient’s energy needs, but if that is not possible, formulas or the label instructions from the
diet of choice can be used. In all cases, frequent adjustments are needed as formulas are very
inaccurate.

Once the energy needs are either estimated or calculated, the daily allowance is calculated by
dividing the maintenance energy requirement (MER) by the energy content of the diet of choice.
If treats are going to be included in the plan, make sure to remove those calories from the
MER first to prevent undesired weight gain. Calculating the allowance in grams (and weighing
the food daily) is indicated in obesity-prone or overweight patients. Cup measurements are
unreliable.6

FEEDING METHOD
Free feeding is indicated in thin cats that are prone to losing weight or those with a waxing and
waning appetite (if the household situation allows), but measuring the daily intake (by weighing

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the dish daily) is required, to have good control of the food intake and identify any changes in
intake quickly. For obesity-prone or overweight cats, portion control is indicated.

Follow-up
The nutritional assessment must be repeated for short-term adjustments (e.g., the cat does not
like the diet, undesired weight changes, the client cannot source the chosen product) but also
in response to longer-term change (disease evolution, new conditions, ageing, etc.).

Resources
◆ WSAVA Global Nutrition Committee website, for nutritional assessment guidelines and tools, including a
document on how to choose a pet food: https://wsava.org/global-guidelines/global-nutrition-guidelines/
◆ FEDIAF nutritional guidelines, which include formulas to calculate MER in cats, and are free to download:
https://europeanpetfood.org/self-regulation/nutritional-guidelines/
◆ Check manufacturers’ websites and product guides for information on the nutritional characteristics of
their veterinary products. They can also provide courses and webinars for those interested in nutrition.
◆ Many major veterinary conferences also provide continuing education on nutrition, ranging from nutrition
for healthy cats to nutritional management of diseases.
◆ Finally, you might need help for complex cases or to get a custom homemade diet. In such cases you can
find a board-certified veterinary nutritionist here: https://ebvs.eu/specialists/find-a-specialist?countryId=0
&specialistTitleId=0 or here: https://www.vetspecialists.com/.

References
1. National Research Council. Nutrient Requirements of Dogs and Cats. Washington, DC: The National
Academies Press; 2006.
2. Davies M. Veterinary clinical nutrition: success stories: an overview. Proc Nutr Soc 2016; 75(3):
392–397.
3. Freeman L, Becvarova I, Cave N, et al. WSAVA Nutritional Assessment Guidelines. J Small Anim Pract
2011; 52(7): 385–396.
4. WSAVA. Global Nutrition Guidelines and toolkit. https://wsava.org/global-guidelines/global-
nutrition-guidelines/
5. Villaverde C, Chandler M. Commercial vs homemade cat diets: what you need to know. J Feline Med
Surg 2022; 24(5): 415–428.
6. German AJ, Holden SL, Mason SL, et al. Imprecision when using measuring cups to weigh out
extruded dry kibbled food. J Anim Physiol Anim Nutr (Berl) 2011; 95(3): 368–373.

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CLINICAL PRACTICE STREAM

Tubes everywhere: practical management of SUBs,

catheters, and urine bags
Laura Jones
BSc (Hons), DipAVN (Small Animal), ISFMDipFN, VTS(SAIM), RVN

Introduction
Veterinary nurses are highly involved in the placement and management of indwelling urinary
catheters. The use of these catheters is not without challenge, with complications such as
hospital-acquired urinary tract infection (UTI) being common. Additionally, they can have
a negative impact on the wellbeing of hospitalised cats, causing discomfort and impacting
normal behaviour. This is a particularly important consideration in cats with conditions such as
feline idiopathic cystitis, which are often stressed when in the hospital.

Subcutaneous ureteral bypass (SUB) devices are placed increasingly frequently to manage
ureteral obstructions in feline patients. The care of these patients is complex, particularly in the
acute postsurgical period. Owing to their need for ongoing device management, these patients
can be challenging to manage for revisits, with increasing stress often noted.

This session will discuss the considerations for placing and managing urinary catheters and the
care of patients with SUBs, both after surgery and ongoing.

Urinary catheters and placement

A variety of urinary catheter types are available; of these, an appropriate catheter should be
selected based on the patient, the anticipated duration of catheterisation and the reason for
catheterisation (i.e., whether it is short term or will be left indwelling).1

In cats, nylon or polypropylene catheters are commonly used. These rigid catheters are useful
for the relief of lower urinary tract obstructions. They should be considered for the relief of
obstructions only and not for indwelling use, since their rigid material can cause trauma to the
urethral mucosa and patient discomfort if left in situ for prolonged periods.1 For indwelling use,
softer, flexible polyurethane catheters should be considered.

Placement in the male cat

Deep sedation or general anaesthesia is typically required for feline urethral catheterisation.
1. Following sedation, the patient is positioned in lateral recumbency.
2. The area around the prepuce is clipped and disinfected using antimicrobial skin
preparation.
3. The catheter is measured from the bladder neck to the prepuce.
4. The thumb and index finger are used to push the prepuce cranially, exposing the
glans penis.
5. The catheter is lubricated using sterile water-based lubricant and advanced into
the urethra aseptically.
6. Once the catheter is advanced into the penile urethra, the prepuce can be
grasped and pulled caudally. This straightens the urethra, facilitating passage of
the catheter.

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7.  he catheter is advanced until it enters the bladder and urine emerges from the
T
catheter hub. The veterinarian/veterinary nurse stops advancing the catheter, and
either obtains a urine sample (if required) or attaches a closed collection system
(if the catheter is to remain indwelling).
8. The catheter, if remaining in situ, is secured to the prepuce with sutures1.

Placement in the female cat

Following sedation, the patient is positioned in either lateral or dorsal recumbency, depending
on individual preference.
1. The area around the vulva is clipped and disinfected using antimicrobial skin
preparation and the vulva is flushed.
2. The catheter is measured from the bladder neck to the vulva.
3. The catheter is lubricated using sterile water-based lubricant.
4. The vulval lips are grasped and extended ventrally, while the catheter is inserted
along the ventral midline of the vestibule.
5. The catheter should advance into the external urethral orifice (which lies on the
ventral floor of the vestibule) without the need for visualisation. However, if desired,
visualisation can be performed using a small sterile otoscope head (depending on
patient size).
6. The catheter is advanced until it enters the bladder and urine emerges from the
catheter hub. The veterinarian/veterinary nurse stops advancing the catheter, and
either obtains a urine sample (if required) or attaches a closed collection system
(if the catheter is to remain indwelling).
7. The catheter, if remaining in situ, is secured to the vulva with sutures.1

Management
Indwelling urinary catheters are frequently placed to assess urine output, maintain comfort
and cleanliness in recumbent patients, manage patients following urethral or bladder surgery
or obstruction, and to decompress a neurogenic bladder. These catheters require careful
management by the veterinary team to maximise patient comfort and minimise the risk of
complications.

Following placement, the catheter should be secured in a way that prevents it being dislodged
while minimising patient discomfort. Foley catheters should be placed, where possible, as they
are held in place by a balloon, preventing the need for sutures, which may pull on the patient’s
vulva or prepuce. Where Foley catheter use is not possible, sutures should be placed through
anchor holes in a suture cuff, via butterfly tape or via a finger trap suture. Excessive tightening of
sutures should be avoided because this can irritate the skin and cause discomfort. Discomfort
associated with pulling on the catheter or sutures can also be minimized by attaching the
catheter or line to the patient’s tail or a hindlimb.

As patients with indwelling urinary catheters are at an increased risk of developing an

ascending UTI1, careful aseptic management of the catheter is vital. Catheters should never
remain open-ended and allowed to drain freely into the environment; instead, a closed
collection system is attached to the catheter. This allows urine output to be measured, the
appearance of the urine to be evaluated and urinalysis to be performed where required,
in addition to maintaining patient and environmental cleanliness, and helping to prevent
secondary infection.

Gloves must be worn whenever the catheter, collection bag or lines are handled, in combination

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with hand hygiene before and after handling. The prepuce/vulva, external portion of the
catheter, collection system and all connections should be cleaned with a non-irritating, diluted
antimicrobial skin solution (e.g., 0.05% chlorhexidine gluconate) every 4–6 hours.

The collection system should not be left to sit on a contaminated surface, such as the floor. The
author places urine collection bags in a clear zip-lock bag on a clean incontinence pad, within
a clean litter tray used only for catheter management.

Prophylactic antibiotics should not be routinely administered to patients with indwelling urinary
catheters, owing to the risk of developing a resistant UTI. Instead, in patients where the risk of
UTI is considered high, a urine sample is collected via cystocentesis after the urinary catheter
is removed. This sample is submitted for bacterial culture, and an appropriate treatment is
administered if required. Alternatively, routine sediment examinations can be performed every
24–48 hours during catheterisation, to detect infection and allow appropriate antibiotic use.

Patient interference should be prevented in patients with indwelling urinary catheters, due to
the risk of self-removal, as well as the risk of catheter contamination. An Elizabethan collar may
be required depending on the individual patient and its demeanour.

Urine collection systems should be emptied at appropriate intervals (typically every 4–8 hours).
The volume of urine collected, in addition to its macroscopic appearance and urine specific
gravity, should be recorded. Urine output should also be calculated in ml/kg/hour and recorded.

Subcutaneous ureteral bypass

The SUB device is commonly used in the management of feline ureteral obstruction. It
consists of locking loop nephrostomy and cystostomy catheters, which are connected to a
subcutaneous shunting port.3 The nephrostomy catheter is inserted into the renal pelvis and
secured using a Dacron cuff and glue; the cystostomy catheter is inserted into the apex of the
urinary bladder and secured using a Dacron cuff, glue and suture.3

Both catheters are tunnelled through the abdominal wall and secured to a shunting port, which
is sutured to the outside of the abdominal wall.3 After placement, the system is flushed using
0.9% saline and an atraumatic Huber needle.

Postoperative management
Care requirements for the postoperative SUB patient are extensive and include:
◆ Analgesia
◆ Fluid therapy monitoring
◆ Urinary catheter management
◆ Monitoring urine output
◆ Nutrition
◆ Monitoring of vital parameters
◆ Assessment of acid–base and electrolyte imbalances
◆ Management of vascular access (central venous catheters are often placed
because they allow frequent sampling in addition to the administration of fluids
and medications).

SUB management
Regular maintenance of the SUB device is required postoperatively. This consists of ultrasound-
guided flushing of the device and urine sample collection 1 month postoperatively, then every

#ISFMRocksDublin 164
 Dublin, 29 June – 2 July

3–6 months for the rest of the patient’s life.

Cystocentesis should not be performed in patients with a SUB due to the risk of puncturing the
device.4 Instead, urine samples are collected via the device port using an atraumatic Huber
needle, which prevents device leakage.

Samples are submitted for microbiological culture, to detect occult infection.5

At the time of sample collection, the device is flushed with 0.9% sodium chloride; the
nephrostomy catheter is flushed first, and ultrasound is used to determine patency (as fluid
can be seen entering the renal pelvis), followed by the cystostomy catheter (with ultrasound
used to watch the fluid entering the urinary bladder). Following flushing, 2% tetrasodium
ethylenediaminetetraacetic acid (tEDTA) solution (T-FloLoc, Norfolk Vet Products) is instilled into
the device to prevent biofilm formation and device mineralisation.6

Strict aseptic technique is required to prevent introduction of infection; the site is clipped and
cleaned as for a surgical procedure, and sterile gloves are worn.

Managing the cat with a SUB

Patients with SUBs require frequent visits to the clinic for SUB management and staging
of chronic kidney disease. These patients often become increasingly stressed with the
frequent visits, venepuncture, handling and examinations. The use of pre-visit anxiolysis
(e.g., gabapentin) is recommended to improve their wellbeing in the hospital and facilitate
procedures such as intravenous catheterisation and blood sampling. Alongside these pre-visit
medications, clients should be given information on how to transport their cat to and from the
clinic in a cat-friendly way.

After admitting the patient, it should be placed in an appropriate kennel (including a hiding
place, and the use of calming pheromones within the ward) and feline-friendly handling
techniques should be used throughout hospitalisation.

Conclusion
Indwelling urinary catheters and SUB devices are commonly placed in the management
of lower and upper urinary tract obstructions, respectively. These devices require careful
management in order to prevent complications, and the veterinary nurse is highly involved in
the care of these patients. Aseptic placement, handling and maintenance of indwelling urinary
catheters is a vital consideration to prevent complications such as infection, and something the
veterinary nurse must strictly adhere to when caring for these patients.

Patients with SUBs are often increasingly nervous and can be challenging to manage in the
hospital. The use of pre-visit anxiolytics alongside feline-friendly nursing techniques can be
incredibly useful in the successful management of these patients.

References
1. Foreman M and Merrill L. Nursing. In Merrill L (ed). Small animal internal medicine for veterinary
technicians and nurses. Ames: Wiley-Blackwell, 2012, pp 449–507.
2. Aldridge P and O’Dwyer L. Practical emergency and critical care veterinary nursing. Chichester: Wiley-
Blackwell, 2013.
3. Berent A and Weisse C. The SUB™ 2.0: a subcutaneous ureteral bypass system; a surgical guide.

#ISFMRocksDublin 165
 Dublin, 29 June – 2 July

https://norfolkvetproducts.com/PDF/SUB/SUB2_Surgical_Guide_2018-03-email.pdf (2018, accessed

10 May 2023).
4. Berent A. Management of feline ureteral obstructions: an interventionalist’s approach. https://www.
acvs.org/files/proceedings/2011/data/papers/051.pdf (2011, accessed 8 May 2023)
5. Casale S. Subcutaneous ureteral bypass (SUB™) for the treatment of ureteral obstruction in cats.
https://www.mspca.org/angell_services/subcutaneous-ureteral-bypass-sub-treatment-ureteral-
obstruction-cats/ (2023, accessed 23 April 2023).
6. Chik C, Berent AC, Weisse CW and Ryder M. Therapeutic use of tetrasodium
ethylenediaminetetraacetic acid solution for treatment of subcutaneous ureteral bypass device
mineralization in cats. J Vet Intern Med 2019; 33(5): 2124–2132.

#ISFMRocksDublin 166
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 ABSTRACTS
A RETROSPECTIVE STUDY OF FELINE GASTROINTESTINAL EOSINOPHILIC
SCLEROSING FIBROPLASIA BASED ON HISTOPATHOLOGY SUBMISSIONS TO A
DIAGNOSTIC LABORATORY
Melanie J. Dobromylskyj1, Agnieszka Zoltowska2
1
Histopathology Department, Finn Pathologists, Diss, UK
2
School of Veterinary Medicine and Science, University of Nottingham, Sutton
Bonington Campus, Loughborough LE12 5RD

Feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) is a distinctive clinico-

pathological entity primarily but not exclusively affecting the gastrointestinal tract and associated
lymph nodes. The condition is characterised by predominantly eosinophilic inflammation
associated with a varied degree of fibroplasia, which together form a mass. Since the first reports
more than ten years ago, the number of cases has slowly increased, although FGESF is still
considered a relatively uncommon differential for an abdominal mass. The aim of this study was
to identify and characterise a large cohort of cases diagnosed as FGESF via biopsy.

Cats with a diagnosis of FGESF based on histopathology samples submitted to a large commercial
diagnostic laboratory between February 2014 and December 2022 were identified by searching
the database for the keywords “eosinophilic sclerosing fibroplasia”. This retrieved 102 “hits”, for
which the histopathology reports were reviewed and 78 cases were deemed suitable for inclusion
in this study. The signalment of cats, the anatomical location of the lesion(s), any clinical history
on the submission form, and any concurrent findings were recorded.

The median age of cases was 8 years 11 months, and slightly more male (62%) than female cats
were affected. The Ragdoll and Birman breeds appeared more frequently affected compared with
the background breed prevalence. The most common sites were the mesenteric lymph nodes,
the root of the mesentery, the stomach (often the pylorus), and the ileo-caeco-colic junction.
More unusual sites included the rectum, caecum and perirenal lymph node, and some cases had
more than one lesion. Reported clinical signs varied widely, including a palpable mass, vomiting,
diarrhoea, anaemia, hypoalbuminaemia, jaundice, lymphadenomegaly, rectal prolapse, lethargy,
pyrexia, weight loss, anorexia/hyporexia, and obstruction. In a small proportion of cases, bacteria
were identified, with a range of different organisms seen. These results are generally supportive
of previous published findings, and this represents a large cohort of cases, potentially setting the
stage for further in-depth studies into the underlying aetiopathogenesis of this intriguing feline
disease entity.

#ISFMRocksDublin 168
 ABSTRACTS
PERIOPERATIVE ANAESTHETIC COMPLICATIONS IN HEALTHY CATS
UNDERGOING ANAESTHESIA FOR NEUTERING IN FIRST-OPINION PRACTICE

Jenny F Brown1, Pamela J Murison2

1
CVS Group, Diss, UK
2
School of Biodiversity, One Health and Veterinary Medicine, University of Glasgow, UK

The objective of this retrospective study was to identify the prevalence of common peri-operative
anaesthetic complications in cats undergoing anaesthesia for neutering in three UK first-opinion
practices.

All cats anaesthetised for neutering at practices 1 and 2 between 9/12/2017 and 02/02/2021 and at
practice 3 between 09/03/2020 and 07/01/2021 were identified by searching practice management
software. Patient characteristics and anaesthetic data were extracted from patient records and
entered into an Excel spreadsheet. Complications were defined after reviewing the literature and
their prevalence determined from the data. Comparisons between different groups of cats in
the study were made using a chi-squared test for homogeneity or Fisher’s exact tests to identify
factors associated with increased prevalence of complications.

Data from 1019 cats were included in the study. The anaesthetic-related mortality was 1/1019
(0.10%), with one cat suffering unrecoverable respiratory arrest in the post-operative period. The
most common complications were hypotension (22.6%), bradycardia (16.7%) and hypothermia
(13.79%). Factors associated with increased risk of hypotension were acepromazine pre-
anaesthetic medication, higher maximum isoflurane dose, longer anaesthetic duration and lower
body weight. Factors associated with increased risk of bradycardia were medetomidine pre-
anaesthetic medication, longer anaesthetic duration and higher body weight. Factors associated
with increased risk of hypothermia were higher maximum isoflurane dose, increased anaesthetic
duration and lower body weight.

This study showed that anaesthetic complications were frequently observed, with complications
documented in 53.4% of the cats in the study. This information in this study may help to guide
prioritisation of monitoring in feline anaesthesia.

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 ABSTRACTS
FACTORS ASSOCIATED WITH LEISHMANIA INFANTUM
INFECTION IN ITALIAN CATS

Eva Spada1, Federica Bruno2, Germano Castelli2, Roberta Perego1, Fabrizio Vitale2,
Antonella Migliazzo3, Sara Accettulli1, Luciana Baggiani1, Daniela Proverbio1

1
Department of Veterinary Medicine and Animal Sciences, University of Milan, Lodi, Italy
2
Istituto Zooprofilattico Sperimentale della Sicilia, Palermo, Italy
3
Dipartimento di Prevenzione UOC Sanità Animale, Igiene degli Allevamenti e delle
Produzioni Zootecniche, ASL Latina, Italy

Leishmania infantum infection was investigated between 2020 and 2023 in 1262 cats using
IFAT (n=1232) and real-time PCR (qPCR) on blood (n=764) and lymph node aspirates (n=296).
Cats with IFAT titer ≥1:80 and/or positive qPCR were considered infected. Season of sampling,
origin (North, Central and South Italy), habitat (owned, stray, shelter), breed (European or not),
hair length (short, medium/long hair), sex (male, female), neutering status (intact, neutered),
age (kitten, adult, senior), prophylaxis against ectoparasites (none, regular, irregular), lifestyle
(indoor, outdoor, indoor/outdoor), cohabitation with dogs, clinical status (weight loss, ocular
and cutaneous signs, lymphadenomegaly) and retroviral status (FIV, FeLV seropositivity) were
evaluated as potential risk or protective factors for infection.

Of 1262 cats, 98 (7.8%) were infected, 2.9%, 0.3% and 4.6% in North, Central and South Italy,
respectively, with a seropositivity rate of 6.5% and qPCR detection rate of 3.6%. Median IFAT
titer was 1:80 (range 1:80–1:2560), median parasite load was 20 Leishmania/ml in blood (range
5–84,400) and 25 in lymph node (range 6–60). Logistic regression analysis found as risk factors
for infection sampling in autumn (OR=3.1, 95%CI:1.7–5.7, P=0.0002) and winter (OR=2.7, 95%CI:1.1–
6.3, P=0.0212), and FIV seropositivity (OR=2.3, 95%CI:1.1–4.7, P=0.0233), while origin from Central
Italy was a protective factor (OR=0.2, 95%CI:0.05–0.6, P=0.0061).

Emergent L. infantum infection in cats is commonly detected at a high level in Italian cats, including
in asymptomatic cats from areas not considered endemic, such as North Italy. Some infected
cats showed parasitemia with high parasite load, especially immediately after the season of
activity for the sand fly vector.

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 ABSTRACTS
ASSESSMENT OF LEFT VENTRICULAR–ARTERIAL COUPLING
BY ECHOCARDIOGRAPHY IN CATS WITH HYPERTROPHIC CARDIOMYOPATHY

Aroonrerm Kittirattanachai, Sirilak D Surachetpong

Department of Veterinary Medicine, Faculty of Veterinary Science, Chulalongkorn
University, Bangkok, Thailand

Ventricular–arterial coupling (VAC) is the interaction between the ventricle and the arterial
system which indicates the cardiovascular performance. It is estimated by the ratio between
effective arterial elastance (Ea) and left ventricular end-systolic elastance (Ees). Inappropriate
VAC has been associated with more advanced heart disease severity and poorer prognosis.
However, no study has been done on VAC in cats with hypertrophic cardiomyopathy (HCM),
which is the most prevalent cardiac disease in cats. Therefore, this study aimed to explore the
echocardiographically estimated VAC in cats with HCM. This retrospective study included data of
39 healthy cats and 77 cats diagnosed with HCM. The HCM group was further divided into stage B1
(n = 19), B2 (n = 17) and C (n = 41) according to the ACVIM consensus guideline. Echocardiographic
profiles of each cat were then used to estimate the Ea and Ees to calculate the VAC index.

Different superscripts indicate differences in VAC value between the groups (P < 0.05).

The VAC value of cats in the HCM stage B2 group was significantly different from that of the
healthy control group (P < 0.001) and the HCM stage C group (P = 0.006). A decrease in VAC from
healthy cats to HCM stage B1, possibly due to left ventricular stiffness from hypertrophy, may aid
in differentiating between the two stages. VAC had a strong negative correlation with fractional
shortening (P <0 .001, r = –0.691), a moderate positive correlation with left ventricular internal
diameter (P < 0.001, r = 0.358) and a weak negative correlation with the thickness of both the
interventricular septum (P = 0.007, r = –0.249) and left ventricular free wall (P = 0.012, r = –0.231),
indicating that there is a correlation between VAC and ventricular wall thickening in HCM.

#ISFMRocksDublin 171
 ABSTRACTS
EPIDEMIOLOGY OF PATHOGENIC RETROVIRUSES AND DOMESTIC
CAT HEPADNAVIRUS IN CLIENT-OWNED AND FREE-ROAMING CATS
IN HONG KONG
Yan Ru Choi1, Regina Hofmann-Lehmann2, Omid Nekouei3,
Vanessa R Barrs1, Julia A Beatty1
1
Department of Veterinary Clinical Sciences & Centre for Animal Health and Welfare,
Jockey Club College of Veterinary Medicine and Life Sciences, City University of
Hong Kong
2
Clinical Laboratory, Vetsuisse Faculty, University of Zurich
3
Department of Infectious Diseases and Public Health, Jockey Club College of
Veterinary Medicine and Life Sciences, City University of Hong Kong

Feline patients comprise 40% of veterinary consultations in Hong Kong. Understanding the threat
posed by feline leukaemia virus (FeLV) and feline immunodeficiency virus (FIV) requires local
data. Domestic cat hepadnavirus (DCH), an emerging hepatitis-B like virus linked to liver disease,
is reported in 11% of client-owned cats in Hong Kong but its molecular prevalence in free-roaming
cats is unknown. This study investigated the serological prevalence of FeLV and FIV in client-
owned cats and in cats enrolled in a trap-neuter-release (TnR) program, and the molecular
prevalence of DCH in TnR cats in Hong Kong.

Residual blood samples were stored at –80°C and age, sex, and source were recorded. Retrovirus
serology was performed using IDEXX SNAP Combo. Results of retrovirus serology and DCH qPCR
were analysed using descriptive statistics.

Among client-owned cats (n=415, median age 121 months [range 2–254 months], male:female
ratio 1.71:1), 5/415 tested FeLV p27 positive (1.2%), and 13/415 (3.1%) tested FIV antibody positive.
Among TnR cats (n=298, median age 18 months [range 5–96 months], male:female ratio 0.75:1),
0/298 tested FeLV p27 positive (0%), 46/298 (15.4%) tested FIV antibody positive, and 34/193 (17.6%)
were positive for DCH by qPCR.

FeLV antigenaemia is uncommon in Hong Kong cats and qPCR confirmation of positive p27 results
is advised. Compared with other regions, TnR cats in Hong Kong acquire FIV relatively young and
infection frequency is high. The molecular prevalence of DCH is similar in TnR and client-owned
cats, and high compared with regions such as the USA and Japan.

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 ABSTRACTS
EPIDEMIOLOGY OF DOMESTIC CAT HEPADNAVIRUS, FELINE LEUKAEMIA VIRUS
AND FELINE IMMUNODEFICIENCY VIRUS IN SANTIAGO, CHILE

Yan Ru Choi1, Maria paz Iturriaga2, Omid Nekouei3, Julia A Beatty1, Vanessa R Barrs1
1
Department of Veterinary Clinical Sciences & Centre for Animal Health and Welfare,
Jockey Club College of Veterinary Medicine and Life Sciences, City University of
Hong Kong
2
Small Animal Unit, School of Veterinary Medicine, Faculty of Life Sciences, Andrés Bello
University, Santiago, Chile
3
Department of Infectious Diseases and Public Health, Jockey Club College of
Veterinary Medicine and Life Sciences, City University of Hong Kong

Domestic cat hepadnavirus (DCH) is an emerging hepatitis-B like virus linked to feline liver disease
in some studies. Global DCH molecular prevalence varies widely from 1% to 18% and retrovirus
coinfection is a risk factor. DCH DNA detection is not yet reported in South America. This study
investigated the epidemiology of DCH, FeLV and FIV in cats in Santiago, Chile.

Residual diagnostic paired serum/blood samples were stored at –80°C. The age, sex, breed,
health status, outdoor access and origin of cats were recorded. The integrity of extracted DNA
was confirmed using glyceraldehyde 3-phosphate dehydrogenase cPCR. Results of DCH cPCR,
retrovirus serology and FeLV qPCR were analysed using descriptive statistics and Fisher’s exact
test.

The study population (n=126) comprised predominantly outbred (98%), desexed (96%) cats, with
a median age of 7 years (range 1–21) and female: male ratio 1.21:1. Of the cats, 2/126 (1.59%) tested
DCH positive, confirmed on sequencing; 10/126 (7.9%) tested retrovirus positive; 4/126 (3.2%) were
FIV antibody positive; and 8/126 (6.3%) were FeLV infected (p27 and qPCR), including 2/126 (1.59%)
dual FIV/FeLV infections. No DCH/retrovirus coinfections were identified. Of 12 cats positive for any
virus, 11 were male. The risk of retrovirus infection was higher in males than females (P = 0.005).

DCH is circulating among cats in Chile with a low molecular frequency compared with Italy and
Asia. Measures to control the spread of FeLV and FIV are indicated in this population.

#ISFMRocksDublin 173
 ABSTRACTS
TRANSIENT BABESIA GIBSONI INFECTION IN A CAT WITH EVANS SYNDROME

Angel Almendros, Yan Ru Choi, Pawel Beczkowski, Kerstin Baiker,

Vanessa R Barrs, Julia A Beatty

Department of Veterinary Clinical Sciences & Centre for Animal Health and Welfare,
Jockey Club College of Veterinary Medicine and Life Sciences, City University of
Hong Kong

The tick-borne haemoparasite Babesia gibsoni commonly infects dogs in Hong Kong either
subclinically or causing babesiosis, a haemolytic anaemia and/or thrombocytopenia and
inflammatory syndrome. Among cats, <20 B. gibsoni infections are documented in apparently
healthy cats in China, Singapore and St Kitts.

A retrospective molecular study of Babesia spp. in Hong Kong cats identified B. gibsoni
infection in a 6-year-old male neutered domestic shorthair presenting with signs consistent
with babesiosis: weakness, melaena, severe regenerative anaemia and thrombocytopenia.
An in-saline agglutination test was positive, whereas retrovirus serology and haemotropic
mycoplasma PCR were negative. Thoracic and abdominal imaging revealed only mild
splenomegaly. Immune-mediated haemolytic anaemia and thrombocytopenia of unknown
aetiology (Evans syndrome) was diagnosed. B. gibsoni DNA was detected in blood taken 24
hours after presentation, using Babesia spp 18S rRNA and mitochondrial cytochrome B PCRs,
sequencing and BLAST analysis. This result was confirmed on repeat DNA extraction and PCR.

Following supportive treatment and glucocorticoids, the cat was clinically stable for 3 months
although reticulocytosis persisted. On day 158, subclinical thrombocytopenia was identified. On
day 180, that cat collapsed and died. A necropsy revealed severe intestinal haemorrhage and
hypocellular bone marrow with megakaryocytosis. DNA from samples stored on days 158 and
180 tested PCR negative for Babesia spp.

The geographic range of feline B. gibsoni infection includes Hong Kong. Although babesiosis is
linked to Evans syndrome in dogs, the role of B. gibsoni in the clinical presentation of this case
is unclear since parasitaemia was apparently cleared, despite iatrogenic immunosuppression,
when signs recurred.

#ISFMRocksDublin 174
 ABSTRACTS
A NOVEL INTERVENTION FOR CAT HOARDING: 3-YEAR FOLLOW-UP

Katherine A Duffy1, Kerry A Williams1, Jodie M Hartley2, Shannon A McCall2,

Jenny H Stavisky3

1
University of Nottingham, UK
2
Manchester RSPCA, UK
3
VetPartners York, UK

This was a follow-up study of a novel intervention for hoarding carried out by the Royal Society for
the Prevention of Cruelty to Animals (RSPCA) Greater Manchester Animal Hospital (GMAH), which
aimed to determine whether observed positive cat population and welfare changes endured
over a 3-year period.

A total of 79 cases of multi-cat households were identified by RSPCA inspectors and referred for
this study. Criteria for inclusion were that households had been visited on at least one occasion
following a public complaint and had five or more cats of breeding age including at least one
female.

All households underwent an initial visit by a veterinary surgeon and follow-up visits at 2 and 12
months. Approximately 3 years later, an RSPCA veterinary surgeon attempted to contact all 79
participants to conduct a telephone follow-up.

A total of 13 usable data sets were obtained and analysed for distribution. Descriptive statistics
were compiled using Microsoft Excel and inferential statistics were calculated using Graphpad.
A Fisher’s exact was used to compare proportions, and the cut-off for significance was P = 0.05.

This study identified a 48.4% reduction in the number of cats living in the 13 households, from 213
to 103. Significant improvements in owner adherence to an effective worming (P = 0.0036) and
flea (P = 0.0414) treatment protocol when compared with initial visit data were noted.

Findings suggest that veterinary home-based welfare interventions which focus on working
collaboratively with multi-cat owners are effective in improving cat welfare in the long term. This
study was limited by loss to follow-up, which was likely due to a combination of the Covid-19
pandemic and the nature of the population under study.

Funding/declarations of interest:
Funding for this research was provided by the Animal Welfare Foundation.

#ISFMRocksDublin 175
 ABSTRACTS
COMPARISON OF THREE DIFFERENT DIAGNOSTIC ASSAYS
FOR DETERMINATION OF FIBROBLAST GROWTH FACTOR-23 IN CATS:
A PILOT STUDY
Ingo Schäfer1, Nicole Nagler1, Simon F Müller1, Annette Holtdirk2, Tanja Kottmann2,
Elisabeth Müller1, Jennifer von Luckner1,3

1
LABOKLIN GmbH and Co KG, Bad Kissingen, Germany
2
Dr med Kottmann – Clinical Research Organization, Hamm, Germany
³ AniCura Ahlen, Ahlen, Germany

Fibroblast growth factor 23 (FGF-23) is a phosphaturic hormone used for monitoring of chronic
kidney disease (CKD) in humans. Its value as a biomarker in feline CKD is questionable. The aim of
this pilot study was to compare three diagnostic assays for FGF-23 and to evaluate the correlation
of FGF-23 with renal parameters in cats.

Cats were recruited into four groups (I: creatinine <1.6 mg/dl, II–IV: creatinine according to IRIS
stages II–IV, n = 10 each). FGF-23 was determined in serum using two different quantitative ELISA
kits (MyBioSource, San Diego, CA, USA; FGF-23 ELISA Kit, Kainos Laboratories, Tokyo, Japan) and an
automated assay for intact FGF-23 on the DiaSorin Liaison platform (FTSE Mid Cap, Italy).

Results for all three assays were available for 38 cats. Spearman’s rho correlation showed high
(ρ = 0.742, P < 0.001) and low (ρ = 0.443, P = 0.005) correlation with the Kainos ELISA for DiaSorin
and MyBioSource, respectively. Results of the Kainos ELISA strongly correlated (ρ > 0.5) with urea
(ρ = 0.835), creatinine (ρ = 0.764), SDMA (ρ = 0.580), and phosphorus (ρ = 0.532) (P < 0.001 each)
while for MyBioSource and DiaSorin this was only the case for urea (ρ = 0.624 and ρ = 0.572,
respectively) and creatinine (ρ= 0.622 and ρ = 0.510, respectively) (P = 0.001 each).

With respect to IRIS staging, the highest correlation was shown for Kainos ELISA (ρ = 0.806),
followed by MyBioSource (ρ = 0.663) and DiaSorin (ρ = 0.580) (P < 0.001 each).

In summary, the best correlation with renal parameters and IRIS staging was shown for the Kainos
ELISA. All three assays showed the highest correlations with urea. Serum phosphorus concentration
did not correlate as well with FGF-23 as would be expected for a phosphaturic hormone.

#ISFMRocksDublin 176
 ABSTRACTS
CLINICOPATHOLOGICAL FINDIGNS OF 7 CATS WITH NEUTROPHILIC AND
ULCTERATIVE BACTERIAL ENTERITIS: A CASE SERIES

Ivan Montañes Sancho1, Silke Salavati Schmitz1, Danièlle Gunn-Moore1, Petra Cerna2,
Grainne Neary3, Kenny Simpson4
1
Department of Small Animal Internal Medicine, The Royal (Dick) School of Veterinary
Studies, University of Edinburgh, UK
2
Department of Clinical Sciences, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, USA
3
Department of Pathological Anatomy, The Royal (Dick) School of Veterinary Studies,
University of Edinburgh, UK
4
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University,
Ithaca, USA

This case series describes a potentially novel gut condition of cats, characterised by neutrophilic
and ulcerative bacterial enteritis (NUBE). The 7 cats included from different geographical locations
were mostly young (median 95 months, range 10–180); breeds included domestic shorthair (4/7)
and other purebreds (3/7). Presenting complaints were chronic insidious weight loss, diarrhoea,
and inappetence. Common findings included poor body condition (6/7), pyrexia (3/7), left-
shifted neutrophilia (3/7), hypoalbuminaemia (4/7), and hypocobalaminemia (5/7). Abdominal
ultrasound revealed enlarged lymph nodes (6/7), loss of intestinal layering (2/7) and marked
thickening of ileal/ileocaecocolic gut segments (4/7) with subsequent intestinal obstruction in 1
cat. Extensive tests for infectious causes (e.g. parasites, mycobacteria, feline infectious peritonitis)
or neoplasia did not reveal a cause. Histopathology of biopsies (mucosal in all cats, additional
full-thickness in 2/7) was consistent with chronic-active neutrophilic (7/7) to pyogranulomatous
(2/7) enteritis with granulomas (2/7), and ulcerations of the epithelium (4/7). Periodic acid-Schiff
stains were negative in all cats. Fluorescent in-situ hybridisation (FISH) revealed invasive and
adherent bacteria in all cases (eubacterial probe in 7/7, probes specific for Escherichia coli in
5/7). Aside from surgical resections of obstructive granulomas, treatments administered were
varied, including antibiotics, glucocorticoids, probiotics, and faecal microbiota transplantations.
Overall, responses were poor, with 4 out of 7 cats being euthanased within a median of 7 months.
NUBE does not seem compatible with other feline gut diseases such as IBD, feline eosinophilic
sclerosing fibroplasia, or previously reported E. coli-associated granulomatous colitis. FISH should
be considered in cats with unusual ileal histopathology, particularly given the poor prognosis
observed.

#ISFMRocksDublin 177
 ABSTRACTS
GASTRIC DIVERTICULA IN SIX CATS: A CASE SERIES (2011–2020)
Kaitlin N Bahlmann, Steven J Bailey, Toni S Brooks
Exclusively Cats Veterinary Hospital, MI, USA

Bahlmann KN, Bailey SJ and Brooks TS. Gastric diverticula in six cats: a case series
(2011–2020). J Feline Med Surg 2021; 24: 407–412.

Gastric diverticulum (GD) is defined as an outpouching of the gastric wall. Gastric diverticula
have not previously been reported in cats. Gastric diverticula were diagnosed in six cats that
presented for a variety of gastrointestinal disorders, including chronic vomiting, weight loss and
anorexia.

All six cats underwent negative contrast radiography to diagnose GD. All but one cat underwent
surgical resection of the GD via partial gastrectomy, while the remaining cat was euthanized.
Resection of the GD was associated with reduction of reported clinical signs.

Negative contrast radiography appears to be a superior imaging technique in the diagnosis of

feline GD. In cats with a vague chronic history, including vomiting, anorexia and weight loss, GD
should be considered among the differential diagnoses. Further study and more cases need to be
identified to better assess clinical problems referable to GD in the absence of other comorbidities.

#ISFMRocksDublin 178
 ABSTRACTS
EPIDEMIOLOGICAL INVESTIGATION OF FELINE UPPER RESPIRATORY TRACT
INFECTION IN CHINA BY A COMMERCIALLY AVAILABLE METHOD

Qipu Feng1, Qiao Qiao2, Hong Jiang3, Liucun Liang4, Xu Zhu5

1
Experimental Animal Center of West China Hospital, Sichuan University,
Chengdu, China
2
AniCura Kleintierzentrum Heilbronn, Heilbronn, Germany
3
Sichuan Tourism Institute, Chengdu, China
4
LABOKLIN GmbH & Co KG, Bad Kissingen, Germany
5
GlinX Biotechnology Co Ltd, Shanghai, China

Feline herpesvirus (FHV-1), feline calicivirus (FCV), Mycoplasma felis (Mf), Bordetella bronchiseptica
(Bb), and Chlamydia felis (Cf) are common pathogens in cats with upper respiratory tract disease
(URTD). A commercially available real-time polymerase chain reaction (PCR)-based assay
device (GlinX inCycle®) was used to rapidly screen all five URTD agents in a single specimen within
half an hour. From July 2021 to April 2022, a total of 1062 household cats exhibiting respiratory
disease clinical signs were included in this multicenter clinical trial. These cats were from 12 small
animal hospitals located in Beijing, Guangzhou, Wuhan, Hangzhou (2 hospitals), Hefei, Qingdao,
Shanghai, Xiamen, Chengdu, Chongqing, and Ya’an. The clinical signs included dyspnea, cough,
sneezing, nasal discharge, ocular signs (secretions, eyelid edema, conjunctival congestion, and
edema), and oral signs (salivation, ulcers, tongue ulcers, hard palate ulcers, and gingivitis). The
results showed that 67.7% of samples were positive for at least one of the five pathogens, with
62.0%, 47.71%, 20.94%, 9.29%, and 8.04% positive for FCV, Mf, FHV-1, Cf, and Bb, respectively.

The results of inCycle® were compared with LABOKLIN in 44 cats; 7% FHV-1, 14% FCV, and 7% Mf were
positive by inCycle® but negative by LABOKLIN, while 11% were negative by inCycle® but positive by
LABOKLIN for Bb.

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 ABSTRACTS
FELINE LEISHMANIOSIS WITH FOCUS ON OCULAR MANIFESTATION:
A CASE REPORT

Ingo Schäfer1, Albert Schmidt², Fritz Gräßer², Andrea Schieszler³, Heike Aupperle-
Lellbach1, Gerhard Loesenbeck1, Michaela Gentil1, Elisabeth Müller1, Torsten J Naucke1,
Jennifer von Luckner1,4

1
LABOKLIN GmbH and Co. KG, Bad Kissingen, Germany
² Small animal practice Dr Fritz Gräßer, Großostheim, Germany
³ Tierärztliches Augenzentrum Frankfurt-Kalbach, Germany
4
AniCura Ahlen, Ahlen, Germany

There is limited knowledge regarding pathogenesis, ocular manifestations, and long-term follow
up in cats with leishmaniosis.

A cat imported from Spain to Germany was presented with lethargy, weight loss, ulcerative lesions
on the limbs, and high-grade uveitis after local glucocorticoid therapy due to respiratory disease.
The diagnosis of Leishmania infantum infection was based on cytological findings of amastigotes
in skin lesions, positive qPCR of EDTA blood, and positive PCR of a cyto-brush sample from the
conjunctiva. Supportive findings included positive serology. Hematological and biochemical
results at first presentation revealed mild leukocytosis with lymphocytosis, monocytosis, and
eosinopenia as well as marked elevation of serum amyloid A (SAA) and hyperglobulinemia. In
serum protein electrophoresis, peaks in alpha2- and gamma-globulin sections were detected.
FeLV antigen and FIV antibody testing were positive. Treatment with allopurinol resulted in
remission of clinical signs.

Enucleation had to be performed on day 288 on both eyes due to refractory glaucoma and
uveitis. The cat was already blind before enucleation. On histologic examination, high numbers
of Leishmania spp. amastigotes were found in histiocytes. Serology and PCR were positive in the
aqueous humor of both eyes.

This case report supports the hypothesis that immunosuppression increases the risk of clinical
signs of leishmaniosis in cats. Alpha2- and gamma-globulin peaks in electrophoresis proved to be
supportive criteria for the diagnosis of feline L. infantum infection. SAA is valuable for monitoring.
For the first time, Leishmania IgG antibodies were demonstrated in the aqueous humor in cats.
Regarding ophthalmology, uveitis and glaucoma may have a poor prognosis.

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 ABSTRACTS
PERFORMANCE OF DAILY APPLICATION OF OPHYTRIUM-CONTAINING PADS IN
ATOPIC CATS: AN EU MULTICENTRIC PROSPECTIVE FIELD TRIAL

Alicia I Cózar1, Chiara Noli2, Marie-Christine Cadiergues3, Pierre Fiora4, Marina Gatellet1

1
Ceva Santé Animale, Libourne, France
2
Dermavet.online, Cuneo, Italy
3
Ecole Nationale Vétérinaire de Toulouse, Toulouse, France
4
Clinique vétérinaire Saint Jacques, Agen, France

Topical products are increasingly part of feline atopic skin syndrome management, as they
bring ingredients directly where they are needed. A multicentric prospective field study was
conducted in Europe to evaluate the performance of daily application of Ophytrium-containing
pads (DOUXO® S3 CALM Pads; Ceva Santé Animale, Libourne, France) in cats suffering from feline
atopic skin syndrome presenting with a localized flare.

Pads were applied daily on the affected areas for 14 days. On D0, D7 and D14, clinical change was
evaluated by the veterinarians, taking a SCORFAD localized scale as a reference (0–4 scale on
excoriations, miliary dermatitis, eosinophilic plaques, self-induced alopecia, sum of each score).
The VAScat dual scale evaluating both licking and scratching was assessed by owners. At the
end of the trial, overall assessment questionnaires were collected.

Nine different body sites from four cats were included in the analysis. Mean localized SCORFAD
value dropped from 3.9 at D0 to 2.2 at D7 and 0.9 at D14, reaching a significant difference (P<0.01)
(mean decrease: 42.2% at D7 and 78.3% at D14). VAScat scores decreased from 5.5 on D0 to 3.2 at
D7 and 1.5 at D14 (mean improvement: 41.3% at D7 and 73.6% at D14). Veterinarians considered the
performance good or excellent in 100% of cases, while 75% of cat owners considered the response
good or very good.

No adverse events were reported. In summary, the Ophytrium-containing pad application

protocol quickly and significantly improved irritation scores and pruritus in atopic cats with a
flare, yielding high satisfaction levels in veterinarians and cat owners.

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 ABSTRACTS
EFFICACY OF ELECTROCHEMOTHERAPY WITH BLEOMYCIN IN FELINE
CUTANEUOUS SQUAMOUS CELL CARCINOMA

Nataša Tozon1, Maša Vilfan1, Sara Suhadolc Scholten1, Urša Lampreht Tratar2, Gregor
Serša2, Maja Čemažar2

1
Veterinary Faculty Ljubljana, Clinic for Small Animals, Cesta v Mestni log 47,
Ljubljana, Slovenia
2
Institute of Oncology Ljubljana, Department of Experimental Oncology,
Zaloška 2, Ljubljana, Slovenia

Thirty-nine cats with squamous cell carcinoma (SCC) were enrolled in a clinical trial between
March 2016 and January 2023 to evaluate the efficacy and safety of electrochemotherapy
(ECT) with intravenous bleomycin in cats. Most cats (31/39) had only one lesion and it was most
frequently (32/39) located on the nasal planum. The remaining cats had lesions on the pinnae
or top of the head, and two of them on the third eyelid. More than half (20/39) were treated with
ECT only once, 11/39 twice, 4/39 three times, 3/39 four times, and one cat was treated five times.

One month after ECT, 82% (32/39) had a complete response (CR) and 18% (7/39) had a partial
response (PR), so that the objective response (OR = CR + PR) was achieved after one month
in all cats (100%). At the end of the observation period (average 7.9 months; 1–49 months) the
percentage of OR was 92% (36/39) as disease progressed in three cats. The time of disease
progression was after an average of 18 months (7–35 months). Of the 39 cats included in the
study, 25 (64%) responded to regular protocol check-ups. In this group, the mean disease-free
period was 6 months.

Based on promising clinical results in cats with SCC, ECT with bleomycin could be the treatment
of choice for local control of smaller tumours. Further studies are needed to evaluate additional
predictive factors, such as those affecting the response to treatment.

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 ABSTRACTS
AN ETHOGRAM OF ACUTE PAIN BEHAVIORS IN CATS BASED ON
EXPERT CONSENSUS

Sabrine Marangoni1, Julia Beatty2, Paulo V Steagall1,2

Department of Clinical Sciences, Université de Montréal, St-Hyacinthe, Canada

1

2
Department of Veterinary Clinical Sciences, Centre of Animal Health and Welfare, City
University of Hong Kong, Hong Kong, China

This study aimed to create and validate an ethogram of acute pain behaviors in cats using
expert consensus.

An inventory of behaviors was created with their respective descriptions to discriminate

painful and non-painful cats based on a literature review using the PubMed, Web of Science
and CAB Abstracts databases. The ethogram was subdivided into 10 categories that could be
evaluated by the duration and/or frequency of behaviors (i.e. repeatability): position in the
cage, exploratory behaviors, activity, posture and body position, affective-emotional states,
vocalization, playing (with an object), feeding, post-feeding and facial expressions/features.
Thirty-six behaviors were analyzed independently by four veterinarians with postgraduate
degrees involving feline medicine and/or behavior as (1) not relevant, (2) somewhat relevant,
(3) quite relevant or (4) highly relevant, and used for content (I-CVI; number of raters who
considered the item relevant (3 or 4) divided by number of raters) and face validity. Items with
I-CVI scores >0.67 were included.

Twenty-four behaviors were included in the final ethogram. A total of 13 items presented full
agreement (i.e. I-CVI = 1): positioned in the back of the cage, no attention to surroundings,
feigned sleep, grooming, attention to wound, crouched/hunched, depressed, difficulty grasping
food, head shaking, eye squinting, blepharospasm, abnormal gait and lowered head position.
Seven descriptors were reworded according to expert suggestions.

This ethogram provides a description of acute pain behaviors after content and face validity.
This tool may be used to determine the duration and/of frequency of specific behaviors during
characterization of different acute painful conditions in hospitalized cats.

The authors are grateful to the expert panel contributing to this study: Dr. Beatriz P Monteiro, Dr.
Diane Frank, Dr. Nathalie Dowgray and Dr. Kelly St-Denis.

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 ABSTRACTS
A FIRST LOOK AT MORTALITY IN A YOUNG COHORT OF DOMESTIC PET CATS

Aimee R Taylor¹, Jennifer McDonald2, Angie Hibbert3, Emily J Blackwell¹

1
Bristol Veterinary School, University of Bristol, UK
2
Feline Welfare Directorate, Cats Protection, National Cat Centre, Haywards Heath, UK
3
The Feline Centre, Langford Vets, UK

The Bristol Cats Study (BCS) is a unique, longitudinal study following a cohort of domestic cats in
the United Kingdom throughout their lifetime. Owners complete regular questionnaires regarding
various aspects of their cat’s life, which contribute to prospectively collected data. All-cause
mortality data represent an important resource that can be used to improve population health,
welfare, and longevity. Previously, this type of data was extrapolated from veterinary records and
represented cats attending veterinary clinics only. Here, we explore causes of death recounted
by cat owners, hence including a previously unreported subset of the feline population.

Data were collated from the first 10 questionnaires of the BCS. Mortality classification was by
system, disease or event. Descriptive statistics were used to summarise the causes of mortality.
Of the 2444 cats recruited into the study, at least 362 died before reaching 9 years old. The most
commonly attributed causes in cats up to 8 years old were road traffic accident (RTA; 45.6%),
non-specified (13.3%), renal disease (6.6%), cardiovascular disease (6.4%) and neoplasia (6.1%).
Mortality causes were also assessed by AAFP life stages. For kittens (cats <1 year old), the most
common causes were RTA (60.6%), feline infectious peritonitis (13.6%), other trauma (6.1%),
surgical complications (6.1%) and toxin ingestion (3.0%). The most common causes of mortality
in young adult cats (1–6 years) were RTA (55.3%), non-specified (15.1%), renal disease (5.5%),
cardiovascular disease (4.5%) and sudden death (4.5%).

RTAs represent the most frequent cause of death during the first two life stages. Kittens are more
likely to succumb to age-related infectious disease, trauma and accidents, whereas young adult
cats can be affected by organ-specific diseases. This study identified important differences in
causes of mortality for different life stages in a population of cats that may not be accounted for
in medical records.

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 ABSTRACTS
COMPARISON OF URINARY CONCENTRATIONS OF PROTEIN
AND CREATININE, AND THEIR RATIO, IN BIRMAN, MAINE COON,
AND DOMESTIC SHORTHAIR CATS

Simona Kovarikova1, Izabela Firlova2, Jana Blahova1

1
Department of Animal Protection and Welfare and Veterinary Public Health,
University of Veterinary Sciences, Brno, Czech Republic
2
Veterinary Clinic, Ostrava, Czech Republic

The concentration of creatinine in the blood can be influenced by various factors, including breed
or the amount of muscle mass. However, little is known about the impact of such factors on urinary
creatinine concentration. The aim of this study was to evaluate the urinary concentrations of
creatinine and protein, and their ratio, in Birman, Maine Coon, and domestic shorthair (DSH) cats.

In total, 76 voided urine samples of clinically healthy cats of three breeds were enrolled. There were
30 Birman, 20 Maine Coon, and 26 DSH cats. The age of the cats ranged from 3 months to 12 years.
In all samples, urine specific gravity was measured by hand refractometer and urine dipstick was
evaluated. Samples positive for blood on dipstick were not included in the study. Urine protein
concentration was measured by use of benzethonium chloride and creatinine concentration
was measured with the Jaffe method, both in an automated biochemical analyser (Konelab 20i;
Thermo Fisher Scientific). The urine protein-to-creatinine ratio (UPC) was then calculated.

There were no significant differences in urine specific gravity and urinary protein concentrations
among the breeds. Statistically significantly higher urinary creatinine concentrations were found
in Birman (median 35.9 mmol/l, P=0.0302) and Maine Coon (median 38.7 mmol/l, P=0.0475)
when compared with DSH cats (median 24.4 mmol/l). In Maine Coon cats, UPC was significantly
lower (median 0.06) in comparison to Birman (median 0.08, P=0.0292) and DSH (median 0.12,
P=0.0002).

Significant differences in urinary creatinine concentrations and UPC were found among clinically
healthy Birman, Maine Coon, and DSH cats. To assess clinical significance, a larger number of
samples, including proteinuric samples, are required.

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 ABSTRACTS
PREDICTIVE HANDLING SCORES ON SHELTER CATS – A PRELIMINARY STUDY

Sabrine Marangoni, Matheus L C Ubiali

Department of Veterinary Medicine, Federal University of Paraná, Curitiba,

Parana, Brazil

Twenty-four male cats from a local shelter were enrolled in a clinical trial. A questionnaire was
devised for measuring a predictive cat handling score (PS). Cats were assigned scores based
on history-social-taking information. A numerical score was used for qualitative assessment for
each item. The final PS score was the sum of these scores, with higher scores assuming a patient
would be more difficult to handle, as follows: very easy (0–4); easy (5–7); difficult (8–10); and very
difficult (>10).

A real-time handling score (RS) was assigned after the cat’s response to the first human–cat
interaction. PS and RS scores have the same qualitative rating. Assessment between PS and
RS was performed after comparisons of scores collected from the same individual. Accuracy
obtained in the PS was 87.5%. The following table represents the planning model of the questions
used in the development of the questionnaire.

Predictive cat handling scores can improve cat-friendly interactions as an easy-to-use tool for
challenging cats. This tool may apply to a different population from this study. Higher scores
would require more expertise from the veterinary team, enhancing appointment efficiency,
reducing fear-anxiety-stress responses and, consequently, improving feline welfare.

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 ABSTRACTS
FELINE INJECTION SITE-ASSOCIATED MAST CELL TUMOR: A CLINICAL AND
PATHOLOGICAL DESCRIPTION OF FOUR CASES

Agustín I Cartes1, Carlos M González2

1
School of Veterinary Medicine, Faculty of Life Sciences, Andrés Bello University, Viña
del Mar, Chile

Four cats were presented for a second-opinion clinical evaluation of a proliferative lesion
associated with a vaccination site. Three of the four cats had been vaccinated against rabies, while
the other one was vaccinated against feline leukemia virus following current recommendations
for vaccination in cats. Two (5-month-old and 2-year-old) females and two (4-month-old and
3-year-old) males developed proliferative, solitary, irregular, pleomorphic, or ovoid cutaneous
growth with well-defined margins, 20 to 30 days after vaccination. All cats underwent surgical
biopsy and the histopathological findings revealed that the predominant cell type was mast
cells, sometimes with mild cellular atypia, arranged as sheets of well-differentiated, slightly
pleomorphic dissociated round cells. A variable amount of granules was detected in the cytoplasm,
with occasional normal mitotic figures. Infiltration of polymorphonuclear eosinophils was present
between collagen fibers surrounding groups of neoplastic cells. Also, abundant vascularization,
intense hyperemia, and edema, in the absence of necrosis (three of four cases), were observed.
The neogrowth was non-encapsulated, poorly defined, but with free surgical margins.

Three cats were diagnosed with a well-differentiated mastocytic mast cell tumor, while one had
an atypical (histiocytic) mast cell tumor. None of the cats required chemotherapy treatment,
and three cats remained healthy during the reporting period. One of the cats developed an
alimentary lymphoma 2 months after this diagnosis; however, presently it is in remission.

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 ABSTRACTS
USE OF NOREPINEPHRINE IN CRITICALLY ILL CATS: SURVIVAL OUTCOMES

Agustín I Cartes1, Valentina N Lepe1, Claudio G Galleguillos1, Eduardo A Bascuñan1

1
School of Veterinary Medicine, Faculty of Life Sciences, Andrés Bello University,
Viña del Mar, Chile

A retrospective analysis was performed on the increased use of different doses of norepinephrine
in 51 critically ill feline patients. Cats were diagnosed with sepsis when they had two or more
criteria for systemic inflammatory response syndrome and if the presence of a septic focus was
confirmed by cytology or microbiology. All cats were diagnosed with dysoxic phenotype septic
shock using the criteria of hypotension (systolic blood pressure <100 mmHg) with refractory fluid
loads and euvolemia with persistent hyperlactatemia (>4 mmol/l).

Twenty-four (47.1%) females and 27 (52.9%) males were included in the study; the median age
was 5.1 years (0.5 ± 19) and the average weight was 3.7 kg (0.4 ± 8). Only 6 cats were positive for
retroviral diseases, 3 (5.8%) for FIV and 3 (5.8%) for FeLV, with 1 (1.9%) positive for both. Underlying
causes for sepsis included urinary tract infections (n = 7), infected wounds (n = 18), pyothorax
(n = 2), pyometra (n = 2), septic peritonitis (n = 12), bacterial cholangitis (n = 3), lumbar abscess
(n = 1) and other infections (n = 6).

Despite there being a tendency for cats treated with a low dose of norephinephrine to have a
higher survival rate, due to a lack of data, it cannot be ensured that there is a statistical difference
between the groups.

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 ABSTRACTS
IMMUNE-MEDIATED HEMOLYTIC ANEMIA IN CATS WITH
FELINE INFECTIOUS PERITONITIS

Petra Černá1, Samantha Evans2, Séverine Tasker3,4, Danièlle A Gunn-Moore5,

Nicole Jacque6, Katie Clemens7, Allison Koonce8, Michael R Lappin1

1
Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA
2
Department of Veterinary Biosciences, The Ohio State University, Columbus, OH, USA
3
Bristol Veterinary School, University of Bristol, Langford, Bristol, UK
4
Linnaeus Veterinary Limited, Solihull, West Midlands, UK
5
The Royal (Dick) School of Veterinary Studies, University of Edinburgh,
Easter Bush Campus, Midlothian, UK
6
Independent Researcher, San Jose, CA, USA
7
Woodcroft Veterinary Group, Handforth, Wilmslow, UK
8
Pleasant Valley Veterinary Clinic, Little Rock, USA

Feline infectious peritonitis (FIP) is a disease caused by feline coronaviruses. Immune-mediated

hemolytic anemia (IMHA) arises due to immune-mediated erythrocyte destruction and can be
non-associative or associative with disease processes such as FIP.

Medical records were reviewed to find cats with FIP and associative IMHA based on exclusion of
other causes of anemia and a positive saline agglutination test or Coombs test.

The inclusion criteria were met for 5 cats with non-effusive FIP and 2 cats with effusive FIP. Mean
hematocrit at presentation was 14.1% and the anemia was non-regenerative in 5 of 6 cats with low
reticulocyte counts. Two of the 7 cats had concurrent thrombocytopenia, and anemia associated
with congestive heart failure was suspected in one cat.

Blood transfusions were administered to 5 cats. All cats were treated with nucleoside analogues
and glucocorticoids. For 2 cats, glucocorticoids were added 14–38 days later after anemia
persisted with antiviral therapy alone. One of the 7 cats was euthanized due to FIP. Long-term FIP
remission occurred in 5 cats and 1 cat relapsed after 8 months. Long-term IMHA remission was
achieved for 3 cats, 1 cat relapsed with IMHA twice despite being in FIP remission, 1 cat relapsed with
IMHA when FIP relapsed, and 1 cat never achieved IMHA remission despite being in FIP remission.

Although FIP is an uncommon cause of associative IMHA, as more cats with FIP are successfully
treated with antiviral therapy, it is important to consider IMHA as a possible cause of anemia with
FIP.

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 ABSTRACTS
SIMPLIFYING SAMPLING: EVALUATION OF A FULL-BODY SAMPLING METHOD
FOR MEASUREMENT OF HAIR CORTISOL IN CATS

Ninni Rothlin-Zachrisson1, Malin Öhlund2, Helena Röcklinsberg3, Bodil S Holst1

1
Department of Clinical Sciences, Swedish University of Agricultural Sciences,
Uppsala, Sweden
2
Swedish Medical Products Agency, Uppsala, Sweden
3
Department of Animal Environment and Health, Swedish University of Agricultural
Sciences, Uppsala, Sweden

With increased use of hair cortisol concentration (HCC) for evaluation of the HPA axis and chronic
stress in cats, more simple and owner-friendly ways of hair sampling are needed.

Hair was sampled from at least one location from 175 cats by clipping the dorsal aspect of the
front leg (n=117) or the ventral aspect of the abdomen (n=29) and by combing, representing a
full-body sample (n=127). The cats differed in coat characteristics and season when sampling
was performed. Cortisol concentrations in hair were analyzed with an ELISA (Salimetrics® Salivary
Cortisol Enzyme Immunoassay Kit) and converted to pg cortisol per mg hair. Data were analyzed
graphically and with a 95% confidence interval using Spearman’s correlation and Bland-Altman
plots for correlation and agreement between sampling locations.

Median HCC was 5.6 (Q1–Q3 4–7.2) for front leg, 6.8 (Q1–Q3 4–8.8) for abdominal and 7.2 (Q1–Q3
4.8–11.7) for full-body samples (pg/mg). A strong positive correlation was seen between HCC in
hair sampled from the front leg and the abdomen (rs=0.76, n=25) and there was good agreement
between the front leg and the full-body sample (rs=0.62, n=65).

We show that hair obtained from combing, representing a full-body sample, can be used for HCC
analysis. This may increase compliance of cat owners when sampling hair for evaluating cortisol
concentrations.

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 ABSTRACTS
FREQUENCY OF MDR1 (ABCB1) VARIANT IN CATS

Ewa Pawlus1, Alexandra Kehl1, Petra Kuehnlein1, Elisabeth Mueller1

1
Laboklin GmbH & Co KG, Bad Kissingen, Germany

The MDR1 gene, also known as ABCB1, encodes for the drug transporter protein P-gp, which is an
important component of the blood–brain barrier. Abnormal P-gp protein synthesis leads to the
accumulation of certain medications in the brain, which result in signs of neurotoxicity after drug
administration.

A canine MDR1 variant has been widely described in different breeds and mixed-breed dogs.
Recent studies found an ABCB1 variant in cats with signs of neurotoxicity.

The aim of this study was to investigate the frequency of this variant, namely ABCB11930_1931delTC,
in different cat breeds. A total of 200 cats, including 174 Maine Coon cats and 26 cats of different
breeds, such as Norwegian Forest, British Shorthair, Ragdoll, Russian Blue and Siberian cats, were
screened by Sanger sequencing.

Of all tested cats, 193 (96.5%) were homozygous for the wild-type ABCB1 allele, 6 (3%) were
heterozygous, and 1 (0.5%) was homozygous for ABCB11930_1931del TC. All 7 cats carrying the
MDR1 variant were Maine Coon cats. The allele frequency in the Maine Coon population was 2.3%,
in agreement with previous studies. The affected cat developed confirmed signs of neurotoxicity
after administration of ivermectin.

Although the frequency of the ABCB1 variant in cats is relatively low and further research is
essential to confirm the allele frequency in other breeds, awareness of this disease should be
spread among veterinarians and breeders to eliminate the risk of dangerous adverse drug
reactions.

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 ABSTRACTS
COLLAGEN DEFICIENCY AND CUTANEOUS MUCINOSIS IN A DOMESTIC
SHORTHAIRED CAT: A CASE REPORT

Nilcéia de V Ramos1,5, Rodrigo V da Motta1, Daniela Murad1, Juliana Werner2, Gabriel

Viegas3, Tábata Maués4, Bárbara B do N Pereira5

1
Faculdade de Ciências Médicas de Maricá, Faculty of Veterinary Medicine,
Maricá, Brazil
2
Laboratório Werner, Curitiba, Brazil
3
Vet Image, Niterói, Brazil
4
Faculty of Veterinary Medicine, Universidade Federal Fluminense, Niterói, Brazil
5
Clinicat, Niterói, Brazil

A 5-month-old female shorthaired cat was presented with extensive oedema that began on
the nasal planum and spread to the eyelids, cranium, rear of the head, and limbs. The cat also
exhibited flaccidity and hyperextensibility of the skin, without skin fragility. The redundant dorsal
cervical skin caused it to hang, and the dorsal thoracic skin sagged towards the ground. The
skin extensibility index was 39.2%. In addition to the cutaneous changes, the sublingual mucosa
was diffusely thickened and abnormally broader. Claudication was observed, and physical
examination showed joint stiffness of the right arm and forearm. None of the cat’s siblings or
parents had exhibited these findings. No follicular parasites were found on parasitological
examination. A full blood count revealed leukocytosis (26,800/μl), neutrophilia (22,780/μl),
and basophilia (536/μl). Serum biochemistry revealed only hypoalbuminaemia (1.98 g/dl).
A FeLV antigen/FIV antibody test was negative. Radiographs revealed mineralisation in the
soft tissues adjacent to the scapulohumeral and radioulnar joints of the right thoracic limb.
During ovariosalpingohysterectomy, inspection of the visceral peritoneum revealed multifocal
areas with a linear and slightly granular appearance. Reconstructive surgery was performed
to excise redundant skin and eradicate skin rashes induced by cutaneous redundancy. About
a month postoperatively, a recurrence of skin redundancy was noted. Histopathological
examination showed diffuse oedema and inflammatory infiltrate consistent with perivascular
to diffuse dermatitis. PAS Alcian Blue staining showed the deposition of mucin in the dermis and
perifollicular area, and also between the epithelial cells of the follicles. Masson’s trichrome staining
showed irregularity of some of the collagen fibres. The findings suggested dermatopathy due
to morphological/structural or biochemical irregularities of the collagen fibres, and cutaneous
deposition of mucin. The cat died prior to any subsequent assessment, 3 months following the
initial consultation. The young age at onset of signs and the findings suggest a possible diagnosis
of collagen deficiency and cutaneous mucinosis of infancy. The mechanisms of this process still
require elucidation in domestic animals and humans.

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HAEMATOLOGICAL, BLOOD BIOCHEMISTRY, AND URINARY SYSTEM
ULTRASOUND ABNORMALITIES IN OVERWEIGHT AND OBESE CATS
Consuelo Pérez, Pedro Sáez, Marla Astudillo, Rafael Gálvez, Claudia Saavedra, Cristóbal
Alcántara, Ángelo Torres
Escuela de Medicina Veterinaria, Facultad de Medicina Veterinaria Y Recursos
Naturales, sede Talca, 3473620, Universidad Santo Tomás, Chile

Being overweight or obese generates physiological alterations that are reflected in haematological
and blood biochemistry analysis. Additionally, being overweight or obese predisposes to other
pathologies, such as urinary tract diseases. Urinary system alterations can be detected through
clinical examination, blood analysis, and ultrasound; however, few studies have attempted to
characterize the haematological, blood biochemistry, and ultrasound abnormalities of the urinary
system observed in overweight and obese cats. This study therefore focused on determining
these.

A total of sixty (20 overweight, 20 obese, and 20 healthy weight) asymptomatic cats of ≥3 years old
and at least 1 year of being overweight were examined, and a blood sample for haematological
and biochemistry analysis was collected. Fructosamine and urine glucose levels were measured
to exclude diabetes. Ultrasounography was performed to evaluate the kidneys, bladder, ureters,
and urethra.

Low MCHC, high MCV, leukocytosis with Table 1. Summary of haematological and biochemistry
eosinophilia, hypophosphataemia, abnormalities in overweight and obese cats.
hyperglycaemia, hypercholesterolaemia,
and high levels of amylase, triglycerides,
AP and albumin/globulin (A/G) index
were observed in the overweight and
obese cats (Table 1). Two cats had
high levels of fructosamine (Table 1).
Among the ultrasonographic findings
were a hyperechoic renal cortex, a loss
of the cortico-medullary relationship,
irregularities in the renal contour, increased
thickness of the bladder wall, and sediment.

Overweight and obese cats have

haematological and biochemical
alterations. Ultrasonographic abnormalities
are compatible with a loss of renal
morphology, episodes of cystitis, and the
presence of sediment. For these reasons,
carrying out a blood analysis and ultrasound
evaluation of the urinary tract in overweight
and obese cats is important to prevent,
detect, and treat associated pathologies
such as urinary system diseases in this type
of cat.

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 ABSTRACTS
OUTCOME OF 307 CATS WITH FELINE INFECTIOUS PERITONITIS TREATED WITH
LEGAL VETERINARY-COMPOUNDED PREPARATIONS OF REMDESIVIR AND/OR
GS-441524, 2020–2022
S Taylor1,2, S Coggins3, D Gunn-Moore4, E Barker5,6, K Jeevaratnam7, R Malik3, S Tasker2,6*

International Cat Care, Tisbury, UK

1

Linnaeus Veterinary Limited, Shirley, UK

2

3
University of Sydney, Australia
4
Royal (Dick) School of Veterinary Studies, University of Edinburgh, UK
5
Langford Vets, University of Bristol, UK
6
Bristol Veterinary School, University of Bristol, UK
7
University of Surrey, Guildford, UK

Feline infectious peritonitis (FIP) is a fatal disease of cats caused by feline coronavirus. Recently,
the nucleoside analogues remdesivir (Rem) and GS-441524 (GS) became legally available for
FIP treatment in Australia, the UK and other countries. The current retrospective study aimed to
describe the outcome of cats treated with legal veterinary-prescribed Rem and/or GS.

Inclusion criteria for cats comprised injectable Rem and/or oral GS treatment for ≥84 days, unless
they died or were euthanased. Data were collected on country of origin, signalment, clinical signs,
physical findings, testing, treatment and outcome.

In total, 307 cats were included (174 UK, 115 Australia, 11 Sweden, 5 South Africa and 2 Japan).
Neutered (76.9%), purebred (63.4%), male (63.2%), and <12 months of age (52.4%) cats were most
common. Most were lethargic (93.8%) and inappetent (75.5%). Pyrexia (67.3%) and abdominal
distension (64.0%) were common, as were hyperglobulinaemia (74.2%) and anaemia (56.3%).
Effusions were common (213/300, 71.0%) and usually abdominal in nature. Neurological signs
occurred in 62/306 (20.3%), diarrhoea in 46/306 (15%) and ocular signs in 40/306 (13.1%). The
table below summarises the treatment response.

Cats with an incomplete response to treatment in the first 30 days of treatment had significantly
shorter survival times than those that had a complete response (P=0.011). Adverse effects included
injection-site pain (Rem; 122/255, 47.8%), raised ALT (71/250, 28.4%), eosinophilia (38/253, 15.0%)
and lymphocytosis (26/244, 10.7%). Vaccination (23) and neutering (21 cats), during or after,
treatment, was not associated with relapse.

* Further authors: Jacqui Norris, David Hughes, Laura MacFarlane, Gerald McLauchlan, Emilie Royaux, Max Foreman, Isabel Calvo Saiz,
Laura Espada Castro, James McMurrough, Bethany Thomas, Jos Bongers, Rachel Korman, Caroline Harlos, Xavier Salord Torres, Aimee
Taylor, Laura Espada Castro, Emily Stacey

#ISFMRocksDublin 194
 ABSTRACTS
COMPARISON OF THE IN VITRO PHOSPHATE-BINDING CAPACITY
OF LANTHANUM CARBONATE WITH THREE FEED SUPPLEMENTS INTENDED
FOR THIS USE
Olaf Hanssen, Mike Wecks, Jörg Hofmann, Lydia Dietzmann
Porus GmbH, Monheim, Germany

Hyperphosphatemia is a major contributor to the progression of chronic kidney disease (CKD).

Intestinal phosphate binders are commonly used in these patients. The aim of this study was to
compare the in vitro phosphate-binding capacity of lanthanum carbonate with a combination
of calcium carbonate and chitosan, a combination of calcium carbonate and magnesium
carbonate, and aluminium hydroxide.

A phosphate-containing solution was prepared in ultrapure water. To simulate the acidic

environment in the stomach, a pH value of 2 was set with hydrochloric acid. For each test product,
one dose as recommended by the manufacturer was added to 50 ml of this solution. After 2 hours,
the phosphate content of each solution was analysed using ion chromatography (Dionex ICS-
1000). After the test at pH 2, the solution was adjusted to pH 8 to simulate the alkaline environment
in the colon and all products were tested again.

In the acidic solution, lanthanum carbonate bound phosphate at its maximum capacity (100%).
Calcium carbonate/chitosan and calcium carbonate/magnesium carbonate bound at 21.5%
and 80.7% of their capacity, respectively, while aluminium hydroxide bound at 21.1% of its capacity.
In total, 2.02 mmol of phosphate was bound by lanthanum carbonate compared with 0.14, 0.28
and 0.54 mmol by calcium carbonate/chitosan, calcium carbonate/magnesium carbonate
and aluminium hydroxide, respectively. In the alkaline solution, lanthanum carbonate, calcium
carbonate/chitosan and calcium carbonate/magnesium carbonate bound phosphate at their
maximum capacity (100%), while aluminium hydroxide reached only 53.2% of its maximum binding
capacity. In total, 2.02 mmol of phosphate was bound by lanthanum carbonate compared
with 0.67, 0.35 and 1.35 mmol by calcium carbonate/chitosan, calcium carbonate/magnesium
carbonate and aluminium, hydroxide respectively.

Lanthanum carbonate was found to be superior to calcium carbonate/chitosan, calcium

carbonate/magnesium carbonate and aluminium hydroxide in binding phosphate in the acid
environment (stomach) as well as in the alkaline environment (colon).

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348 CPD Points

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