A logical approach to the bleeding or anaemic patient

Jill E. Maddison
The Royal Veterinary College, London, UK

THE BLEEDING PATIENT

Bleeding is a potentially life-threatening clinical sign that often requires prompt assessment
and management. As with all clinical signs, a structured approach is key to ensuring that
important differentials are not overlooked. Understanding the pathophysiology of bleeding is
also important particularly in relation to interpreting relevant clinical pathology. Three major
bleeding sites are discussed in these notes but the principles of the approach apply to any
site of bleeding – most importantly – is this animal bleeding because of local disease or
systemic disease?

Define the problem

The potential for confusing bleeding as a clinical sign with another clinical sign is variable
dependent on the site of bleeding. The issue can be “is this blood”? (e.g. red urine), or “is
the cause pathological?” (e.g. melaena).

Epistaxis

Epistaxis is defined as bleeding from the nose. It is unlikely that identification of the problem
will pose any difficulties although confirming the blood is coming from within the nasal cavity
as opposed to peri-nasal skin is important (the latter almost always due to local trauma or
skin pathology).

Melaena

Melaena is presence of digested blood in the faeces and is manifested as black tarry faeces.
It can also be detected using tests for occult faecal blood. It is important to determine
whether the melaena is due only to the dog having eaten a very high meat meal (so
obtaining a dietary history is important and faeces may be black but not tarry) or has
swallowed blood – i.e. is bleeding in the mouth or nasal cavity, coughing up blood then
swallowing it or licking a bleeding wound.

Red urine

Red urine may be due to haematuria, haemoglobinuria, myoglobinuria or even ingestion of

beetroot (beeturia). Hence, for the animal presenting with what the owner describes as
’blood in the urine an important first step is to confirm that the urine discolouration is in fact
due to the presence of red blood cells.

Clinical signs may assist (see below) or a simple method is to spin some urine down and
examine the sediment and supernatant. In cases of ’pseudohaematuria‘ the supernatant will
remain discoloured. Urine dipsticks cannot differentiate between lysed blood cells, ‘pure’
haemoglobin and myoglobin.

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Define the system

Any site of bleeding such as epistaxis, melaena and haematuria may be due to local
disorders or systemic disorders – this is the key question to answer to which has a profound
impact on the diagnostic pathway and potential differentials. Systemic disorders include
bleeding disorders (coagulopathy), hypertension, polycythaemia, hyperviscosity and
systemic vasculitis.

Define the lesion

We will first consider local disorders for the specific signs and then the diagnostic approach
to bleeding disorders in general.

LOCAL DISORDERS

Epistaxis

Local disorders that can cause epistaxis include:

• Neoplasia
• Inflammatory/infectious
o Immune mediated or allergic rhinitis
o Fungal infection
o Local vasculitis
• Severe dental disease e.g. tooth root abscess
• Trauma
• Foreign bodies

Melaena

Melaena can occur due to gastrointestinal (GI) ulceration or due to bleeding disorders. In the
latter case there is no overt ulceration and use of anti-ulcer drugs in the management of
these cases is not indicated.

Melaena due to GI ulceration may occur due to primary GI disease (neoplasia, parasites
such as hookworms, foreign bodies) or secondary GI diseases that cause ulceration (e.g.
liver disease, mast cell tumours, gastrinoma, NSAID toxicity, hypoadrenocorticism). It is
therefore important that you do not immediately assume that the presence of melaena
indicates primary GI disease, even if vomiting is also present, as many of the secondary GI
causes of ulceration will also cause vomiting. Failure to recognise this may result in very
inappropriate diagnostic procedures (e.g. endoscopy) being performed.

Haematuria

Haematuria is most commonly due to local disease but like other sites of bleeding can occur
as a consequence of systemic disease.

Local disorders
The causes of haematuria due to local disease include:
• Urinary calculi
• Neoplasia
o bladder neoplasia (most commonly transitional cell carcinoma)
o neoplasia of the renal pelvis
o polyps
• Inflammatory/infectious

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 o bacterial cystitis
o prostatitis
o interstitial cystitis (cats)
• Idiopathic
o idiopathic renal haemorrhage
• Vascular anomalies

Causes of Haemorrhage

Bleeding may occur if there is:

• An abnormality of the vessel wall (trauma, vasculitis)

• Reduced platelet numbers (thrombocytopenia)
• Platelet dysfunction (lack of von Willebrand's factor - vWF, defect in activation and
aggregation)
• A defect in the extrinsic or intrinsic coagulation cascade

In addition, disorders such as hypertension and hyperviscosity will increase the tendency for
exudation to occur and will perturb platelet function.

Clinical signs

• Reduced platelet numbers or impaired platelet function usually manifests as bleeding

from mucosal surfaces e.g. petechiation.
• In contrast, clotting factor deficiencies (from any cause) usually manifest as deeper
tissue (ecchymosis) and body cavity haemorrhages.
• Petechiation can also occur with vasculitis.

Causes of bleeding disorders

REMEMBER
When considering the causes of abnormal/unexpected bleeding
THINK

LOCAL DISEASE?
neoplasia, calculi, foreign body, infection, inflammation, polyps, vasculitis
OR
SYSTEMIC DISEASE?
Coagulopathy, hypertension, dysproteinaemia, systemic vasculopathy

The most common causes of impaired coagulation in cats and dogs are:
• Immune-mediated thrombocytopenia
• von Willebrand's disease
• Drug-induced platelet dysfunction
• Rodenticide poisoning
• DIC

Other less common causes include:

• Inherited platelet dysfunction
• Inherited coagulation factor deficiencies

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 • Malabsorption of vitamin K
• Acquired disorders of platelet function

In conclusion

As with many other clinical signs, the assessment of the bleeding patient requires a
structured approach. This must be underpinned by appreciation of pathophysiology so that
the results of diagnostic tests can be appropriately assessed. The very first step when faced
with a bleeding patient is to ask – is the bleeding due to local or systemic disease? The
answer can be obvious or require investigation but keep the aim is to avoid a serious clinical
error by neglecting to ensure that coagulation is normal before proceeding with invasive
diagnostic tests such as biopsy.

THE ANAEMIC PATIENT

Define the problem

Anaemia is a relatively common disorder with a multitude of causes. Animals with anaemia
often present with pale mucous membranes - the first step is therefore to differentiate those
animals with pale mucous membranes due to poor peripheral perfusion (i.e. hypovolaemic,
cardiogenic or obstructive shock) and those who have a reduced red blood cell mass.

Is the anaemia primary or secondary?

Once it has been confirmed that true anaemia is the cause of the animal's pale mucous
membranes, it is important to assess whether the anaemia is the primary disease process or
secondary i.e. is it causing the animal's presenting clinical signs or is it secondary to an
underlying disorder.

Often the clinical significance of mild to moderate anaemia is overestimated - mild to

moderate anaemia is a common feature of many chronic disorders (more details later in this
module) and anaemia of chronic disease is the most common cause of mild anaemia.
Classification of the severity of anaemia is arbitrary but can be as follows in dogs for
example: mild anaemia (PCV 30–36%), moderate anaemia (PCV 18–29%) and severe
anaemia (PCV < 18%).

Clinical signs relate to rapidity of onset

The rapidity with which anaemia develops also will influence its clinical effect - for example a
dog with a PCV of 20% may show only mild clinical signs if the anaemia is chronic, but will
be more severely affected if the PCV has decreased to this level suddenly.

Define the system

The system involved in the problem of anaemia is the haemopoietic system. The system
may be further refined by determining how the haemopoietic system is affected i.e. by
destruction or loss of RBCs (usually, though not always, causing regenerative anaemia) or
by a failure to effectively produce RBCs (causing non-regenerative anaemia).

Non-regenerative anaemia can be refined further to consider whether the problem is a

structural problem of the bone marrow or whether the problem is functional (i.e. local versus
systemic bone marrow disease).

Is the anaemia regenerative or non-regenerative?

It is imperative to ascertain whether the anaemia is regenerative or non-regenerative.

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The work-up and aetiologies for regenerative and non-regenerative anaemia are very
different and inappropriate tests will be ordered and time wasted if the type of anaemia is not
established as soon as possible.

How long does the bone marrow take to respond?

Be aware that it takes 3-5 days for the bone marrow to respond to acute anaemia therefore
signs of complete regeneration may not be present if peracute red blood cell loss (from
haemorrhage or haemolysis) has occurred.

Regenerative anaemia

Haemorrhage or haemolysis?

Regenerative anaemia may be the result of haemorrhage or haemolysis.

HAEMORRHAGE

If the haemorrhage is acute, there may initially be no change in the PCV as both plasma and
RBCs have been lost. However, after a few hours the plasma will equilibrate and the
reduced PCV will become apparent.

Acute haemorrhage is often associated with decreased plasma protein concentrations

especially if the haemorrhage is external. If a patient has developed an acute anaemia and
the plasma protein is high normal or above normal then haemolysis is more likely than
external haemorrhage.

Chronic external haemorrhage (e.g. gastroduodenal ulceration, bleeding GIT or skin tumour)
will eventually cause iron deficiency although the anaemia often remains moderately
responsive. Anaemia due to chronic gut haemorrhage is usually associated with mild to
moderate hypoproteinaemia. Platelet count is often high normal or slightly elevated in
chronic blood loss.

Internal Haemorrhage
Internal haemorrhage into a body cavity may be difficult to detect if the volume is small.

With internal haemorrhage, the protein usually is less reduced than with external
haemorrhage, because the protein is not “lost” and plasma levels will increase more quickly
after the bleed. Plasma levels will not usually however be above normal, however, unless
the patient is also dehydrated.

HAEMOLYSIS

Haemolysis may occur extravascularly (RBCs are broken down in the reticuloendothelial
system in the spleen predominantly, but also the liver and bone marrow) or intravascularly
(RBCs are broken down within the bloodstream releasing haemoglobin) or both. Increased
serum bilirubin is observed in the majority (but not all) cases of extravascular IMHA although
overt clinical jaundice may be less common. The diagnosis of IMHA should therefore never
be excluded on the basis of absence of overt jaundice. Intravascular haemolysis can be
easily demonstrated as the plasma of a centrifuged (and appropriately collected*) sample
will be red if the intravascular haemolysis is moderate to severe. Haemoglobinuria is often
also present – this can be differentiated from haematuria by centrifuging urine and observing
the supernatant - it will be clear if haematuria is present, and red if haemoglobinuria is
present.

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*Haemolysis is commonly caused ex vivo by improper sampling methods such as strong
suction during blood collection, small needle gauge or vigorous shaking of the blood tube.

Causes of haemolysis are:

• Immune-mediated haemolytic anaemia

• Microangiopathic anaemia e.g.
o Iron deficiency
• Congenital haemolytic anaemia
• Infectious haemolytic anaemia
• Drug/Toxins

Non-regenerative anaemia

• Anaemia of chronic disease

• Chronic kidney disease
• Bone marrow disorders
• Iron deficiency
• Precursor-directed immune mediated anaemia (PIMA)

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 Anorexia and normal blood work
Jill E. Maddison
The Royal Veterinary College, London, UK

Can’t eat or won’t eat?

Loss of appetite is a frequent presenting complaint as owners will usually be aware of the
amount of food eaten by their animal and it is often the first indication to an owner that there
is something wrong with their pet. Feeding is a core part of their care for their animal and
contributes to the human-animal bond so refusal of food can be extremely worrying for an
owner.

If the owner reports an animal is not eating, the first key question is “Is it because the animal
can’t eat or won’t eat?” It is important to ensure that the animal does not have any condition
causing difficulties in prehending food, mastication difficulties, dysphagia or swallowing
defects (“can’t eat”).

Appetite is controlled by the feeding-satiety centre of the hypothalamus and many factors will
directly or indirectly influence this centre and thus cause anorexia (“won’t eat”). These
include body temperature, metabolic products, neural input from the gastrointestinal tract,
substances released by neoplasia, psychic factors.

CAN’T EAT
Dysphagia
Dysphagia is defined as difficulties in prehension, mastication and swallowing. The animal
with prehension or mastication difficulties can appear hungry and interested in food. They
are either unable to pick food up properly, show evidence of pain when trying to eat or drop
food from their mouth when chewing. Prehension and mastication difficulties are most often
associated with disorders of the mouth and pharynx.

Less commonly, dysphagia may be due to inflammation of the muscles of mastication

(myositis) or neuromuscular lesions resulting in paralysis of the muscles of the jaw or
tongue. The jaw is innervated by cranial nerve V (trigeminal), the tongue by cranial nerve XII
(hypoglossal).

Difficulties in swallowing
Difficulties in swallowing are indicated by excessive, forceful attempts to swallow or by
regurgitation of food from the mouth or nostrils.

Difficulties in swallowing can be due to:

• Local disorders in the pharynx such as inflammation, foreign bodies, or neoplasia.

• Rarely, neurological disorders involving cranial nerve IX (glossopharyngeal) or cranial
nerve X (vagus) may be responsible.
• Cricopharyngeal achlasia is a rare congenital disorder of young animals in which the
cricopharyngeal sphincter fails to relax when animal swallows. Its aetiology is
unknown but it is surgically correctable by a cricopharyngeal myotomy.

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Assessment of inflammation
Inflammation of the lips, tongue or gingiva may cause prehension, mastication or swallowing
difficulties. Inflammation can be due to local disease or systemic disease. Thus a key
question when inflammation is noted is: “Is the cause due to local disease or systemic
disease?”

Examples of systemic disorders causing oral inflammation include uraemia due to renal
failure and viral infections in cats. Local causes of inflammation include irritants (plant,
chemical), foreign bodies (always check the hard palate), dental disease (but must be
severe), lymphocytic/plasmacytic stomatitis and neoplasms - either benign or malignant.
Unfortunately, the majority of oral tumours are malignant. The most common ones are
malignant melanoma, squamous cell carcinoma and fibrosarcoma.

WON’T EAT
Anorexia/inappetance
Anorexia is defined as complete loss of appetite. Inappetance or hyporexia is defined as
reduced appetite.

Loss of appetite may occur in many disease conditions. Often anorexia or hyporexia is just
one of many clinical signs and thus does not need to be the diagnostic focus. It is when
there are apparently no other clinical signs present that it can become a diagnostic challenge
especially as our patients cannot tell us they feel nauseous or have a headache or feel
general unwell. Particularly in cats, loss of the sense of smell may cause anorexia, hence
nasal disorders may need to be investigated.

If an animal is presented because of anorexia or inappetanceand there are no other clinical

signs reported by the owner, in many cases a thorough physical examination will reveal
more specific abnormalities that can be investigated e.g. pyrexia, masses, severe
constipation, severe heart disease, anaemia. Nausea can be cause of anorexia/hyporexia
and may not be recognised. Subtle clinical signs that may be present but missed include
ptyalism, restlessness and anxiety and lip licking or smacking.

However, in some cases, an underlying cause cannot be found on physical examination

alone. In these cases, the diagnostic approach is partly dependent on the length of time the
animal has been anorectic/hyporectic and the degree of weight loss that has been sustained.

For an animal that has not eaten for 24-48 hours and is in good bodily condition with no
evidence of malaise, it may be most appropriate to adopt a "wait and see" approach. To
advise the owner that if the cause of the loss of appetite is serious, the animal is most likely
to develop other clinical signs such as vomiting or diarrhoea that may help localise the
problem. It is important in these cases to determine whether the diet has been changed
recently or whether there are environmental conditions that may be responsible e.g. very hot
weather, absent owner, loss of a companion pet, new pet or baby in the house, change of
ownership or house, administration of medications that may have anorexia or nausea as a
side effect.

If the anorexia is prolonged and/or the animal has lost weight and/or is exhibiting signs of
non-specific malaise, then further diagnostic procedures are indicated. As a plethora of
disease processes can cause anorexia e.g. liver disease, renal failure, neoplasia, infection,
electrolyte imbalance, endocrine abnormalities, anaemia, toxins, it can appear a daunting
task to determine the cause.

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Diagnostic procedures should be directed at trying to determine the system involved and
should if possible start the more simple inexpensive tests, then proceed to more expensive
procedures if indicated.

Appropriate tests to evaluate inflammation/infection, serum protein, liver and renal function,
electrolyte abnormalities (sodium and potassium) and calcium levels should be used. In
cats, viral infections, such as FeLV, FIV and more commonly, FIP should be considered.

All the bloods are normal – help!

In the very uncommon cases where the anorexia/hyporexia is persistent and causing weight
loss, you are sure there is nothing stopping the patient from eating, there are no other
clinical signs (perhaps other than lethargy) and routine haematology and biochemistry are
normal then a few specific causes should be considered.

In appropriate areas, lead toxicity should be considered as cats with lead toxicity may
present with anorexia as their only clinical sign.

Cats with pancreatitis may have anorexia/hyporexia as their only clinical sign. Assessment
for pancreatitis is problematical as the SNAP fPLI test done in-house has too many false
positives and negatives to be of much help. The SPEC fPLI test done in the laboratory may
be more useful – there is a much smaller chance of false negatives (around 10%) but
unfortunately a rather large number of false positives (around 40%). So the test can be used
to support a suspected diagnosis, but not rule it out. Abdominal ultrasound in skilled hands is
a very useful tool for the diagnosis of pancreatitis but again cannot rule it out –
approximately 20% of cats with pancreatitis may have normal ultrasound findings.

Cats with significant liver pathology can have normal liver enzymes and further assessment
of the liver through measurement of bile acids and abdominal ultrasound may be
appropriate.

In an older animal, a more rigorous search for occult neoplasia (e.g. abdominal and thoracic
radiographs, abdominal ultrasound, CT scan) may be indicated.

Ultimately it may be necessary to investigate the brain (imaging, CSF tap) as

anorexia/hyporexia may be one of the early and only clinical signs of CNS neoplasia or
inflammation.

Conclusion

Provided a through history is taken and a thorough physical examination performed, the
number of cases where anorexia/hyporexia is the only clinical sign are few. They are even
less common if, in addition, standard haematology and biochemistry results are normal.

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 Clinical pathology relating to the liver and pancreas
Jill E. Maddison
The Royal Veterinary College, UK

Liver disease can be difficult to diagnose and frustrating to treat. Clinical signs are usually
non-specific. Clinical pathology often indicates liver pathology exists but not what type – e.g.
neoplastic, inflammatory, infectious, toxic, fibrotic.It can be difficult to differentiate the
location of the pathology – i.e. is it hepatic parenchymal disease or post-hepatic disease. Yet
it is important to do so as there are different aetiologies and treatment for hepatic
parenchymal disease compared with post-hepatic disorders which can need surgical
management.
ASSESSING THE LIVER
Alanine Aminotransferase (ALT, Formerly SGPT)
This is a liver-specific enzyme in the dog and cat. Highest cellular concentrations occur in
the cytosol therefore the enzyme is released following acute and diffuse hepatocellular
necrosis. However, the insult does not need to be severe –being central to many body
functions, the liver is easily affected by disorders of other organs and has been described as
a sympathy organ. Thus, in general, serum levels are not regarded as definitively indicating
hepatocellular pathology unless they are at least two to three times above the upper
reference limit. Even at this level, non-hepatic disorders can cause moderate increases and
the level probably needs to be approaching 5-10 times above the upper reference limit to
conclude that the increase is due to primary hepatocellular disease.

As a rule of thumb, levels of ALT that are elevated more than 5 times should be investigated.
Levels less than this may not need to be if the animal appears otherwise well. However, if
the level is increasing or is persistently increased over a prolonged period of time (even if
only 2-3 fold) further investigation may be warranted. See comment re cats below.

Non-hepatic disorders that will cause ALT to be moderately (3-5 times reference range)
increased include:
• Treatment with anticonvulsants or glucocorticoids
• Biliary stasis for any reason
• Hypoxia
• GI disease - especially if inflammatory or infectious
• Haemolysis (in the cat but not the dog)

The serum half-life of ALT is approximately 30 hours in dogs. Levels peak two to three days
after hepatic insult and return to normal in one to three weeks if hepatic insult resolves.
Persistent increase indicates continuing hepatocellular insult.

The half-life of ALT is shorter in cats than dogs (3-5 hours). This tends to mean that levels
that occur in hepatic disorders in cats may be lower than those achieved by a similar degree
of pathology in dogs. As such I suspect clinically significant hepatocellular disease even with
mild ALT increases (2-3 times reference range) in cats.

AST
AST levels are also increased in dogs and cats with hepatic necrosis. The enzyme is not
specific for liver disease as it may increase with muscle necrosis. However, it has been
suggested (but not to my knowledge conclusively demonstrated in dogs or cats) that

1
because AST represents liberation of mitochondrial isoenzymes, if AST is higher than ALT
(and the CPK is normal, ruling out muscle disease) this may reflect the presence of severe
hepatocellular injury associated with organ devitalisation. AST does not appear to be
increased by phenobarbitone treatment (in contrast to ALT).

Alkaline Phosphatase (ALP)

ALP is bound to membranes of bile canaliculi and bile ducts. Values are increased by any
condition causing cholestasis, either intra- or extra-hepatic. Cholestasis results in increased
synthesis and regurgitation of the enzyme from the biliary system into the serum.

Other isoenzymes of ALP are also found in bone, intestine, kidney tubules and the placenta.
However, the half-life of the intestinal, renal and placental isoenzymes are so short (two to
six minutes) that serum elevations of ALP would rarely occur from these organs.

Usually an elevation in ALP is due to hepatic or bone isoenzymes. However, exogenous

and endogenous glucocorticoids can induce a specific isoenzyme and thus result in elevated
serum levels in the dog (but not in the cat). The value in measuring the ALP isoenzyme in
the diagnosis of hyperadrenocorticism is questionable (see reference in Module 4).

ALP levels will be increased in young growing animals (bone isoenzyme) and in destructive
bone disease. ALP is also increased in certain carcinomas and mammary gland tumours,
and with anticonvulsant therapy in dogs but not cats. ALP is commonly increased in cats
with hyperthyroidism.

The half-life of ALP varies between dogs and cats. In the dog, the half-life is 72 hours, in the
cat only six hours. As well, feline bile canaliculi do not excrete as much ALP in cholestasis
as dogs. Therefore, any elevation in cats is very significant and cholestasis and jaundice will
occur often without an elevation in ALP. In contrast to the dog, systemic conditions, other
than hyperthyroidism and bone growth, do not cause induction of ALP synthesis without
concurrent cholestatic disease.

The pretenders
Non-hepatic disorders that can result in a substantial increase in ALP include:
• Glucocorticoid administration or hyperadrenocorticism – in dogs but not cats
• Some tumours e.g. mammary tumours
• Pancreatitis
• Old dogs (nodular hyperplasia, asymptomatic vacuolar hepatopathy)

Asymptomatic vacuolar hepatopathy

These patients have a high ALP but no clinical signs. They are often detected because of a
routine pre-anaesthetic screen. If a biopsy is done the histopathological changes seen are
similar to glucocorticoid hepatopathy. It appears to be breed associated in Scottish terriers.
Some patients can have hypertension and proteinuria - monitor and treat as necessary

Gamma Glutamyl Transpeptidase (GGT)

GGT levels are increased in most conditions that cause elevation in ALP, i.e. cholestasis,
glucocorticoid therapy, hyperadrenocorticism. However, unlike ALP, GGT is not elevated
with increased osteoblastic activity (e.g. growing dogs) and may not be elevated in dogs on
anticonvulsant medication. It is not increased by corticosteroids or anticonvulsants in cats.

ALP is slightly more sensitive than GGT for detection of cholestatic disease in dogs but GGT
is significantly more sensitive than ALP in cats – therefore it is a useful enzyme to include in

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the biochemical profile of the cat (but not much use in the dog). GGT increases may be
greater than ALP in feline extrahepatic bile duct obstructions, cholangio-hepatitis and
cirrhosis. Disproportionately low GGT with high ALP can be a useful pointer to hepatic
lipidosis. In both dogs and cats, acute hepatic necrosis is unlikely to cause an increase in
GGT whereas ALP may be elevated.

Liver Enzymes - General comments

In acute hepatic injury, enzyme (ALT, AST) release is proportional to the amount of affected
tissue. However, note that liver enzymes are not liver function tests and in sub-acute and
chronic hepatic disorders there is no correlation between the magnitude of the enzyme
increase and severity or reversibility of the condition though they might be used to monitor
the progress of an individual patient. Several serious and potentially irreversible liver
diseases such as cirrhosis and portocaval shunts may be associated with only mild-
moderate enzyme changes.

Bile Acids
‘Primary’ bile acids (cholic, chenodeoxycholic) are synthesised only in the liver and are
secreted into bile after being conjugated with various amino acids (primarily taurine). Once
released into the small intestine when the gall bladder contracts (where they facilitate fat
absorption) ’primary‘ bile acids are efficiently reabsorbed into the portal vein and returned to
the liver for reuptake and resecretion into bile. A small percentage of primary bile acids
escape reabsorption and are converted by intestinal bacteria to secondary bile acids
(deoxycholic, lithocholic), some of which are also reabsorbed into the portal circulation.

Absorption of bile acids by the intestine is extremely efficient, but hepatic extraction from the
portal vein is not, which results in a small proportion of the bile acids being present in the
blood of normal cats and dogs.

Abnormally high levels occur if there is disturbance of hepatic excretion into bile or disruption
at any point along the path of portal venous return to the liver and hepatocellular uptake.

Bile acid levels will increase in blood when there is:

• Decreased clearance of bile acids from portal blood

o Diffuse hepatocellular disease
o Portacaval shunting
Or
• Decreased bile acid excretion in bile
o Obstructive cholestasis – intrahepatic
o Post-hepatic cholestasis
Bile acids can be increased well above normal by GI bacterial metabolism so levels should
be interpreted with care in patients with diarrhoea where the bacterial flora balance may be
disturbed.

Serum bile acids are a sensitive test for the presence of liver, biliary or hepatic vasculature
pathology in the cat and dog. They should be considered when other routine clinical
pathology results do not permit an unequivocal diagnosis of liver disease to be made. It is
not necessary to do the test if the patient is jaundiced and not anaemic or if liver enzyme
changes permit an unequivocal diagnosis of liver disease to be made.

Bile acids cannot be used to estimate the severity or extent of liver injury nor determine the
type or distribution of pathology. Quantification of bile acids only indicates the presence of

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‘significant’ liver injury (if there are few hepatocytes available to recycle bile acids, increased
amounts spill into blood), altered bile flow or altered hepatic vasculature usually due to portal
vein abnormalities or development of collateral shunts as a result of portal hypertension.
Relative changes to abnormal values cannot be used to quantify the improvement or
worsening of a condition. A value is either abnormal or normal and has no linear relationship
to the extent of circulatory or tissue compromise due to the many variables involved in
increasing or decreasing their levels in the blood.

They are useful as a screening test for hepatic encephalopathy (except in Maltese dogs -
see reference). Their major advantage in this context is the lack of stringent requirements for
sample collection and processing in contrast to blood ammonia determination. The
sensitivity of a post-prandial bile acid test for detecting portacaval shunting is close to 100%,
though there are the occasional patients with shunts who will have normal bile acids.

Bile acids can be normal in patients with hepatic disease depending on the reference range
used. Reviewing the results of various studies it would appear that roughly 20-25% of cases
of confirmed hepatobiliary disease can have fasting bile acids less than 20µM and
postprandial bile acids less than 25µM.

In a recent study at the RVC of 217 dogs (99 with normal livers, 218 with confirmed hepatic
disease – parenchymal, vascular or biliary), 40 dogs with confirmed level disease had pre-
prandial BAs < 25 µg/L. 16 dogs had post-prandial levels less than 25 µg/L. The bile acid
level both pre- and post-prandially was less than 25 µg/L in 9 dogs. These were the “false
negatives”.

With reference to the “false positives”, 9 dogs without liver disease had a pre-prandial bile
acid level > 25 µg/L and 19 has a post-prandial level >25 µg/L. It was only when results were
greater than 34 µmol/L that the false positive rate was less than 10% and the cut off for
100% specificity (i.e. no false positives) was 58 µmol/L.There were smaller number of cats in
the study (18 with normal livers, 21 with hepatic disease).
• 11 cats with confirmed liver disease (52%) had pre-prandial BAs < 25 µg/L
• 7 cats with confirmed liver disease (33%) had post-prandial BAs < 25 µg/L
• 5 (24%) cats with confirmed liver disease had both pre and post BAs < 25 µg/L

The take home message is to interpret bile acid results with great care as they neither rule
hepatic pathology in or out. It is usually recommended that values greater than 40µM
warrant biopsy if possible to determine the aetiology (unless due to portocaval shunting).

Serum bile acid concentrations are usually not affected by corticosteroid administration but
occasionally they can be markedly altered due to alteration of hepatic architecture as a result
of hepatic glycogen accumulation. Serum bile acids are therefore useful but not infallible for
differentiating elevated ALP values due to steroids (endogenous or exogenous) or
hepatobiliary disease. About 20% of patients with hyperadrenocorticism will have increased
bile acids.

Portal vein hypoplasia

Dogs with portal vein hypoplasia (PVH) have no clinical signs but their bile acids are
increased. Breeds affected similar to portacaval shunts (PSS)e.g. Yorkshire terriers,
Maltese, Cairn terriers. You may become aware of them because of a slight increase in ALT
on a routine blood profile e.g. pre-anaesthetic which is further investigated by doing bile
acids. Dogs with PVH can have a low Protein C wheras dogs with PSS do not. They require
no treatment and 95% live normal lives although very occasionally a dog may develop
ascites.

4
CLINICAL PATHOLOGY RELATED TO THE DIAGNOSIS OF PANCREATITIS
Clinical Signs
Pancreatitis occurs most frequently in obese, middle-aged female dogs. However, any age
and type of dog can be affected. Pancreatitis is usually due to acute inflammation in dogs.
In cats it is often due to low grade oedematous inflammation; however, acute pancreatitis
may also occur and has been reported in cats ranging in age from four weeks to 18 years.
Siamese cats have been over-represented in some case series.

Dogs usually present with a sudden onset of acute vomition, often initially food, although
they then become anorectic. Thus, they present similarly to animals with primary GI disease
where the lesion is high in the GI tract. They may have recently ingested a large amount of
fat but not always. Increased thirst with vomition after drinking is often noted and the
presence of diarrhoea is variable. The most common clinical findings in cats are lethargy,
anorexia and weight loss, in contrast to dogs where acute vomiting related to eating or
drinking would be the most common presenting sign, vomiting is reported in less than 50%
of cats. In contrast to dogs, abdominal pain is uncommon in cats and dietary factors do not
seem to be a trigger. Other clinical signs that may be observed in cats with pancreatitis are
icterus, diarrhoea and polyuria/polydipsia.

Pain may be localised to the anterior abdomen. Hyperthermia is common initially, but may
give way to hypothermia if shock ensues. The animal may have abdominal distension, which
is more often due to rigidity of abdominal muscles and less often due to fluid accumulation.

Clinical pathology

The problem for assessing diagnostic tests for pancreatitis is that there is no gold standard
that is easily accessible – some studies are based on post mortem findings, others on a
combination of clinical signs and other diagnostic tests, others on pancreatic biopsy.

Lipaemic Serum
Lipaemic serum in a fasting animal with acute abdominal signs is very suggestive of
pancreatitis.

Amylase & Lipase

Increased serum levels of amylase or lipase in dogs but not cats are also suggestive of
pancreatitis but there are some grey areas, e.g. normal levels in animals with pancreatitis or
moderately increased levels in other diseases such as renal, enteric (small intestinal mucosa
secretes amylase) and liver disease, or after administration of morphine.

Interpret with care!

In general, levels in these latter diseases are not as high as in pancreatitis. Amylase levels
of two to three times normal could be due to anything - consider pancreatitis if the clinical
signs are appropriate and the serum is lipaemic but don't overinterpret. Amylase and/or
lipase levels that are elevated more than three-fold, if associated with appropriate clinical
signs, are virtually diagnostic for pancreatitis.

Amylase or lipase
Lipase levels are thought to be more reliable than amylase levels but there is still some
controversy and they can be normal even when amylase levels are elevated in dogs with
pancreatitis (although this is uncommon) and vice versa. They may be more useful in cats
but very little work has been done in this area.

5
Cats
In general, amylase and lipase levels are of little value in the diagnosis of pancreatitis in
cats.

Pancreatic lipase immunoreactivity

PLI is believed to be a highly sensitive marker for canine and feline pancreatitis. The original
assays were termed cPLi and fPLi but were modified to permit commercial production and
wider availability. These have been known as Spec cPL and Spec fPL since 2007 and 2008
respectively. The reference interval for the canine assay, Spec cPL, is < 200µg/L and values
> 400 µg/L are considered consistent with pancreatitis. Values between 200 and 400 µg/L
are considered in the grey zone. In cats the reference interval is < 3.5 µg/L, values > 5.3
µg/L are considered consistent with pancreatitis and values between 3.5 and 5.3 µg/L are in
the grey zone.

The SNAP® cPL™ Test and The SNAP® fPL™ Test are rapid assays that can be
performed in house and interpreted as normal or abnormal. The upper limit of the reference
interval for each species is used as the cut off – values above 200 µg/L in the dog and 3.5
µg/L in the cat.

The data on the sensitivity and specificity of these tests can be challenging to interpret.

Sensitivity indicates the number of false negatives i.e. the number of animals with the
disease who do not test positive. If a test has 100% sensitivity it will detect all of the true
positives in the group (i.e. there will be no false negatives). However, there may be many
false positives - animals who do not have the disease. If it has a sensitivity of 50%, it will
incorrectly identify 50% of the patients with the disease as negatives i.e. patients who had
the disease but did not test positive for it (false negatives).

Specificity is a measure the number of false positives. In a test with 100% specificity all of
the positives will be true positives in a population (i.e. there will be no false positives).
However, there may be false negatives - i.e. animals with the disease who do not test
positive. A test with 50% specificity will incorrectly identify 50% of the group as positive when
they are not (false positives). The problem for assessing diagnostic tests for pancreatitis is
that there is no gold standard that is easily accessible – some studies are based on post
mortem findings, others on a combination of clinical signs and other diagnostic tests, others
on pancreatic biopsy.

In dogs, the sensitivity of Spec cPL has been reported to be up to 78% though can be as low
as 21% for mild, though potentially clinically insignificant, pancreatitis. The sensitivity is lower
for chronic pancreatitis than acute pancreatitis – in one study only 26%. Thus at least 20% of
patients with pancreatitis may have a Spec cPL in the reference range i.e. 20% of animals
with pancreatitis will have a false negative result.

The specificity has been reported to be between 81% and 96% depending on the study. In
healthy dogs, there is considerable variability in serum Spec cPL values between dogs and
within the same dog. As a result values in an individual healthy dog can be in the diagnostic
range for pancreatitis. A broad interpretation would be that up to 20% of dogs that test
positive (values > 400 µg/L) may not have pancreatitis.

The sensitivity of the SNAP® cPL™ Test is higher than Spec cPL – around 94%. Thus if the
test is negative this rules out pancreatitis in the vast majority of cases. However, there is the
occasional case that has a confirmed diagnosis of pancreatitis but had a negative SNAP®
cPL result. Based on the above sensitivity data, around 6% of cases can be false negatives.

6
The specificity of the test is lower – between 71% and 78%. As the cutoff is at the top end of
the reference range (and therefore at the bottom end of the grey zone) it is not surprising
that almost 30% of animals may have a false positive result. A positive result may need to be
confirmed by Spec cPL unless all other clinical and clinical pathology data is consistent with
pancreatitis. And also noting that the SpecPL test can have up to a 20% false positive rate.

A study published in 2014 has highlighted the care that must be taken when interpreting PLI
results in dogs with GI signs. Howarth et al (2014) – see additional reading - compared two
groups of dogs with acute abdominal signs – one group had confirmed pancreatitis, the other
group had other causes of their clinical signs. In that study (full results in the reference list)
the SNAP cPLhas a sensitivity 82% i.e. there were 18% false negatives and a specificity of
59% i.e. there were 41% false positives. The Spec cPL had a sensitivity of 70% i.e. there
were 30% false negatives and a specificity of 77% i.e. there were 23% false positives.

The validation of the diagnostic performance of Spec fPL and SNAP® fPL™ in the diagnosis
of feline pancreatitis is even more challenging. As well as an imperfect gold standard for the
disease (pancreatic biopsy), other markers of pancreatitis that are of some use in dogs such
as amylase and lipase are of no value in cats. In addition the clinical signs of pancreatitis in
cats are often ill defined and the cats present with non-specific signs of malaise –
inappetance and weight loss. Vomiting and abdominal pain are often absent. Studies of the
variability of feline Spec fPL in healthy cats and the performance characteristics of SNAP®
fPL™ have not been published.

The sensitivity of fPLI is reported to be around 67% with higher sensitivity (79-100%) for
moderate to severe pancreatitis and lower for chronic pancreatitis without an acute
component. Specificity has been reported to range from 67% to 100%. In a recent study at
the RVC of 275 cats (Lee, Kathrani & Maddison, 2020), Spec fPLI had a false positive
rateof 10%andafalsenegativerateof24%.Soapositiveresultindicatedadiagnosisofpancreatitis
was very likely (though may not be the only pathology) but the diagnosis could not be ruled
out if the fPLI was in the referencerange.

Critical review of the sensitivity and specificity of PLI emphasises that although the tests are
the most useful serum markers for pancreatitis in both species, pancreatitis remains a
diagnosis that often requires the consideration of a range of clinical and diagnostic
information.

Liver Enzymes
Alkaline phosphatase levels are almost always increased in dogs, but not necessarily in
cats, due to stasis of the common bile duct. Increased alanine aminotransferase (ALT)
levels are also common (but only moderate increases occur) due to central lobular necrosis
of the liver.

Serum Bilirubin
Bilirubin is also often increased due to bile duct compression (swollen pancreas) or
secondary cholestasis. For some reason, a dog may become icteric in the recovery phase
of pancreatitis. Although this may indicate bile duct obstruction due to development of a
pancreatic abscess or pseudo-cyst, in my experience, the icterus usually resolves over
several weeks without specific treatment.

7
 Diarrhoea
Jill E. Maddison
The Royal Veterinary College, London, UK

Introduction and classification

Diarrhoea is a common clinical sign in animals presented to veterinarians in small animal

practice. Similar to vomiting, the clinical consequences can range from insignificant to
life threatening, although the latter is less common than the former. Many acute cases
require little diagnostic intervention and resolve with or without symptomatic treatment.
Chronic diarrhoea, however, can be a diagnostic challenge and the source of much
frustration for the client and veterinarian.It is defined as diarrhoea that lasts for more
than three weeks, or intermittent diarrhoea over a period of one month or more. Animals
can have chronic diarrhoea for months to years. Often, the animal may not be
particularly unwell, the diarrhoea may be chronic but intermittent and may respond
partially but not entirely to different therapeutic interventions.

Diagnostic investigation of chronic diarrhoea can involve various procedures that range
from the inexpensive to the expensive and the non-invasive to the invasive. Unlike many
clinical problems, therapeutic trials often play an important role in helping the clinician
reach a probable diagnosis. However, trials need to be conducted logically and the
outcomes reviewed critically.

The temptation to give multiple treatments aimed at different aetiologies in the hope that
something will work is understandable. However, even if there is a positive response to
multi-modal therapy, if the diarrhoea recurs once treatment stops (as it often does), the
clinician is no wiser about the underlying cause and how to manage the patient long
term. Patience is needed by all parties, and excellent communication between the
veterinarian and the client is imperative. As such, the clinician needs to have a rational
diagnostic and therapeutic approach to chronic diarrhoea in the dog and cat and this will
be dependent on the classification of the type of diarrhoea that is present and its
potential causes.

Classification of diarrhoea

Although symptomatic therapy (or no therapy!) is appropriate for the majority of animals
with acute diarrhoea, chronic diarrhoea does not usually respond to non-specific
symptomatic treatment and will often present the veterinarian with a diagnostic challenge
where the more routine laboratory aids are not useful.

The diagnostic work-up, differential diagnoses and therapy for small and large bowel
diarrhoea may differ, although there are some causes common to both. Therefore, it is of
utmost importance that before embarking on invasive diagnostic procedures or extensive
therapy, an assessment is made as to whether the diarrhoea is:
• Acute or chronic
• Relatively mild or more severe with the presence of secondary systemic
effects
• Small bowel or large bowel origin, or mixed
• Due to primary or secondary GI disease.

1
Failure to elicit sufficient information from the client about the characteristics of the
diarrhoea, so as to allow appropriate classification as small bowel, large bowel or mixed,
may result in inappropriate diagnostic procedures or therapeutic trials with increased
expense to the client and frustration of the veterinarian, client and patient.

Define the problem

Diarrhoea is defined as an alteration in the normal pattern of defaecation, resulting in the
passage of soft, unformed stools with increased faecal water content and/or increased
frequency of defecation. It is important to consider the animal’s previous pattern of
defecation, as the frequency of defaecation and the nature of faeces vary between
individuals.

There are a few uncommon situations where it may not be obvious to the owner that
their animal has diarrhoea. Occasionally, they may mistake anal or vaginal discharges
for diarrhoea, or see vomitus on the floor and think it is diarrhoea. The patient with
constipation may pass small amounts of liquid faeces, which the owner thinks is
diarrhoea. Conversely, the patient who is straining to defaecate and attempting to
defaecate frequently because of large bowel disease may be interpreted by the owner
as being constipated. Therefore, it is important that the clinician is cognisant of these
issues and aims to define the problem as a first priority in the consultation.

Define the location

In cases of diarrhoea, the problem-based system we discussed in Chapter 2 is applied,

but in a slightly different order. Identification of the location occurs first, which then
assists in defining the system. This is because, almost always, large bowel diarrhoea
reflects primary GI disease, whereas small bowel diarrhoea can occur with either
primary or secondary GI disease. Thus, defining the location first aids in defining the
system.

A thorough history is essential to differentiate small from large bowel disease. It is

important to carefully question the owner as to the character of the faeces and to elicit
information regarding consistency, colour, frequency and presence of blood or mucus.
Related abnormalities should also be assessed, such as whether there has been
significant weight loss, loss of appetite or vomiting. The characteristics of small and large
bowel diarrhoea are detailed in Table 4.1.

Because large bowel diarrhoea has fewer and more specific characteristics than small
bowel diarrhoea, it is often easiest to note if there is any fresh blood, mucus and small
amounts of faeces passed frequently. If the diarrhoea has none of these characteristics,
then the patient has small bowel diarrhoea. Note also that diarrhoea may have features
of both small and large bowel, which indicates either primary small bowel with secondary
effects on the lower bowel or diffuse disease involving both the small and large intestine.

2
Table 1 Characteristics of small and large bowel diarrhoea.

Small bowel diarrhoea Large bowel diarrhoea

Consistency, • Faecal volume and/or water content is • Small amounts of faecal

volume and increased. Diarrhoea may be projectile material are passed frequently.
pattern and does not usually involve significant Tenesmus and urgency are
tenesmus or urgency. often present, particularly if the
lower colon or the rectum is
involved.
Blood • If blood is present, it is usually digested • If blood is present, it will be
(melaena) or in acute diarrhoea, undigested (haematochezia).
reddish-brown.
Appearance • Colour may be grey if large amounts of • Mucus is often present either
undigested fat are present. A yellow- on the surface (indicating the
green coloration is common and due to lesion is in the lower colon or
malabsorbed bile salts. rectum) or throughout the
faeces (indicating a lesion in
the higher colon).
Weight loss • Chronic small bowel diarrhoea is often • Usually there is no weight loss
(but not always) associated with weight caused by large bowel
loss. diarrhoea per se but there may
be as a result of the pathology
such as severe inflammation or
neoplasia.
Vomiting • Vomiting may also be present (but • Vomiting can occur
need not be). Relationship to eating occasionally but is infrequent
can be variable depending on the and is unrelated to eating.
location of the lesion.
Borborygmus • Gas commonly occurs with small bowel • Uncommon
and flatulence diarrhoea, as malabsorbed
carbohydrates are fermented by colonic
bacteria producing CO 2 and H 2 S.
Appetite • Appetite may be variable depending on • Usually, the appetite is
the underlying aetiology. unaffected.
Water balance • If the diarrhoea is severe, the animal • Large bowel diarrhoea per se
may be dehydrated. If the diarrhoea is does not usually adversely
very watery, the patient may have an affect water balance.
increased water intake.
Physical • Physical examination may reveal • Physical examination is often
examination increased gas or thickened loops of unremarkable, but it is
bowel but is often unrewarding. Always imperative to do a rectal
do a rectal examination to check for examination if possible to
melaena or large bowel signs such as check for strictures, masses or
mucus and fresh blood about which the thickened mucosa.
owner may not be aware of.

3
Define and refine the system
Diarrhoea can be due to primary disorders of the small bowel and/or large bowel or due
to other systemic, secondary GI disorders such as hepatic disease, exocrine pancreatic
insufficiency, pancreatitis, hyperthyroidism or hypoadrenocorticism. As discussed earlier,
large bowel diarrhoea is almost always due to primary GI disease, whereas small bowel
diarrhoea may occur with either primary or secondary GI disease.

Severe systemic diseases such as sepsis and uraemia can cause large bowel diarrhoea,
but this will be a very minor clinical sign in relation to the patient’s other systemic clinical
signs. Thus, secondary disordersare not usuallylikelydifferentials when considering the
work-up of a patient whose primary problem is large bowel diarrhoea.

Diarrhoea due to primary GI disease is more common than diarrhoea due to secondary
GI disease. In animals with secondary GI disease, with the exception ofexocrine
pancreatic insufficiency and some dogs with hypoadrenocorticism, diarrhoea is not
usually the primary presenting complaint.

Define the lesion

The following tables summarise the causes of acute and chronic small and large bowel
diarrhoea (Tables 2–4).

4
Table 2: Causes of Acute Small Bowel Diarrhoea in Dogs and Cats

Cause Examples Comments

• Overeating (especially • Including change to food that causes
Diet related
puppies) allergy/hypersensitivity.
• Dietary change
• Spoiled food
• Dietary indiscretion
• Parasites
Parasites/protozoa
o most commonly ascarids
(Toxocara and
Toxascaris spp., also
hookworms Ancylostoma
and Uncinaria spp.)
• Protozoa
o Giardia spp.
o Coccidia, for example
Cystisospora spp.
(formerly called Isospora) • Zinc sulphate flotation is a sensitive
o Cryptosporidiumspp test for Giardia cysts, provided three
faecal samples collected over 5 days
are examined (∼95% sensitive).
• The ELISA test can identify Giardia
antigen in faeces. The test is reported
to be about 90% sensitive and is
probably more sensitive than
performing zinc sulphate flotation
examination on a single faecal
sample.
• Faecal IFA and PCR are also
available.
• A negative result does not necessarily
exclude Giardia infection, and some
clinicians will treat with metronidazole
or fenbendazole regardless and
proceed with further investigations
only if the diarrhoea persists.
• Viral enteritis
Infection
o Parvo/panleukopaenia
(bacterial/viral)
o corona
o distemper
o FIV/FeLV
o other viruses (e.g.
adenovirus, norovirus,
torovirus)
• Bacterial enteritis • Microbial culture of faeces is often
o Campylobacter spp. unrewarding due to the abundant
o Salmonella spp. normal flora in the gut and the
o E. coli predominance of anaerobes.
o Clostridium spp. • E. coli is frequently, and Salmonella is
sometimes, isolated from faeces of
normal animals, and therefore their
presence does not necessarily imply
that they are the cause of the

5
 diarrhoea. Campylobacter spp. and
Clostridium spp. are also found in
animals with and without diarrhoea,
which makes interpretation of results
quite difficult.
• Clostridium perfringens and
Clostridium difficile have equal
prevalence in dogs with and without
diarrhoea. However, there is a
correlation between the presence of
diarrhoea and the detection of toxins
that are produced by these bacteria
although enterotoxin can also be
found in healthy dogs.
• Identification of an overgrowth of
Clostridia or Clostridial spores on
faecal smears means nothing
diagnostically and will occur in many
situations when gut flora is disturbed
by a variety of GI disorders.

• Toxins • Plants that may cause diarrhoea if

Toxins
o lead ingested (as well as other clinical
o organophosphates signs) include:
o plants o Lily of the Valley
o Daffodil bulbs
*ingestion of many toxins
o Aloe vera
can cause acute
o Asparagus fern
diarrhoea sometimes in
o Chrysanthemums
combination with other
o Cyclamens.
systemic signs
• Acute haemorrhagic • Previously called haemorrhagic
Unknown
diarrhoea syndrome (AHDS) gastroenteritis (HGE). This is a
syndrome causing acute onset of
vomiting and bloody diarrhoea.
• Characteristically the patient will have
significant haemoconcentration
(increased PCV) with a normal or low
plasma protein due to protein loss into
the bowel. It is typically described in
small breed dogs, but any size/breed
can be affected.
• It is now believed that the cause may
be novel necrotising toxin produced
by Type A Clostridia perfringens.
• However, antimicrobial therapy does
not improve outcome unless the
patient is septic.
• Acute pancreatitis • See previous comments regarding
Secondary GI
disease • Severe systemic disease presence of other clinical signs.

Table 2: Causes of Chronic Small Bowel Diarrhoea in Dogs and Cats

6
Cause Examples Comments
Diet related • Diet-responsive disease or • Food intolerance is a non-
food- responsive enteropathy immunological reaction to a
(FRE) component of food, for
example gluten,
preservative, bony material
and other irritants.
• Food
allergy/hypersensitivity is an
immunological reaction to a
component of food, for
example beef, chicken and
dairy.
• Diagnosis of dietary allergy
or intolerance is usually a
process of trial and error by
using elimination diets, as
there is no sensitive or
specific diagnostic test.
• Current evidence would
suggest that blood tests for
anti-food antibodies are not
specific and not clinically
useful for dogs and cats
with FRE.
Parasites/protozoa • Intestinal parasites (as See comment in Table 2.
previously mentioned)
• Protozoa (as previously
mentioned)
‘Infection’/bacterial/viral • Campylobacter/Salmonella Note comments in Table 2 in
• Feline infectious peritonitis relation to bacterial causes of
diarrhoea.

Antibiotic responsive • Antibiotic responsive • Antibiotic responsive

diarrhoea (ARD) diarrhoea: small intestinal
• Secondary SIBO diarrhoea that is responsive
to antibacterials but no
underlying cause can be
identified.
• SIBO: small intestinal
bacterial overgrowth
secondary to an underlying
problem such as exocrine
pancreatic insufficiency,
inflammatory bowel
disease, partial obstruction
or motility disorders.
Infiltrative • Immunosuppressive- • Diarrhoea is the most
responsive or non-responsive common clinical signs of
chronic enteropathy (IRE and IBD in dogs.
NRE) - also termed • Vomiting is the more
common clinical sign in
inflammatory bowel disease
cats.
[IBD] e.g: • Intestinal biopsy is primarily

7
 o Lymphocytic-plasmacytic required to characterise
enteritis infiltrative inflammatory gut
o Eosinophilic enteritis disease (IBD vs. neoplasia)
and/or protein-losing
• Diffuse or focal lymphoma
enteropathy.
• Adenocarcinoma/adenoma
• Mast cell tumour (feline)
• Smooth muscle/stromal cell
tumours (canine)

Miscellaneous • Lymphangiectasia • Lymphangiectasia is usually

• Inherited selective cobalamin secondary to IBD but
deficiency primary forms exist.
• Chronic intussusception
• Chronic partial obstruction
Secondary GI (not an • Hypoadrenocorticism - dogs
exhaustive list) • Hyperthyroidism - cats
• Exocrine pancreatic
insufficiency
• Chronic pancreatitis
• Liver disease (hepatocellular
failure, cholestasis, portal
hypertension)
• Severe systemic disease

8
Table 4 Causes of acute and chronic large bowel diarrhoea in dogs and cats.
Parasites / protozoa • Giardia spp. (more commonly small-bowel can affect
both)
• Tritrichomonas foetus (cats).
• Entamoeba spp.
• Trichuris vulpis(whipworm)
• Ancylostoma caninum (hookworm)

Infection (bacterial/viral) • Campylobacter spp. (interpret positive results with

caution).
• Clostridiumperfringens; Clostridium difficile *
• Salmonella spp.*
• Yersinia enterocolitica *
• FIP
• Granulomatous colitis (Boxers, French Bulldogs) –
caused by invasive and adherent E. coli

* These bacteria are rarely identified as causal agents in

canine chronic diarrhoea; they may be more commonly
identified in faecal samples from raw fed pets but raw food is
not currently proven to cause diarrhoea more often than
commercial pet food.

Diet related • Food responsive enteropathy (FRE)

• Passing foreign material.
• Fibre deficient diet.

Inflammatory • Immunosuppressive-responsive or non-responsive

enteropathy = Inflammatory bowel disease (IBD). E.g.
• Lymphocytic-plasmacytic enteritis (colitis).
• Eosinophilic enteritis (colitis).

Neoplasia • Diffuse or focal lymphoma.

• Adenocarcinoma/adenoma.
• Mast cell tumour (feline).
• Smooth muscle/stromal cell tumours (canine).

Miscellaneous • Stress induced colitis can occur relatively commonly in

hospitalisedor newly kenneled dogs. This may be due to
an overgrowth of Clostridium perfringens.
• Structural disease such as caecocolic intussusception
(rare)

9
Diagnostic approach to the patient with diarrhoea

Small bowel diarrhoea

Acute vs. chronic

It is important to ascertain the duration the diarrhoea has been present. Acute diarrhoea
that is not severe, fulminating and potentially life threatening does not usually require
extensive diagnostic investigation and will usually respond to non-specific therapy.
Fulminating acute diarrhoea e.g. viral and acute haemorrhagic diarrhoea syndrome
(AHDS) may not require extensive diagnostic testing but will require intense supportive
therapy and should not be treated on an outpatient basis if at all possible. In contrast,
chronic diarrhoea persisting for weeks to months indicates that a structured approach to
therapeutic trial and investigation is required.

When to investigate?
If diarrhoea persists despite symptomatic treatment or is chronic, severe and associated
with significant weight loss and/or evidence of hypoproteinaemia, dehydration or
systemic illness, then a more detailed investigation is indicated. Only a small proportion
of diarrhoea cases requires investigation as chronic disorders. An animal presenting with
intermittent but repetitive episodes of diarrhoea over many months should also be
considered for investigation unless there is a proven cause (e.g. regular garbage bin
raiding).

The following is a general outline that can be used to approach stable cases of diarrhoea
in adult dogs and cats in general practice. More severely affected animals and very
young animals will require investigation and/or more intensive supportive treatment
earlier in the course of their disease. Every case should be considered individually and
client factors such as budget must be taken into account.

1. Take a detailed history to assess for trigger factors (bin raiding, extra table scraps
from the roast dinner, inappropriate diet or snacks, hunting etc). Perform a thorough
physical examination to look for relevant abnormalities (e.g. palpable bowel lesion,
dehydration, weight loss).

2. Ensure anthelmintic history is up to date and if in doubt treat with an appropriate

anthelmintic (usually more appropriate in young animals). For example,
fenbendazole.

3. Recommend low fat, highly digestible food until diarrhoea resolves. If animal is not
eating, monitor the situation in case intervention is needed (e.g. recheck in
appropriate time period between 24-72 hours).

4. Antibiotic treatment is rarely indicated in acute diarrhoea unless the animal is

systemically unwell and even then it may not be warranted.

5. Consider faecal culture:

• If the animal is systemically unwell
• When diarrhoea is acute and haemorrhagic
• If the diarrhoea is very severe
• In multiple animals in a crowded environment such as a kennel environment

10
 • If the owner or the pet is immunocompromised or if the owner is also affected
with diarrhoea

Overall, most dogs and cats with chronic diarrhoea do not require faecal culture; it
rarely adds to the clinical picture, and it increases the overall cost of investigation.

Treat with antibiotics if bacterial cause is strongly suspected but culture is not
possible.Select antibiotics following appropriate rational antibiotic therapy guidelines.

6. The majority of acute diarrhoea cases will resolve or improve within 24-48 hours.
However if the problem becomes chronic…..

7. Consider the merits of faecal parasitology and Giardia testing depending on age of
animal and previous treatments/response to fenbendazole treatment. Note that
some dogs with Giardia infection will respond to fenbendazole but relapse
afterwards.

8. Recommend a diet trial (commercial or homemade, novel protein source or

hydrolysed).
• Use the animal’s diet history to choose a ‘novel’ protein source diet or choose a
hydrolysed diet if many different foods have been given.
• The diet must be fed for 2-3 weeks initially by which time some response is
expected and up to 12 weeks if successful before other foods are introduced.
• If the diarrhoea does not resolve (and assuming the patient is otherwise well),
try another diet and even a 3rd diet.
• No other foods (including table scraps, food consumed illicitly e.g. by fed by
toddlers, dental chews, supplements or drinks other than water should be given.
Diet trials are important as food-responsive chronic enteropathy is common and
the next diagnostic step is often invasive and costly (gut biopsy).
• If the diarrhoea is large bowel in origin in a dog, diets can be similar to those
mentioned above or a fibre-enriched diet can be trialled – commercial high fibre
diets or psyllium/bran added to a balanced diet can be used.
• Care must be used if fibre is given to underweight animals as overall calorie
intake tends to become reduced especially if appetite is low.
• Diet trial alone is rarely appropriate in significantly underweight, anorexic,
hypoproteinaemic or systemically unwell animals.
9. Before any invasive, costly or extensive diagnostic plans ensure that secondary GI
disease is not present e.g. exocrine pancreatic insufficiency (EPI), hyperthyroidism
in cats, hepatic disease, hypoadrenocorticism in dogs, by performing routine
haematology and biochemistry +/- total T4 (cats), basal cortisol/ACTH stimulation
test (dogs), TLI. Secondary disease is more likely if diarrhoea is small bowel or
mixed in origin.
• Even if the electrolytes are normal, if a dog is systemically unwell and does not
have a stress leukogram consider doing a basal cortisol/ACTH stimulation test
to rule out hypoadrenocorticism before any invasive tests e.g. biopsy.
• Measurement of serum cobalamin is routinely done at this point to assess
whether supplementation is needed. Low serum cobalamin is seen with distal
SI disease but normal levels don’t rule it out.

11
10. Test for Tritrichomonas with PCR if it is a cat with large bowel signs (may do this
earlier in the process if it is a pure bred cat or from a multi-cat household or shelter).

11. Perform an abdominal ultrasound to assess for structural bowel lesions that may
occur with chronic diarrhoea (e.g. hyperechoic mucosal speckles/striations;
intestinal wall thickening, intestinal masses, lymph node enlargement in neoplasia)
and for other disorders which may cause diarrhoea e.g. abdominal neoplasia,
intussusception. Ultrasound is indicated sooner if there is a palpable abnormality in
the abdomen or if diarrhoea is severe and accompanied by weight loss or severe
vomiting.

12. Assuming that secondary GI disease has been ruled out, if small bowel diarrhoea
persists after points 1-10 for more than a month or so and, depending on the
severity, species and breed (German Shepherd/young large breed dog), the
animal’s clinical condition and owner concerns, consider treating for antibiotic-
responsive diarrhoea with metronidazole (10 mg/kg PO BID) or tylosin (5-10 mg/kg
PO SID).
• Four to six weeks of therapy is usually the recommended treatment. The most
appropriate drug has not been determined by controlled clinical trials.
• Relapse following the treatment course is common.
• The role of pre/probiotics in cases of idiopathic ARD has yet to be determined.
• Relapses may be reduced or less severe in patients fed a high fibre diet

13. If all the above fails or if the patient is hypoproteinaemicor significantly underweight
or if neoplasia is suspected on physical examination or imaging, biopsy is indicated.
• Endoscopic biopsy is preferred if appropriate expertise and facilities are
available.
o Whilst there are some limitations with this technique, surgical biopsy may
be overly invasive for many cats and dogs with chronic diarrhoea.
• Exploratory laparotomy may be required:
o If endoscopic equipment and expertise are not available
o Diagnostics have indicated that the disease is a focal lesion that may be
unreachable with an endoscope e.g. a jejunal mass
• If possible, consult a medicine specialist prior to biopsy if you are unsure.

14. If biopsy is not an option for cost reasons or lack of access to appropriate
facilities/expertise, following careful client discussion of the risks of misdiagnosis
and inappropriate treatment …..
• Treat with prednisolone 2-3mg/kg once daily and observe response.
• Large dogs should have no more than 40mg/m2 once daily.
• If good response is seen taper the prednisolone dose by 20-25% every 4
weeks.
• Consider a second immunosuppressive drug (e.g. azathioprine, ciclosporin,
chlorambucil, mycophenolate orleflunamide) if steroid side-effects are moderate
to severe to allow more rapid tapering of prednisolone.

Summary

Acute and chronic diarrhoea are common clinical signs in small animal practice. Cats
and dogs with mild chronic diarrhoea can usually undergo dietary or anthelmintic trials

12
before costly investigation. Further investigation may be appropriate due to the severity
of diarrhoea, concurrent clinical signs such as weight loss or due to a lack of response to
therapeutic trials.

Clinical pathology is frequently normal in dogs and cats with diarrhoea but it is an
important step during investigation to rule out non-gastrointestinal disorders.

Intestinal biopsy is usually the final step during investigation of diarrhoea and is not
necessary in many cases. Inflammatory change on intestinal biopsy is non-specific and
may be seen in FRE, ARD and IRE. Treatment trials are still required to differentiate
between these causes.

13
 GI drugs – useful or useless?
Jill E. Maddison
The Royal Veterinary College, UK

SYMPTOMATIC TREATMENT OF THE VOMITING PATIENT

If possible, identify and remove the cause of vomition.Regardless of whether further

investigation is planned, it is usually prudent to withhold food for u to 24 hours (less in young
animals) to rest the GI tract from physical trauma and to eliminate stimulation of secretions
that could further damage an already abnormal mucosa. Water may be given in small
frequent amounts or iceblocks, but withhold if this stimulates vomiting.

Intravenous fluid therapy

Intravenous fluid therapy should be commenced if the animal is dehydrated. Subcutaneous
fluids are only appropriate if dehydration is slight as they are slowly absorbed (particularly in
dehydrated, hypotensive patients). Only isotonic fluids can be given by this route.

• Correct dehydration and replace continuing losses.

• Correct electrolyte imbalances - vomiting patients lose chloride and potassium
particularly, and sodium if severe.
• Acid/base: alkalosis occurs if vomiting is severe and high duodenal or pyloric
lesions are present. Acidosis occurs if there is chronic reflux of duodenal
contents into the stomach or if vomiting is accompanied by severe diarrhoea
(NB: acidosis occurs much more commonly than alkalosis). It is rare that
specific management of acid base status is required.

Antiemetics?
Consider use of antiemetics if vomiting is protracted or as specific therapy for drug-induced,
radiation or motion sickness.

Oral protectants?
Oral protectants such as kaolin and pectin are generally not useful as they do not protect or
soothe injured gastric mucosa and may stimulate further vomiting.

Antacids?
Antacids e.g. cimetidine, sucralfate - are useful in management of severe gastric ulceration
and may have protective value against development of oesophagitis secondary to prolonged
and severe vomiting. However, whether or not they are necessary in the vast majority of
vomiting patients is highly debatable and in many cases just adds to treatment costs.

Antibiotics?
Antibiotics are rarely indicated for the patient that is vomiting due to primary GI disease,
although they are frequently administered. The only specific indication for antibiotics for
vomiting due to primary GI disease is to treat Helicobacter infection and it should be noted
that many confirmed infections with Helicobacter are clinically irrelevant.

Bland diet
If no vomiting has occurred after withholding food, gradually introduce water (small amounts)
then small meals, bland diet (cottage cheese, rice, chicken without the skin).

1
ANTIEMETIC DRUGS

Antiemetic therapy should only be considered as symptomatic therapy.

The clinician's attention should be primarily directed at determining and resolving the
underlying disease process. Antiemetic drugs may be used as specific therapy for vomiting
induced by drugs, radiation therapy, motion sickness and psychosomatic disturbances.

Inappropriate use of antiemetics

Use of antiemetics in the following situations is inappropriate:
• Gastrointestinal infections - antiemetics may prolong gastrointestinal infections,
particularly bacterial infections.
• Gastrointestinal obstruction - some antiemetics increase gastric motility which could
result in perforation.
• Gastrointestinal toxicity - antiemetics may prevent the patient from eliminating the
toxin.
• Systemic hypotension - the phenothiazines and other α 2 -adrenergic antagonists can
worsen hypotension.
• Epilepsy - phenothiazines tend to lower the seizure threshold.

It is important to recognise that an antiemetic may not be very effective against nausea. In
human medicine, all anti-emetic drugs have label claims that they reduce nausea since it is
accepted that, in most cases, nausea is a prerequisite of emesis. Although there are some
stimuli that induce emesis with little nausea, the two are generally associated. However, it is
purely assumption that if a drug prevents emesis, it will also prevent nausea.

It is recognised that nausea is more difficult to prevent and treat than emesis. Emesis is an
all-or-nothing event and an antiemetic drug is effective if it inhibits emetic stimuli to such a
degree that the threshold for the emetic reflex is not reached. However, this could still leave
the patient feeling somewhat nauseous, since nausea is a graded phenomenon i.e. one can
feel mildly, moderately or severely nauseous. This graded phenomenon can also be implied
from observations in veterinary patients of the frequency and severity of nausea behaviours.

Maropitant (Cerenia)

Clinical applications
Maropitant is the first drug of its class registered (in some markets) for veterinary use. It is
indicated for the prevention and treatment of general emesis in the dog, and the prevention
of motion sickness in the dog. It may not be as a particularly effective anti-nausea drug.

Metoclopramide

Clinical applications
Metoclopramide is indicated for control of vomiting associated with:

• Various emesis-inducing disorders that involve central or peripheral activation of

vomiting.
• Gastroesophageal reflux.
• Decreased gastric emptying associated with:
- Inflammatory gastrointestinal disorders.
- Gastric ulcers.
- Gastric neoplasia.
- Autonomic neuropathy (diabetes mellitus).
- Pyloric stenosis.
- postoperative gastric volvulus patient.
2
 - Hypokalaemia.
- Abnormal gastric motility.

Although metoclopramide is sometimes recommended for endoscopic procedures to facilitate

passage of the endoscope through pylorus this effect was not confirmed in a well-controlled
study of the effect of pharmacologic agents on the ease of endoscopic intubation in dogs.

A search of the published literature provides no evidence for the anti-nausea effects of
metoclopramide in the dog. In the study of low dose cisplatin-induced nausea and vomiting in
dogs by Kenwood et al (2017), metoclopramide did not reduce nausea.

Antihistamines

Examples
Diphenhydramine (Benadryl), promethazine (Phenergan), dimenhydrinate (Dramamine).

Mechanism of action
Act directly on neural pathways arising in the vestibular nucleus. Therefore can be effective
in control of motion sickness and vomiting associated with middle ear infections but have
little effect on emesis produced by other stimuli. They have no effect on stimuli from viscera
as they don't act directly on the vomiting centre. They do have some effect on the CRTZ but
effectiveness against vomiting caused by metabolic toxins and drugs is inconsistent.
Antiemetic effect appears to be independent of the antihistaminic or sedative potencies.

Side effects
Drowsiness and xerostomia (dry mouth).

Phenothiazines

Examples
Prochlorperazine (Stemetil, Compazine).

Mechanism of action
Block CRTZ at low doses (antidopaminergic) and vomiting centre at higher doses
(anticholinergic). Also block peripheral dopamine receptors in stomach. However, cannot
block visceral afferent (vagal) impulses associated with severe visceral pain and
contractions.

Side effects
May cause hypotension due to α-adrenergic receptor blocking action  arteriolar
vasodilation. Therefore, should not be included at high doses in the therapeutic regime until
dehydration is corrected by intravenous fluid therapy.

5-HT 3 antagonists

Examples
Dolasetron(Anzemet), ondansetron (Zofran), granisetron (Kytril).

Clinical indications
The 5-HT3 receptor antagonists are extremely potent antiemetics used in the management of
cancer therapy-induced emesis in humans. Their effectiveness as antiemetics is orders of
magnitude better than metoclopramide (e.g. 100 times better in the ferret).

The anti-nausea effect of ondansetron is well documented in human patients but less so in
veterinary species. Ondansetron has been shown to significantly reduce nausea induced by

3
anaesthesia, cyclophosphamide and cisplatin in humans. In the Kenward et al (2017) study
ondansetron was far more effective at suppressing nausea behaviour or its biomarker
(vasopressin) than metoclopramide or maropitant.

Mechanism of action
Although initially thought to have a central action on the CRTZ, recent work suggests that
their main mode of action is through antagonism of peripheral 5-HT3 serotonergic receptors
in the gut.

Side effects
Experimental studies suggest that the 5-HT 3 antagonists are very safe with animals showing
minimal toxicity at doses up to 30 times greater than those needed to abolish vomiting. In
humans, constipation, headaches, occasional alterations in liver enzymes and rarely
hypersensitivity reactions have been reported.

Anticholinergics

Examples
Atropine, hyoscine (scopolamine), propanthaline, isopropamide.

Anticholinergics have been used frequently in the past as antiemetics but usually
inappropriately. These drugs are usually not effective unless vomition is due to smooth
muscle spasm (an extremely uncommon occurrence). They do not stop vomiting caused by
stimulation of peripheral receptors by other means such as inflammation. If they can cross
the BBB (e.g. hyoscine) they are effective for motion sickness due to antagonism of M 1
receptors in vestibular apparatus.

Anticholinergics have been used in the management of pancreatitis on the basis that they
may reduce pancreatic secretion. However, no appreciable benefit has been demonstrated
experimentally or clinically from this treatment.

BEWARE!Anticholinergic drugs reduce gastrointestinal motility, which can act as a stimulus

for further vomiting. Overuse can result in gastric atony and intestinal ileus, which may
predispose to absorption of endotoxins through damaged mucosa. Don't use in dogs with
parvovirus infection as the potential for endotoxaemia is increased.

GASTRIC ULCERATION

The protective barrier that prevents gastric mucosa from being damaged by gastric acid
includes:

Gastric protective barrier

• Mucus, with bicarbonate incorporated into the mucosal gel layer - this buffers
influxing luminal protons and establishes a pH gradient across the mucosal layer from
a pH of 2-3 at the luminal surface to a pH of 7 near the epithelium.

• High epithelial turnover - there is continual rapid cell turnover (2-4 days). Cell
restitution (migration of surviving cells from the edge of the defect) is the most rapid
means of repair. Minor damage to the epithelial surface can be repaired within 15-30
minutes.

• Tight junctions and lipoprotein layer of epithelial cells.

4
 • Surface-active phospholipids contributing to mucosal hydrophobicity, which
excludes or retards the absorption of potentially damaging water-soluble luminal
contents by mucosa.

• Rich vascular supply - the high rate of mucosal blood flow supplies oxygen and
nutrients to the epithelium and also allows for rapid removal of substances that have
penetrated the epithelial barrier. Maintenance of mucosal blood flow is essential for
the maintenance of mucosal defence and the extent of damage to this component is
central to whether on-going mucosal damage or restoration will ensue following an
insult.

• Prostaglandins - PGE series and PGI 2 protective:

- Inhibit gastric acid secretion.
- Maintain mucosal blood flow.
- Involved in secretion and composition of healthy mucus.
- May be intercellular messengers for stimulus of mucosal cell turnover and
migration.

Causes of GI ulcers

GIT ulceration may occur for variety of reasons but in most cases the primary pathogenic
mechanism is disruption of mucosal defence rather than increased acid secretion:
• Drugs (aspirin, PBZ, corticosteroids).
• Uraemia (toxins, increased gastrin).
• Liver disease (cause not known).
• Stress.
• Increased production of HCl (mast cell tumour at any site, gastrin-producing tumour of
the pancreas = Zollinger-Ellison syndrome).
• Hypotension e.g. during surgery.
• Hypoadrenocorticism.
• Increased incidence associated with spinal cord disease.

Consequences of damage to the mucosal barrier

Damage to the gastric mucosal barrier allows back-diffusion of gastric acid into the
submucosa which  mast cell degranulation  histamine release  stimulation of acid
production by gastric parietal cells  enhanced inflammation and oedema in submucosa.

The aim of antiulcer therapy is to reduce the amount of gastric acid produced or to
neutralise its effect and hence stop the vicious cycle of gut damage.

ANTIULCER DRUGS

Antiulcer drugs are useful in the specific management of GIT ulceration and reflux
oesophagitis. They are not usually used or needed for treatment of simple acute gastritis.

The most comprehensive review of gastroprotectants is the ACVIM Consensus statement

(2018).

Histamine receptor antagonists

Examples
Cimetidine (Zitac), ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid).

Clinical indications
5
The H 2 antagonists have efficacy in treating gastric ulceration caused by a variety of agents
including NSAIDs and uraemia. However, they do not appear to be effective in preventing
NSAID-induced ulcers.

Although there are difference in potency (i.e. the relationship between amount of drug and
effect) between cimetidine, ranitidine and famotidine, they are equally effective at promoting
ulcer healing if given at the correct dose and dose frequency and drug choice should be
based on considerations of cost, client convenience and concurrent drug therapy.

Cimetidine must be given at least every 6 hours as it only suppresses acid production for 3-5
hours. Ranitidine can be dosed every 8-12 hours and famotidineevery 12-24 hours.

Sucralfate

Clinical indications
Sucralfate (Carafate) is indicated for the symptomatic treatment of gastric ulceration from a
variety of causes. In humans sucralfate is as effective as antacids or H 2 receptor antagonists
in healing ulcers. It does not appear to be successful, however, in preventing corticosteroid-
induced ulceration in dogs subjected to spinal surgery. Its prophylactic efficacy in preventing
NSAID-induced ulcers has also not been proved in the dog. Sucralfate has also been used
for treatment of oral and oesophageal ulcers.

Misoprostol

Clinical indications
Misoprostol (Cytotec) is a synthetic PGE 1 (prostaglandin). In human medicine, there is
conflicting data about whether misoprostol is as effective or more so than H 2 antagonists in
healing ulcers. It is, however, most useful for prevention of NSAID-induced ulceration and its
efficacy in this regard has been demonstrated in dogs. This is in contrast to the lack of
prophylactic efficacy of other anti-ulcer drugs such as cimetidine.

Other less common uses include intravaginal administration in conjunction with PGF 2α for
pregnancy termination (mid to late gestation). It has also been reported to have some
efficacy in the treatment of atopic dermatitis in dogs.

Omeprazole

Clinical indications
Omeprazole (Prilosec, Losec) has slightly greater efficacy in healing ulcers in humans than
H 2 antagonists but is more expensive. Its use in veterinary medicine was initially primarily for
refractory ulcers or ulcers associated with gastrinomas or mastocytosis although it is being
used more commonly as a “routine” anti-ulcer drug – often with little justification. It is used
peri-operatively for brachycephalic dogs at risk of gastric reflux. Excellent long term clinical
outcomes have been reported in humans and dogs with non-resectablegastrinomas treated
with omeprazole.

Omeprazole has been reported to be useful in the management of severe erosive

oesophagitis, gastritis or gastric ulcer disease in dogs that are refractory to therapy with H 2
receptor antagonists and sucralfate. It has been used successfully to treat severe erosive
oesophagitis in one cat but had no effect in two other similarly affected cats.

Omeprazole was not reported to significantly reduce mechanically-induced gastric ulceration

and/or prevent aspirin-induced gastritis in dogs although there was a non-statistically
significant trend that suggested that omeprazole was more effective than cimetidine in this
regard.

6
Non-systemic antacids

Examples
Non-systemic antacids included a variety of oral preparations containing aluminium
hydroxide, calcium carbonate and magnesium compounds.

Clinical indications
Non-systemic antacids are probably most frequently used in management of uraemia as
aluminium hydroxide binds phosphate thus reduces hyperphosphataemia as well as having
an antacid effect.

Although they are inexpensive, non-systemic antacids must be administered orally (which
may be problematical in a vomiting patient) and frequently, which results in poor owner
compliance. Dosages are empirical as no specific dosages have been defined for animals.

Effective doses are estimated to be 0.5 - 1.0 mL/kg. To be effective, antacids must be
administered at least every four hours. Daily treatment for four to six weeks is required.

DIARRHOEA

For most cases of acute diarrhoea, the mainstay of therapy is to replace fluid losses, modify
the diet and to treat the specific cause (infectious, immune-mediated etc.) where possible.
Symptomatic treatment of diarrhoea does not often require the use of drugs but they may be
considered when symptomatic relief of discomfort will be beneficial to the patient, provided
that their use does not increase the risk of exacerbating the diarrhoea or causing systemic
effects.

Motility modifying drugs

Intestinal transit time is predominantly determined by the balance between peristalsis, which
moves ingesta in an aboral direction, and segmental contractions which narrow the bowel
lumen and increase the resistance to flow. Peristalsis is influenced by the cholinergic system
and gut hormones such as motilin. Segmental contractions are cholinergic dependent.
Although it is theoretically possible to reduce diarrhoea by either decreasing peristalsis or
increasing segmental contractions, reducing peristalsis is of little clinical benefit and is
generally contraindicated. This is because, in most cases of diarrhoea, the gut is hypomotile
not hypermotile and peristalsis and segmental contractions are already reduced.

Gastrointestinal motility may be modified by two groups of agents - narcotic analgesics,

which increase segmental contractions, and anticholinergic drugs, which decrease both
segmental contractions and peristalsis.

Opioid analgesics

Example

Diphenoxylate (Lomotil), loperamide (Imodium), paregoric.

Clinical indications

7
These drugs are effective for the symptomatic treatment of diarrhoea as they increase
segmental contractions, thus delaying gut transit time. They will effectively relieve abdominal
pain and tenesmus and reduce the frequency of defecation.

Are they often needed?

They are rarely required, however, in management of diarrhoea in small animals. Acute
diarrhoea is usually self-limiting with appropriate symptomatic treatment and chronic
diarrhoea does not usually respond to symptomatic therapy, and requires a definitive
diagnosis to be established to allow specific therapy to be instituted. They are occasionally
useful in chronic colitis that cannot be controlled by other means.

Any risks?

The use of motility modifiers is not without risk as the diarrhoea may be beneficial in
removing toxins and inhibition of movement may be counterproductive. Reduced motility may
allow enterotoxin-producing organisms to remain in the small intestine, resulting in increased
fluid loss.

In addition, in cases of diarrhoea caused by invasive bacteria, the diarrhoea itself is a

protective mechanism, probably by hastening the elimination of the organism. Slowing the
transit time may prolong the time the bacteria is resident in the bowel resulting in a greater
opportunity for proliferation of the organism, invasion of the mucosa and absorption of toxic
products.

Loperamide, however, appears to be anti-secretory and therefore may have value in the
treatment of animals with secretory diarrhoea due to E. coli.

Mechanism of action

Opioids increase the amplitude of rhythmic contraction and decrease propulsive contractions.

They directly affect intestinal smooth muscle producing both tonic and phasic contractions of
the circular muscle. They also act centrally and on synapses to augment segmentation.

Opioids either have no effect on longitudinal muscle or they relax it. The net effect of these
actions is to inhibit the flow of intestinal contents, delay gastric emptying and increase the
tone of the ileocolic valve and anal sphincter.

Some opioids such as loperamide and to a lesser extent diphenoxylate, also increase fluid
and water absorption, possibly by a calcium blocking effect or by inhibition of calmodulin, the
intrinsic calcium binding protein. Loperamide and diphenoxylate also inhibit the activity of
secretagogues such as E. coli enterotoxin, VIP, bile acids and PGE2.

Lomotil contains atropine as well as diphenoxylate. This is to discourage abuse of the drug
by people and at therapeutic doses the atropine has no clinical effect.

Side effects

Signs of systemic opioid intoxication may occur with use of the opioid antidiarrhoeal agents,
particularly in cats. Neurological disturbances such as ataxia, hyperexcitability, circling, head
pressing, barking and prostration may occur with overdosage.

8
In dogs there has been a suggestion that Collies may be more sensitive to the toxic effects of
loperamide. Treatment of side effects or overdosage involves use of the opioid antagonist
naloxone and recovery is usually uneventful.

Drug interactions

Other CNS depressants such as anaesthetic agents, antihistamines, phenothiazines,

barbiturates and tranquillisers may cause increased CNS or respiratory depression when
used with opiate antidiarrhoeal agents.

Opiate antidiarrhoeal agents are contraindicated in patients receiving monoamine oxidase

inhibitors e.g. L-deprenyl (selegeline) for at least 14 days.

Anticholinergic drugs

Anticholinergics have little use in the management of diarrhoea in small animals although
they are frequently prescribed, usually in combination products. As discussed previously,
most diarrhoeal disorders in small animals are associated with a hypomotile rather than a
hypermotile gut and the risk with anticholinergics is that they will produce adynamic ileus
especially if electrolyte imbalances such as hypokalaemia are also present.

Anticholinergics reduce but do not abolish peristalsis, but significantly decrease segmental
contractions. As long as some peristaltic activity is present, no matter how weak, it can
propel liquid intestinal contents along the flaccid intestine and diarrhoea will occur.

Although anticholinergics reduce gastric secretions, including protein exudation induced by

histamine, they have little effect on intestinal secretions. They may be justified in the short
term symptomatic relief of pain and tenesmus associated with large bowel inflammatory
disease. They also may be indicated in stress-induced colitis where cholinergic mechanisms
might be involved.

Absorbents and protectants

Kaolin and Pectin

Kaolin and pectin are in many preparations that are widely used for the management of
diarrhoea in small and large animals. They are purported to soothe irritated gastrointestinal
mucosa and bind toxins and pathogenic bacteria. However, their clinical efficacy is unproven.

There is no evidence that kaolin and pectin reduce gastrointestinal fluid or electrolyte loss
and kaolin may in fact increase faecal sodium loss.

Many preparations contain combinations of kaolin and pectin, and/or antibiotics and/or
anticholinergics. As discussed previously the value of the latter two types of compounds in
the treatment of diarrhoea is limited in small animals and may be detrimental.

Activated Charcoal

Activated charcoal has been used for many years in the treatment of toxicosis. It is thought to
absorb toxic substances and bind bacterial toxins although there are no controlled studies
that evaluate its efficacy.

Bismuth Salicylate

Bismuth salicylate is reported to be an effective agent for the treatment and prevention of
enterotoxigenic diarrhoea. Nausea, abdominal pain and diarrhoea are reduced in humans
with infective diarrhoea treated with bismuth salicylate. Bismuth salicylate has modest
9
antibacterial effects against enteropathogens such as E. coli,Salmonella and Campylobacter
jejuni.

The salicylate moiety is believed to decrease intestinal secretion by inhibiting prostaglandin

production and has an inhibitory effect on generation of cAMP by the enterotoxin.

Preparations that contain bismuth salicylate (Pepto-Bismol,Peptosyl) can be clinically useful

in the management of acute diarrhoea. However, usually such conditions resolve with
appropriate non-pharmacological symptomatic therapy.

Overdosage can result in salicylate toxicity especially in cats. A safe dose in dogs and cats is
0.25 mL/kg q4-6h. Dosages greater than 0.7 mL/kg could result in toxicity.

Fluid therapy

Fluid therapy is required if the animal is dehydrated. Intravenous administration is necessary

if the dehydration is severe and/or associated with vomiting. The loss of bicarbonate ions
may result in acidosis, however this does not require specific therapy. Potassium loss is
important and in severe diarrhoea the animal will have a total body potassium deficiency. It
is therefore important to supplement fluids with potassium and to monitor plasma
concentrations.

Oral fluid therapy

In pure secretory diarrhoea (more common in calves and pigs with E. coli infection than small
animals), glucose and amino acid absorption are intact and thus fluids containing these
substances can be given orally and will facilitate absorption of water and sodium. Oral
rehydration therapy is effective in calves and piglets. Small animals with severe acute
diarrhoea often will not voluntarily drink or are vomiting as well, therefore oral fluids are of
little value.

Antimicrobial therapy

Antimicrobial therapy is not indicated for routine nonspecific acute or chronic diarrhoea in
small animals, where primary bacterial causes are uncommon and indiscriminate use may
alter normal flora sufficiently to allow pathogens to proliferate.

Parenteral antibiotics may be indicated in small animal patients with haemorrhagic diarrhoea
where there is loss of the intestinal mucosal barrier and therefore the potential for bacterial
invasion and septicaemia (although this is difficult to reproduce experimentally). This is
particularly so if leucopenia is also present as in parvovirus infection or where the presence
of leucocytosis and pyrexia may suggests systemic bacterial invasion. There is no indication
for use of antibiotics in haemorrhagic diarrhoea if there is no evidence of systemic signs
supporting bacteraemia.

Bacteria play a pathogenic role in parvo virus (germ free dogs infected with parvovirus have
very mild clinical signs) so it is appropriate to use antibiotics in these cases – parenteral
amoxicillin-clavulanate is probably the best and safest choice although some recommend
gentamicin (ensure the patient is appropriately hydrated before commencing therapy) and
penicillin. (I personally think this combination is a bit risky in a critically ill patient).

Infectious diarrhoea

Antibiotics are frequently used in the treatment of diarrhoea and their use is logical in cases
of enteropathogenic E. coli infections. However, in some experimental studies, while
antibiotic treatment was superior to placebo, it had similar efficacy to oral rehydration therapy
with glucose-glycine electrolyte formulation. Use of antibiotics oral antibiotics in
10
Salmonellosis is controversial, as it is believed they may cause prolongation of the carrier
state. Erythromycin is the drug of choice for Campylobacter infections. Ronidazole is used for
T. foetus.

Histiocytic colitis

Clinical evidence has accumulated over several years that histiocytic colitis in Boxers may be
resolved with enrofloxacin therapy. The reason for this positive response has been recently
identified by some elegant research from Kenny Simpson’s lab in Cornell. His work has
shown that histiocytic colitis in boxers is associated with selective intramucosal colonisation
by E.coli strains which are adherent and invasive.

Probiotics

The clinical efficacy of probiotics in the management of GI disorders has been demonstrated
in several studies in humans. However, there have been few studies in pets and the
evidence for their efficacy is not, as yet, particularly encouraging especially given the
prevalence with which they are currently used in general practice.

In one study of acute diarrhoea in 36 dogs, those receiving probiotics made a statistically
significant faster recovery but as the difference was only between 1.2 days to recover for the
probiotic dogs and 2.2 days for those not treated with probiotics, it is hardly an earth
shattering difference. In another study in dogs with acute diarrhoea there was no significant
benefit noted in the probiotic treated dogs. To date there has only been one study in dogs
with chronic diarrhoea. In a group of dogs with food responsive diarrhoea where there was
no additional benefit seen by addition of probiotic to the management regimen.

Studies in cats with diarrhoea are a little more positive. In a study of 33 kittens with acute
diarrhoea due to Giardia significantly fewer of those receiving probiotics needed additional
support (9.5% probiotic treated vs. 60% placebo treated). In another study of 30 cats with
chronic diarrhoea, 30% of cats treated with E. faecium improved but none in the placebo
controlled group did.

It is therefore prudent to consider the cost:benefit of probiotic treatment especially in dogs at

this time with current products. Future products may differ in composition and as we learn
more about gut flora in dogs and cats they may be better targeted to be of clinical benefit.

Currently, in the author’s opinion the major benefit of using probiotics in dogs and cats is that
it may reduce the inappropriate use of antibioticsin patients with diarrhoea.

Diet

Diet-responsive chronic enteropathy may be due to dietary allergy (hyperimmune response

to a dietary allergen) or intolerance (non immune-mediated response to a dietary substance).
Patients with food allergy can also have dermatological signs though they can be subtle. The
anatomic location of lesions in dogs is often feet and axilla, in cats, face and ears.
Diagnosis is usually a process of trial and error by using elimination diets as there is no
sensitive or specific diagnostic test. True dietary hypersensitivity/allergy may or may not be
associated with peripheral eosinophilia (i.e., it should not be ruled out if the eosinophil count
is normal). Current evidence would suggest that blood tests for anti-food antibodies are not
specific nor clinically valuable.
The aim of an elimination diet is to feed the animal a single novel protein source – i.e., one
which it has not previously been exposed to (sometimes this can be very difficult to find – fish
is often good for dogs but not cats) and ideally a single carbohydrate source that is gluten
11
free (i.e., rice, sweet potato). Both commercial prescription and homemade diets can be
utilised for this purpose. If the diarrhoea does not resolve (and assuming the patient is
otherwise well), try another diet and even a 3rd diet.Although a 12-week dietary trial has been
recommended in some texts, most animals that have diarrhoea secondary to food
hypersensitivity or intolerance will respond in two to three weeks – and most owners will not
tolerate diarrhoea and dietary trials for 12 weeks. If the diarrhoea has still notnot resolved,
then a dietary cause is unlikely or the wrong diet has been chosen - provided you are 100%
sure that the owners have been 100% compliant i.e., nothing else has been fed including
treats, dental chews, table scraps, food material ingested illicitly (e.g. in households with
toddlers) and other creatures (especially relevant to cats that hunt). If the diarrhoea does
resolve, then in theory single items are gradually added to the diet to attempt to identify the
offending food/s. Some owners don’t want to do this and would rather just continue with the
new diet than risk a return of the clinical signs.
If the patient is unwell, seriously underweight and/or has low albumin then multiple diet trials
are not appropriate and biopsy or immunosuppressive treatment (along with diet) should be
pursued.
The hydrolysed protein commercial diets that contain fragments of protein (i.e., supposedly
too small to be immunogenic) can be useful especially in patients who have had a wide and
varied diet so that finding a novel protein is almost impossible. However, these diets may not
be entirely hypoallergenic as the hydrolysates will occasionally still trigger an allergic reaction
in very susceptible patients. Apparently, if proteins are completely hydrolysed so that their
capacity to induce an immune or allergic reaction is entirely eliminated, the taste is so bitter
the diet is unpalatable.
We will recommend an elimination diet prior to biopsy if the animal is essentially well, has not
lost a large amount of weight and is not hypoproteinaemic. If the diet is unsuccessful (and at
least one further diet trial has been conducted) and there is has been no response to a
metronidazole or tylosin trial biopsy is often the next step.

12
 GI drugs – useful or useless?
Jill E. Maddison
The Royal Veterinary College, UK

SYMPTOMATIC TREATMENT OF THE VOMITING PATIENT

If possible, identify and remove the cause of vomition.Regardless of whether further

investigation is planned, it is usually prudent to withhold food for u to 24 hours (less in young
animals) to rest the GI tract from physical trauma and to eliminate stimulation of secretions
that could further damage an already abnormal mucosa. Water may be given in small
frequent amounts or iceblocks, but withhold if this stimulates vomiting.

Intravenous fluid therapy

Intravenous fluid therapy should be commenced if the animal is dehydrated. Subcutaneous
fluids are only appropriate if dehydration is slight as they are slowly absorbed (particularly in
dehydrated, hypotensive patients). Only isotonic fluids can be given by this route.

• Correct dehydration and replace continuing losses.

• Correct electrolyte imbalances - vomiting patients lose chloride and potassium
particularly, and sodium if severe.
• Acid/base: alkalosis occurs if vomiting is severe and high duodenal or pyloric
lesions are present. Acidosis occurs if there is chronic reflux of duodenal
contents into the stomach or if vomiting is accompanied by severe diarrhoea
(NB: acidosis occurs much more commonly than alkalosis). It is rare that
specific management of acid base status is required.

Antiemetics?
Consider use of antiemetics if vomiting is protracted or as specific therapy for drug-induced,
radiation or motion sickness.

Oral protectants?
Oral protectants such as kaolin and pectin are generally not useful as they do not protect or
soothe injured gastric mucosa and may stimulate further vomiting.

Antacids?
Antacids e.g. cimetidine, sucralfate - are useful in management of severe gastric ulceration
and may have protective value against development of oesophagitis secondary to prolonged
and severe vomiting. However, whether or not they are necessary in the vast majority of
vomiting patients is highly debatable and in many cases just adds to treatment costs.

Antibiotics?
Antibiotics are rarely indicated for the patient that is vomiting due to primary GI disease,
although they are frequently administered. The only specific indication for antibiotics for
vomiting due to primary GI disease is to treat Helicobacter infection and it should be noted
that many confirmed infections with Helicobacter are clinically irrelevant.

Bland diet
If no vomiting has occurred after withholding food, gradually introduce water (small amounts)
then small meals, bland diet (cottage cheese, rice, chicken without the skin).

1
ANTIEMETIC DRUGS

Antiemetic therapy should only be considered as symptomatic therapy.

The clinician's attention should be primarily directed at determining and resolving the
underlying disease process. Antiemetic drugs may be used as specific therapy for vomiting
induced by drugs, radiation therapy, motion sickness and psychosomatic disturbances.

Inappropriate use of antiemetics

Use of antiemetics in the following situations is inappropriate:
• Gastrointestinal infections - antiemetics may prolong gastrointestinal infections,
particularly bacterial infections.
• Gastrointestinal obstruction - some antiemetics increase gastric motility which could
result in perforation.
• Gastrointestinal toxicity - antiemetics may prevent the patient from eliminating the
toxin.
• Systemic hypotension - the phenothiazines and other α 2 -adrenergic antagonists can
worsen hypotension.
• Epilepsy - phenothiazines tend to lower the seizure threshold.

It is important to recognise that an antiemetic may not be very effective against nausea. In
human medicine, all anti-emetic drugs have label claims that they reduce nausea since it is
accepted that, in most cases, nausea is a prerequisite of emesis. Although there are some
stimuli that induce emesis with little nausea, the two are generally associated. However, it is
purely assumption that if a drug prevents emesis, it will also prevent nausea.

It is recognised that nausea is more difficult to prevent and treat than emesis. Emesis is an
all-or-nothing event and an antiemetic drug is effective if it inhibits emetic stimuli to such a
degree that the threshold for the emetic reflex is not reached. However, this could still leave
the patient feeling somewhat nauseous, since nausea is a graded phenomenon i.e. one can
feel mildly, moderately or severely nauseous. This graded phenomenon can also be implied
from observations in veterinary patients of the frequency and severity of nausea behaviours.

Maropitant (Cerenia)

Clinical applications
Maropitant is the first drug of its class registered (in some markets) for veterinary use. It is
indicated for the prevention and treatment of general emesis in the dog, and the prevention
of motion sickness in the dog. It may not be as a particularly effective anti-nausea drug.

Metoclopramide

Clinical applications
Metoclopramide is indicated for control of vomiting associated with:

• Various emesis-inducing disorders that involve central or peripheral activation of

vomiting.
• Gastroesophageal reflux.
• Decreased gastric emptying associated with:
- Inflammatory gastrointestinal disorders.
- Gastric ulcers.
- Gastric neoplasia.
- Autonomic neuropathy (diabetes mellitus).
- Pyloric stenosis.
- postoperative gastric volvulus patient.
2
 - Hypokalaemia.
- Abnormal gastric motility.

Although metoclopramide is sometimes recommended for endoscopic procedures to facilitate

passage of the endoscope through pylorus this effect was not confirmed in a well-controlled
study of the effect of pharmacologic agents on the ease of endoscopic intubation in dogs.

A search of the published literature provides no evidence for the anti-nausea effects of
metoclopramide in the dog. In the study of low dose cisplatin-induced nausea and vomiting in
dogs by Kenwood et al (2017), metoclopramide did not reduce nausea.

Antihistamines

Examples
Diphenhydramine (Benadryl), promethazine (Phenergan), dimenhydrinate (Dramamine).

Mechanism of action
Act directly on neural pathways arising in the vestibular nucleus. Therefore can be effective
in control of motion sickness and vomiting associated with middle ear infections but have
little effect on emesis produced by other stimuli. They have no effect on stimuli from viscera
as they don't act directly on the vomiting centre. They do have some effect on the CRTZ but
effectiveness against vomiting caused by metabolic toxins and drugs is inconsistent.
Antiemetic effect appears to be independent of the antihistaminic or sedative potencies.

Side effects
Drowsiness and xerostomia (dry mouth).

Phenothiazines

Examples
Prochlorperazine (Stemetil, Compazine).

Mechanism of action
Block CRTZ at low doses (antidopaminergic) and vomiting centre at higher doses
(anticholinergic). Also block peripheral dopamine receptors in stomach. However, cannot
block visceral afferent (vagal) impulses associated with severe visceral pain and
contractions.

Side effects
May cause hypotension due to α-adrenergic receptor blocking action  arteriolar
vasodilation. Therefore, should not be included at high doses in the therapeutic regime until
dehydration is corrected by intravenous fluid therapy.

5-HT 3 antagonists

Examples
Dolasetron(Anzemet), ondansetron (Zofran), granisetron (Kytril).

Clinical indications
The 5-HT3 receptor antagonists are extremely potent antiemetics used in the management of
cancer therapy-induced emesis in humans. Their effectiveness as antiemetics is orders of
magnitude better than metoclopramide (e.g. 100 times better in the ferret).

The anti-nausea effect of ondansetron is well documented in human patients but less so in
veterinary species. Ondansetron has been shown to significantly reduce nausea induced by

3
anaesthesia, cyclophosphamide and cisplatin in humans. In the Kenward et al (2017) study
ondansetron was far more effective at suppressing nausea behaviour or its biomarker
(vasopressin) than metoclopramide or maropitant.

Mechanism of action
Although initially thought to have a central action on the CRTZ, recent work suggests that
their main mode of action is through antagonism of peripheral 5-HT3 serotonergic receptors
in the gut.

Side effects
Experimental studies suggest that the 5-HT 3 antagonists are very safe with animals showing
minimal toxicity at doses up to 30 times greater than those needed to abolish vomiting. In
humans, constipation, headaches, occasional alterations in liver enzymes and rarely
hypersensitivity reactions have been reported.

Anticholinergics

Examples
Atropine, hyoscine (scopolamine), propanthaline, isopropamide.

Anticholinergics have been used frequently in the past as antiemetics but usually
inappropriately. These drugs are usually not effective unless vomition is due to smooth
muscle spasm (an extremely uncommon occurrence). They do not stop vomiting caused by
stimulation of peripheral receptors by other means such as inflammation. If they can cross
the BBB (e.g. hyoscine) they are effective for motion sickness due to antagonism of M 1
receptors in vestibular apparatus.

Anticholinergics have been used in the management of pancreatitis on the basis that they
may reduce pancreatic secretion. However, no appreciable benefit has been demonstrated
experimentally or clinically from this treatment.

BEWARE!Anticholinergic drugs reduce gastrointestinal motility, which can act as a stimulus

for further vomiting. Overuse can result in gastric atony and intestinal ileus, which may
predispose to absorption of endotoxins through damaged mucosa. Don't use in dogs with
parvovirus infection as the potential for endotoxaemia is increased.

GASTRIC ULCERATION

The protective barrier that prevents gastric mucosa from being damaged by gastric acid
includes:

Gastric protective barrier

• Mucus, with bicarbonate incorporated into the mucosal gel layer - this buffers
influxing luminal protons and establishes a pH gradient across the mucosal layer from
a pH of 2-3 at the luminal surface to a pH of 7 near the epithelium.

• High epithelial turnover - there is continual rapid cell turnover (2-4 days). Cell
restitution (migration of surviving cells from the edge of the defect) is the most rapid
means of repair. Minor damage to the epithelial surface can be repaired within 15-30
minutes.

• Tight junctions and lipoprotein layer of epithelial cells.

4
 • Surface-active phospholipids contributing to mucosal hydrophobicity, which
excludes or retards the absorption of potentially damaging water-soluble luminal
contents by mucosa.

• Rich vascular supply - the high rate of mucosal blood flow supplies oxygen and
nutrients to the epithelium and also allows for rapid removal of substances that have
penetrated the epithelial barrier. Maintenance of mucosal blood flow is essential for
the maintenance of mucosal defence and the extent of damage to this component is
central to whether on-going mucosal damage or restoration will ensue following an
insult.

• Prostaglandins - PGE series and PGI 2 protective:

- Inhibit gastric acid secretion.
- Maintain mucosal blood flow.
- Involved in secretion and composition of healthy mucus.
- May be intercellular messengers for stimulus of mucosal cell turnover and
migration.

Causes of GI ulcers

GIT ulceration may occur for variety of reasons but in most cases the primary pathogenic
mechanism is disruption of mucosal defence rather than increased acid secretion:
• Drugs (aspirin, PBZ, corticosteroids).
• Uraemia (toxins, increased gastrin).
• Liver disease (cause not known).
• Stress.
• Increased production of HCl (mast cell tumour at any site, gastrin-producing tumour of
the pancreas = Zollinger-Ellison syndrome).
• Hypotension e.g. during surgery.
• Hypoadrenocorticism.
• Increased incidence associated with spinal cord disease.

Consequences of damage to the mucosal barrier

Damage to the gastric mucosal barrier allows back-diffusion of gastric acid into the
submucosa which  mast cell degranulation  histamine release  stimulation of acid
production by gastric parietal cells  enhanced inflammation and oedema in submucosa.

The aim of antiulcer therapy is to reduce the amount of gastric acid produced or to
neutralise its effect and hence stop the vicious cycle of gut damage.

ANTIULCER DRUGS

Antiulcer drugs are useful in the specific management of GIT ulceration and reflux
oesophagitis. They are not usually used or needed for treatment of simple acute gastritis.

The most comprehensive review of gastroprotectants is the ACVIM Consensus statement

(2018).

Histamine receptor antagonists

Examples
Cimetidine (Zitac), ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid).

Clinical indications
5
The H 2 antagonists have efficacy in treating gastric ulceration caused by a variety of agents
including NSAIDs and uraemia. However, they do not appear to be effective in preventing
NSAID-induced ulcers.

Although there are difference in potency (i.e. the relationship between amount of drug and
effect) between cimetidine, ranitidine and famotidine, they are equally effective at promoting
ulcer healing if given at the correct dose and dose frequency and drug choice should be
based on considerations of cost, client convenience and concurrent drug therapy.

Cimetidine must be given at least every 6 hours as it only suppresses acid production for 3-5
hours. Ranitidine can be dosed every 8-12 hours and famotidineevery 12-24 hours.

Sucralfate

Clinical indications
Sucralfate (Carafate) is indicated for the symptomatic treatment of gastric ulceration from a
variety of causes. In humans sucralfate is as effective as antacids or H 2 receptor antagonists
in healing ulcers. It does not appear to be successful, however, in preventing corticosteroid-
induced ulceration in dogs subjected to spinal surgery. Its prophylactic efficacy in preventing
NSAID-induced ulcers has also not been proved in the dog. Sucralfate has also been used
for treatment of oral and oesophageal ulcers.

Misoprostol

Clinical indications
Misoprostol (Cytotec) is a synthetic PGE 1 (prostaglandin). In human medicine, there is
conflicting data about whether misoprostol is as effective or more so than H 2 antagonists in
healing ulcers. It is, however, most useful for prevention of NSAID-induced ulceration and its
efficacy in this regard has been demonstrated in dogs. This is in contrast to the lack of
prophylactic efficacy of other anti-ulcer drugs such as cimetidine.

Other less common uses include intravaginal administration in conjunction with PGF 2α for
pregnancy termination (mid to late gestation). It has also been reported to have some
efficacy in the treatment of atopic dermatitis in dogs.

Omeprazole

Clinical indications
Omeprazole (Prilosec, Losec) has slightly greater efficacy in healing ulcers in humans than
H 2 antagonists but is more expensive. Its use in veterinary medicine was initially primarily for
refractory ulcers or ulcers associated with gastrinomas or mastocytosis although it is being
used more commonly as a “routine” anti-ulcer drug – often with little justification. It is used
peri-operatively for brachycephalic dogs at risk of gastric reflux. Excellent long term clinical
outcomes have been reported in humans and dogs with non-resectablegastrinomas treated
with omeprazole.

Omeprazole has been reported to be useful in the management of severe erosive

oesophagitis, gastritis or gastric ulcer disease in dogs that are refractory to therapy with H 2
receptor antagonists and sucralfate. It has been used successfully to treat severe erosive
oesophagitis in one cat but had no effect in two other similarly affected cats.

Omeprazole was not reported to significantly reduce mechanically-induced gastric ulceration

and/or prevent aspirin-induced gastritis in dogs although there was a non-statistically
significant trend that suggested that omeprazole was more effective than cimetidine in this
regard.

6
Non-systemic antacids

Examples
Non-systemic antacids included a variety of oral preparations containing aluminium
hydroxide, calcium carbonate and magnesium compounds.

Clinical indications
Non-systemic antacids are probably most frequently used in management of uraemia as
aluminium hydroxide binds phosphate thus reduces hyperphosphataemia as well as having
an antacid effect.

Although they are inexpensive, non-systemic antacids must be administered orally (which
may be problematical in a vomiting patient) and frequently, which results in poor owner
compliance. Dosages are empirical as no specific dosages have been defined for animals.

Effective doses are estimated to be 0.5 - 1.0 mL/kg. To be effective, antacids must be
administered at least every four hours. Daily treatment for four to six weeks is required.

DIARRHOEA

For most cases of acute diarrhoea, the mainstay of therapy is to replace fluid losses, modify
the diet and to treat the specific cause (infectious, immune-mediated etc.) where possible.
Symptomatic treatment of diarrhoea does not often require the use of drugs but they may be
considered when symptomatic relief of discomfort will be beneficial to the patient, provided
that their use does not increase the risk of exacerbating the diarrhoea or causing systemic
effects.

Motility modifying drugs

Intestinal transit time is predominantly determined by the balance between peristalsis, which
moves ingesta in an aboral direction, and segmental contractions which narrow the bowel
lumen and increase the resistance to flow. Peristalsis is influenced by the cholinergic system
and gut hormones such as motilin. Segmental contractions are cholinergic dependent.
Although it is theoretically possible to reduce diarrhoea by either decreasing peristalsis or
increasing segmental contractions, reducing peristalsis is of little clinical benefit and is
generally contraindicated. This is because, in most cases of diarrhoea, the gut is hypomotile
not hypermotile and peristalsis and segmental contractions are already reduced.

Gastrointestinal motility may be modified by two groups of agents - narcotic analgesics,

which increase segmental contractions, and anticholinergic drugs, which decrease both
segmental contractions and peristalsis.

Opioid analgesics

Example

Diphenoxylate (Lomotil), loperamide (Imodium), paregoric.

Clinical indications

7
These drugs are effective for the symptomatic treatment of diarrhoea as they increase
segmental contractions, thus delaying gut transit time. They will effectively relieve abdominal
pain and tenesmus and reduce the frequency of defecation.

Are they often needed?

They are rarely required, however, in management of diarrhoea in small animals. Acute
diarrhoea is usually self-limiting with appropriate symptomatic treatment and chronic
diarrhoea does not usually respond to symptomatic therapy, and requires a definitive
diagnosis to be established to allow specific therapy to be instituted. They are occasionally
useful in chronic colitis that cannot be controlled by other means.

Any risks?

The use of motility modifiers is not without risk as the diarrhoea may be beneficial in
removing toxins and inhibition of movement may be counterproductive. Reduced motility may
allow enterotoxin-producing organisms to remain in the small intestine, resulting in increased
fluid loss.

In addition, in cases of diarrhoea caused by invasive bacteria, the diarrhoea itself is a

protective mechanism, probably by hastening the elimination of the organism. Slowing the
transit time may prolong the time the bacteria is resident in the bowel resulting in a greater
opportunity for proliferation of the organism, invasion of the mucosa and absorption of toxic
products.

Loperamide, however, appears to be anti-secretory and therefore may have value in the
treatment of animals with secretory diarrhoea due to E. coli.

Mechanism of action

Opioids increase the amplitude of rhythmic contraction and decrease propulsive contractions.

They directly affect intestinal smooth muscle producing both tonic and phasic contractions of
the circular muscle. They also act centrally and on synapses to augment segmentation.

Opioids either have no effect on longitudinal muscle or they relax it. The net effect of these
actions is to inhibit the flow of intestinal contents, delay gastric emptying and increase the
tone of the ileocolic valve and anal sphincter.

Some opioids such as loperamide and to a lesser extent diphenoxylate, also increase fluid
and water absorption, possibly by a calcium blocking effect or by inhibition of calmodulin, the
intrinsic calcium binding protein. Loperamide and diphenoxylate also inhibit the activity of
secretagogues such as E. coli enterotoxin, VIP, bile acids and PGE2.

Lomotil contains atropine as well as diphenoxylate. This is to discourage abuse of the drug
by people and at therapeutic doses the atropine has no clinical effect.

Side effects

Signs of systemic opioid intoxication may occur with use of the opioid antidiarrhoeal agents,
particularly in cats. Neurological disturbances such as ataxia, hyperexcitability, circling, head
pressing, barking and prostration may occur with overdosage.

8
In dogs there has been a suggestion that Collies may be more sensitive to the toxic effects of
loperamide. Treatment of side effects or overdosage involves use of the opioid antagonist
naloxone and recovery is usually uneventful.

Drug interactions

Other CNS depressants such as anaesthetic agents, antihistamines, phenothiazines,

barbiturates and tranquillisers may cause increased CNS or respiratory depression when
used with opiate antidiarrhoeal agents.

Opiate antidiarrhoeal agents are contraindicated in patients receiving monoamine oxidase

inhibitors e.g. L-deprenyl (selegeline) for at least 14 days.

Anticholinergic drugs

Anticholinergics have little use in the management of diarrhoea in small animals although
they are frequently prescribed, usually in combination products. As discussed previously,
most diarrhoeal disorders in small animals are associated with a hypomotile rather than a
hypermotile gut and the risk with anticholinergics is that they will produce adynamic ileus
especially if electrolyte imbalances such as hypokalaemia are also present.

Anticholinergics reduce but do not abolish peristalsis, but significantly decrease segmental
contractions. As long as some peristaltic activity is present, no matter how weak, it can
propel liquid intestinal contents along the flaccid intestine and diarrhoea will occur.

Although anticholinergics reduce gastric secretions, including protein exudation induced by

histamine, they have little effect on intestinal secretions. They may be justified in the short
term symptomatic relief of pain and tenesmus associated with large bowel inflammatory
disease. They also may be indicated in stress-induced colitis where cholinergic mechanisms
might be involved.

Absorbents and protectants

Kaolin and Pectin

Kaolin and pectin are in many preparations that are widely used for the management of
diarrhoea in small and large animals. They are purported to soothe irritated gastrointestinal
mucosa and bind toxins and pathogenic bacteria. However, their clinical efficacy is unproven.

There is no evidence that kaolin and pectin reduce gastrointestinal fluid or electrolyte loss
and kaolin may in fact increase faecal sodium loss.

Many preparations contain combinations of kaolin and pectin, and/or antibiotics and/or
anticholinergics. As discussed previously the value of the latter two types of compounds in
the treatment of diarrhoea is limited in small animals and may be detrimental.

Activated Charcoal

Activated charcoal has been used for many years in the treatment of toxicosis. It is thought to
absorb toxic substances and bind bacterial toxins although there are no controlled studies
that evaluate its efficacy.

Bismuth Salicylate

Bismuth salicylate is reported to be an effective agent for the treatment and prevention of
enterotoxigenic diarrhoea. Nausea, abdominal pain and diarrhoea are reduced in humans
with infective diarrhoea treated with bismuth salicylate. Bismuth salicylate has modest
9
antibacterial effects against enteropathogens such as E. coli,Salmonella and Campylobacter
jejuni.

The salicylate moiety is believed to decrease intestinal secretion by inhibiting prostaglandin

production and has an inhibitory effect on generation of cAMP by the enterotoxin.

Preparations that contain bismuth salicylate (Pepto-Bismol,Peptosyl) can be clinically useful

in the management of acute diarrhoea. However, usually such conditions resolve with
appropriate non-pharmacological symptomatic therapy.

Overdosage can result in salicylate toxicity especially in cats. A safe dose in dogs and cats is
0.25 mL/kg q4-6h. Dosages greater than 0.7 mL/kg could result in toxicity.

Fluid therapy

Fluid therapy is required if the animal is dehydrated. Intravenous administration is necessary

if the dehydration is severe and/or associated with vomiting. The loss of bicarbonate ions
may result in acidosis, however this does not require specific therapy. Potassium loss is
important and in severe diarrhoea the animal will have a total body potassium deficiency. It
is therefore important to supplement fluids with potassium and to monitor plasma
concentrations.

Oral fluid therapy

In pure secretory diarrhoea (more common in calves and pigs with E. coli infection than small
animals), glucose and amino acid absorption are intact and thus fluids containing these
substances can be given orally and will facilitate absorption of water and sodium. Oral
rehydration therapy is effective in calves and piglets. Small animals with severe acute
diarrhoea often will not voluntarily drink or are vomiting as well, therefore oral fluids are of
little value.

Antimicrobial therapy

Antimicrobial therapy is not indicated for routine nonspecific acute or chronic diarrhoea in
small animals, where primary bacterial causes are uncommon and indiscriminate use may
alter normal flora sufficiently to allow pathogens to proliferate.

Parenteral antibiotics may be indicated in small animal patients with haemorrhagic diarrhoea
where there is loss of the intestinal mucosal barrier and therefore the potential for bacterial
invasion and septicaemia (although this is difficult to reproduce experimentally). This is
particularly so if leucopenia is also present as in parvovirus infection or where the presence
of leucocytosis and pyrexia may suggests systemic bacterial invasion. There is no indication
for use of antibiotics in haemorrhagic diarrhoea if there is no evidence of systemic signs
supporting bacteraemia.

Bacteria play a pathogenic role in parvo virus (germ free dogs infected with parvovirus have
very mild clinical signs) so it is appropriate to use antibiotics in these cases – parenteral
amoxicillin-clavulanate is probably the best and safest choice although some recommend
gentamicin (ensure the patient is appropriately hydrated before commencing therapy) and
penicillin. (I personally think this combination is a bit risky in a critically ill patient).

Infectious diarrhoea

Antibiotics are frequently used in the treatment of diarrhoea and their use is logical in cases
of enteropathogenic E. coli infections. However, in some experimental studies, while
antibiotic treatment was superior to placebo, it had similar efficacy to oral rehydration therapy
with glucose-glycine electrolyte formulation. Use of antibiotics oral antibiotics in
10
Salmonellosis is controversial, as it is believed they may cause prolongation of the carrier
state. Erythromycin is the drug of choice for Campylobacter infections. Ronidazole is used for
T. foetus.

Histiocytic colitis

Clinical evidence has accumulated over several years that histiocytic colitis in Boxers may be
resolved with enrofloxacin therapy. The reason for this positive response has been recently
identified by some elegant research from Kenny Simpson’s lab in Cornell. His work has
shown that histiocytic colitis in boxers is associated with selective intramucosal colonisation
by E.coli strains which are adherent and invasive.

Probiotics

The clinical efficacy of probiotics in the management of GI disorders has been demonstrated
in several studies in humans. However, there have been few studies in pets and the
evidence for their efficacy is not, as yet, particularly encouraging especially given the
prevalence with which they are currently used in general practice.

In one study of acute diarrhoea in 36 dogs, those receiving probiotics made a statistically
significant faster recovery but as the difference was only between 1.2 days to recover for the
probiotic dogs and 2.2 days for those not treated with probiotics, it is hardly an earth
shattering difference. In another study in dogs with acute diarrhoea there was no significant
benefit noted in the probiotic treated dogs. To date there has only been one study in dogs
with chronic diarrhoea. In a group of dogs with food responsive diarrhoea where there was
no additional benefit seen by addition of probiotic to the management regimen.

Studies in cats with diarrhoea are a little more positive. In a study of 33 kittens with acute
diarrhoea due to Giardia significantly fewer of those receiving probiotics needed additional
support (9.5% probiotic treated vs. 60% placebo treated). In another study of 30 cats with
chronic diarrhoea, 30% of cats treated with E. faecium improved but none in the placebo
controlled group did.

It is therefore prudent to consider the cost:benefit of probiotic treatment especially in dogs at

this time with current products. Future products may differ in composition and as we learn
more about gut flora in dogs and cats they may be better targeted to be of clinical benefit.

Currently, in the author’s opinion the major benefit of using probiotics in dogs and cats is that
it may reduce the inappropriate use of antibioticsin patients with diarrhoea.

Diet

Diet-responsive chronic enteropathy may be due to dietary allergy (hyperimmune response

to a dietary allergen) or intolerance (non immune-mediated response to a dietary substance).
Patients with food allergy can also have dermatological signs though they can be subtle. The
anatomic location of lesions in dogs is often feet and axilla, in cats, face and ears.
Diagnosis is usually a process of trial and error by using elimination diets as there is no
sensitive or specific diagnostic test. True dietary hypersensitivity/allergy may or may not be
associated with peripheral eosinophilia (i.e., it should not be ruled out if the eosinophil count
is normal). Current evidence would suggest that blood tests for anti-food antibodies are not
specific nor clinically valuable.
The aim of an elimination diet is to feed the animal a single novel protein source – i.e., one
which it has not previously been exposed to (sometimes this can be very difficult to find – fish
is often good for dogs but not cats) and ideally a single carbohydrate source that is gluten
11
free (i.e., rice, sweet potato). Both commercial prescription and homemade diets can be
utilised for this purpose. If the diarrhoea does not resolve (and assuming the patient is
otherwise well), try another diet and even a 3rd diet.Although a 12-week dietary trial has been
recommended in some texts, most animals that have diarrhoea secondary to food
hypersensitivity or intolerance will respond in two to three weeks – and most owners will not
tolerate diarrhoea and dietary trials for 12 weeks. If the diarrhoea has still notnot resolved,
then a dietary cause is unlikely or the wrong diet has been chosen - provided you are 100%
sure that the owners have been 100% compliant i.e., nothing else has been fed including
treats, dental chews, table scraps, food material ingested illicitly (e.g. in households with
toddlers) and other creatures (especially relevant to cats that hunt). If the diarrhoea does
resolve, then in theory single items are gradually added to the diet to attempt to identify the
offending food/s. Some owners don’t want to do this and would rather just continue with the
new diet than risk a return of the clinical signs.
If the patient is unwell, seriously underweight and/or has low albumin then multiple diet trials
are not appropriate and biopsy or immunosuppressive treatment (along with diet) should be
pursued.
The hydrolysed protein commercial diets that contain fragments of protein (i.e., supposedly
too small to be immunogenic) can be useful especially in patients who have had a wide and
varied diet so that finding a novel protein is almost impossible. However, these diets may not
be entirely hypoallergenic as the hydrolysates will occasionally still trigger an allergic reaction
in very susceptible patients. Apparently, if proteins are completely hydrolysed so that their
capacity to induce an immune or allergic reaction is entirely eliminated, the taste is so bitter
the diet is unpalatable.
We will recommend an elimination diet prior to biopsy if the animal is essentially well, has not
lost a large amount of weight and is not hypoproteinaemic. If the diet is unsuccessful (and at
least one further diet trial has been conducted) and there is has been no response to a
metronidazole or tylosin trial biopsy is often the next step.

12
 Vomiting, regurgitation& reflux
Jill E. Maddison
The Royal Veterinary College, UK

ASSESSMENT OF THE PATIENT REPORTED TO BE VOMITING

Define the problem

It’s important to differentiate vomiting from regurgitation, which involves the retrograde
movement of food and fluid from the oesophagus, pharynx and oral cavity without
initiation of reflex neural pathways other than the gag reflex.

It’s also important to differentiate vomiting from gastric reflux which involves retrograde
movement of food and fluid from the stomach into the oesophagus. This material may
then travel some or all of the way to the pharynx and nasopharynx and may be inhaled,
causing acid damage to mucosae it contacts. The severity ranges from subclinical to
severe and life threatening. Many patients present for the respiratory consequences of
“silent reflux” but in this chapter we will focus on the presentation that can be confused
with vomiting because material from the stomach comes out of the mouth.

It is also important to differentiate vomiting from coughing followed by gagging, which is

often confused by owners with vomiting. Cat owners in particular may confuse vomiting
and coughing in their pets.

Owners are often unable to differentiate vomiting, regurgitating, refluxing and gagging
and therefore it is important to ask specific questions to elicit appropriate information,
e.g. amount of effort involved, character of vomitus etc. If still uncertain, the veterinarian
may need to observe the animal. Even with veterinary observation, it is difficult and
sometimes impossible to differentiate reflux and regurgitation without fluoroscopy.
Without fluoroscopy, the concurrent problems need to be considered to reach a
reasonable conclusion. Patients with nausea, vomiting and gastric dysmotility are
predisposed to reflux, as are brachycephalic breeds.

Why is it important to differentiate vomiting from regurgitation, reflux and

coughing?

The differential diagnoses, appropriate diagnostic tools and management strategies are
completely different for patients who are truly vomiting compared with patients who are
regurgitating, gagging or coughing. There is much in common in the treatment of
vomiting and reflux because diseases that lead to vomiting may subsequently lead to
reflux. It is important to appreciate this so that a gastric antacid can be prescribed to
reduce the risk of reflux oesophagitis which can be the reason a patient with an acute
vomiting disorder does not recover as expected and which can contribute significantly to
patient morbidity and mortality.

Patients who are vomiting (due to primary GI or secondary GI disease) may be treated
symptomatically or investigated, depending on the case, using a variety of diagnostic
tools, including clinical pathology, diagnostic imaging, endoscopy and exploratory
laparotomy.

1
When regurgitation is the predominant clinical sign, it will usually be due to oesophageal
disease (very occasionally pharyngeal) and usually carries a poor or guarded prognosis
due to the type of lesion – for example foreign body, stricture or megaoesophagus. The
patient should not be treated symptomatically without diagnostic investigation to define
the lesion where possible. In addition, the investigation of regurgitation essentially
involves visualising the oesophagus (by endoscopy and/or diagnostic imaging tools) – it
is rare for routine clinical pathology to be of diagnostic value in defining the type of lesion
(megaoesophagus, foreign body etc.), although it may be of value once
megaoesophagus is diagnosed in assessing possible metabolic causes.

Similarly, the patient who is gagging most likely has a lesion in the pharyngeal region or
upper oesophagus, and visualising the lesion is the appropriate diagnostic path. Clearly,
the animal that is coughing has respiratory or cardiac disease and requires an entirely
different diagnostic approach.

Failure to define the problem appropriately can therefore potentially endanger the patient
and may lead to wasted time and money and impair the veterinarian–client relationship
and trust.

Clues to help differentiation of vomiting, regurgitation and reflux

The associated behaviour of patients who vomit differs from those who regurgitate or
reflux. As discussed, vomiting is a neurologically coordinated activity with defined stages
and physical manifestations. The patient will exhibit abdominal effort prior to bringing up
material and vomiting is often preceded by hypersalivation – manifested by licking of lips
and repeated swallowing. The vomiting may be projectile.

In contrast, regurgitation and reflux are passive processes - there are no coordinated
movements. Regurgitation is often induced or exacerbated by alterations in food
consistency and exercise and facilitated by gravity when the head and neck are held
down and extended. Patients who regurgitate will often gag as material accumulates in
the pharynx. Reflux is often watery and low in volume but acidic and patients may exhibit
behaviour indicating local irritation as it enters the airways.

The character of the vomitus may also give the clinician clues. While undigested food
may be brought up by vomiting or regurgitation, if the food is partially digested and/or
contains bile, the patient is vomiting and/or refluxing not regurgitating. The pH of the
vomitus is occasionally, but not always, useful. Acidic material strongly suggests
vomiting or reflux but pH neutral material may be the product of vomiting, reflux or
regurgitation.

As mentioned, because the epiglottis does not close, regurgitating patients are at
considerable risk of aspirating gastric contents. Thus, if an owner reports that his/her
animal developed a cough at the same time it started ‘vomiting’, the clinician should be
alert to the possibility that aspiration has occurred and that this is more likely to occur
with regurgitation than vomiting.

There is a caveat, however, which should be kept in mind. Patients who have
experienced serious vomiting of acidic gastric contents may develop a secondary
oesophagitis and present with signs suggestive of both vomiting and regurgitation or

2
reflux. Usually, vomiting will have been the first sign noted. Animals that ingest caustic or
irritant material causing oesophagitis and gastritis may also present with signs of both
vomiting and regurgitation.

Define and refine the system

Primary vs. secondary gastrointestinal disorders

Reviewing the physiology of vomiting as discussed in the previous section and as shown
in Figure 1, it is apparent that vomiting may occur due to primary GI disease or from
secondary or non-GI disease.

Figure 1 The relationship between the elements of the emetic reflex.

In contrast, regurgitation is almost always due to primary oesophageal disease (Table

1).

Primary GI diseases are those where there is specific primary GI pathology such as gut
disturbance due to dietary indiscretion, inflammation, infection, parasites, obstruction or
neoplasia. There may be metabolic consequences of the GI disease, but the primary
pathology is in the GI tract.

Secondary GI disease is where the vomiting or regurgitation has occurred due to

pathology elsewhere in the body – the gut is just the ‘messenger’. Abnormalities of other
body systems may indirectly cause vomiting either due to the action of toxins on the
CRTZ, vomiting centre and vestibular system or by stimulation of peripheral non-GI-
associated vomiting receptors.

Examples would include renal failure, liver disease, ketoacidososis, pancreatitis,

hypercalcaemia, hypoadrenocorticism and other metabolic disorders. In most cases,
there is no pathology identifiable in the gut, or where there is, for example ulceration
secondary to liver disease, uraemia or hypoadrenocorticism, the primary cause is the
metabolic disorder. While symptomatic management strategies might be directed at the
gut pathology in these cases (such as the use of anti-ulcer drugs), there is no diagnostic
benefit to imaging the gut, for example by endoscopy.

3
Why is it important to differentiate primary from secondary GI disease?

It is important to determine whether primary or secondary GI disease is occurring in the

vomiting or regurgitating animal, as much time and money can be wasted if the wrong
system is investigated. As discussed in Chapter 2, the range of diagnoses to consider,
diagnostic tools used and potential treatment or management options for primary,
structural problems of a body system such as the GI tract are often very different
compared to those relevant to secondary, functional problems of that system.
Investigation of primary GI disease often involves some form of imaging modality
(radiology, ultrasound, endoscopy and surgery) and/or biopsy. Routine haematology and
biochemistry are often of little diagnostic value in GI disease, although they may give
clues about the clinical status of the patient. In contrast, for secondary GI disorders,
haematology, biochemistry and other tests are often critically important in progressing
towards a diagnosis.

It is also important to appreciate that there are cases of primary GI disease causing
vomiting such as gastroenteritis caused by dietary indiscretion or other irritants that can
be safely treated symptomatically, as the cause is transient and will resolve within days
without specific treatment. Symptomatic management such as withholding food,
antiemetic treatment and/or dietary change is appropriate for these patients. However,
there are few, if any, secondary GI causes of vomiting (such as liver disease, renal
failure, hypoadrenocorticism and hypercalcaemia) where the cause is transient, which
will respond to symptomatic treatment and/or will resolve without specific therapeutic
intervention.

The uncommon secondary GI causes of regurgitation all cause megaesophagus (Table

1), so the clinical decision pathway leading to their diagnosis begins with the diagnosis
of megaoesphagus by endoscopy or diagnostic imaging and then the search for a
metabolic cause. As mentioned, symptomatic treatment of regurgitation without
establishing the cause is not prudent.

Thus, the clinician’s clinical reasoning, in the consultation room, about whether primary
or secondary GI disease is likely to be present is a crucial component of the rational
management of patients reported to be vomiting or regurgitating and of clear
communication with the client.

What are the clues that the patient has primary or secondary GI disease causing
vomiting?

Primary GI disease should be strongly suspected if:

• An abnormality is palpable in the gut, for example foreign body and intussusception
• The vomiting is associated with significant and concurrent diarrhoea
• The patient is clinically and historically normal in all other respects
• The onset of vomiting significantly preceded any development of signs of malaise –
depression and/or anorexia
• The vomiting is consistently related in time to eating (although this can also occur
with pancreatitis).

4
It is important to note, however, that primary GI disease cannot be ruled out even if none
of the aforementioned features are present. For example, vomiting may be delayed for
some hours (up to 24 hours) in animals with non-inflammatory gastric disorders. Animals
with foreign bodies or secretory disorders of the bowel often vomit despite not eating. In
lower bowel disorders, vomiting more commonly occurs at variable times after eating.

Animals with primary GI may also be depressed and inappetant due to the lesion (there
are neural inputs to the satiety centre in the hypothalamus from the gut) or due to the
secondary effects of prolonged vomiting such dehydration or electrolyte disturbances.
Usually, the malaise will occur at the same time or after the onset of vomiting.

Thus, the features in the aforementioned bulleted list are strong clues that primary GI
disease is present, but their absence does not preclude it.

Animals with secondary GI disease are vomiting due to the effect of toxins on the
vomiting centre or CRTZ or because of the stimulation of non-GI-associated peripheral
receptors. The vomiting is usually unrelated to eating – except pancreatitis in dogs.

Animals with secondary GI disease will:

• Often have evidence from the history and/or clinical examination of abnormalities
affecting other organ systems, for example jaundice, polydipsia/polyuria.
• Vomiting is usually intermittent, unrelated to eating and may often occur subsequent
to the onset of other signs of malaise.
• In general, animals that are vomiting due to extra-GI disease are metabolically ill and
are not usually bright, alert and happy.
• If a patient has been metabolically ill (depressed and inappetant) for a significant
period before vomiting was observed, then secondary GI disease is more likely.

Secondary GI causes of regurgitation will frequently have other systemic signs such as
generalised weakness or metabolic malaise. It is usually only patients with
megaoesophagus due to focal myasthenia gravis who present with regurgitation as their
only clinical sign.

Exceptions to the ‘rules’

The exception to these generalisations about the features of secondary GI disease is

pancreatitis in dogs. Canine pancreatitis behaves similarly to a primary GI disease in
that it causes acute-onset vomiting in an initially often otherwise well dog and
subsequent to an episode of dietary indiscretion. The vomiting often occurs immediately
after eating, and decreased appetite and depression may not precede the onset of
vomiting.

Pancreatitis in cats, however, usually behaves similarly to a secondary GI disease. Cats

with hyperthyroidism may also vomit intermittently over a prolonged period and seem
otherwise well (although, of course, they may also have other clinical signs suggestive of
hyperthyroidism).

Define the location

5
If primary GI disease is determined to be present, the temporal relationship of vomiting
to eating and the character of the vomitus should be used to assess where the lesion is
likely to be – the upper or lower GI tract.

Diagnostic tools such as contrast radiography may be appropriate to localise the lesion.
An assessment of the likely location of the lesion is important, as this may determine
what further diagnostic procedures are suitable. For example, endoscopy would be
appropriate for examining the stomach and possibly duodenum but will be of little use if
lower small bowel disease is suspected.

Defining the location for secondary GI disease usually involves routine clinical pathology,
dynamic or function tests +/− imaging to localise the organ affected, for example liver,
kidney, pancreas and adrenals.

The location of the problem for patients who are regurgitating is almost always the
oesophagus (occasionally the pharynx), whether the cause is primary or secondary GI.
Thus, regurgitation is a clinical sign where location is considered first and then the
question is asked – is this a primary or secondary GI lesion?

Define the lesion

Primary GI diseases causing vomiting

Once the lesion has been located within the GI tract, it must now be identified. Biopsy
may be appropriate or the type of lesion may be evident by visual inspection (e.g. foreign
body).

In the GI tract, as elsewhere, neoplasia and inflammation often look grossly identical and
biopsies should always be taken even if the GI tract looks grossly normal.

Diseases of the stomach

• Gastritis
∘ dietary indiscretion
∘ drug induced
∘ immune mediated
∘ eosinophilic
∘ infection, for example Helicobacter pylori
• Gastric foreign bodies
• Gastric ulceration
∘ Note that gastric ulceration can be due to either primary GI lesion, for example
secondary to a foreign body, inflammatory disease or neoplasia but can also be
caused by secondary GI disease such as mastocytoma, liver disease, uraemia,
pancreatic neoplasia (gastrinoma) and drugs such as NSAIDs.
• Disorders of the pylorus
∘ Pylorospasm
∘ Pyloric obstruction
∘ Congenital pyloric stenosis
∘ Chronic hypertrophic gastropathy
• Abnormal gastric motility

6
Intestinal disease

Those intestinal diseases for which vomiting is a predominate clinical feature include the
following:
• Infectious enteritis, for example parvovirus, corona virus (diarrhoea will usually also
be present)
• Dietary indiscretion (diarrhoea often present)
• Intestinal obstruction – foreign body and intussusception
• Inflammatory bowel disease especially in cats (dogs tend to more commonly present
with diarrhoea as the major clinical sign).

The closer the obstruction is to the pylorus, the more frequent and severe the vomiting.

Secondary GI diseases causing vomiting

A large number of secondary GI disorders can cause vomiting. However, most of these
can be eliminated with relatively few tests – at least in dogs. Cats are more problematic
especially in the diagnosis of pancreatic and hepatic disease. In Table 3.2, the most
important secondary GI disorders are listed with tests that are useful in their diagnosis.

You should consult other textbooks to read about specific details of primary and
secondary GI diseases causing vomiting and regurgitation.

Causes of regurgitation

Table 1Oesphageal disorders causing regurgitation.

Megaoesophagus • Congenital
• Acquired – primary GI • Idiopathic
• Acquired – secondary GI • Polymyositis
• Myasthenia gravis
• Polyneuritis
• Hypothyroidism
• Hypoadrenocorticism
• Neoplastic
neuromyopathy
• Lead toxicity
• Tick paralysis
(Ioxodesholycyclus)
External compression • Persistent right aortic
arch
• Mediastinal lymphoma
• Thyroid tumours
Internal obstruction – • Foreign body
physical or functional • Oesophagitis
• Stricture
Intramural Lesions • Neoplasm

7
 • Abscess
• Granuloma e.g. Spirocerca lupi in
endemic areas

Table 2 Secondary gastrointestinal causes of vomiting in cats and dogs.

Disorder Clinical pathology that may be useful
Pancreatitis Pancreatic lipase immunoreactivity (PLI),
amylase (not in cats), lipase (not in cats),
white blood cell count (WBC), ALP, presence
of lipaemic serum
Hepatic disease ALT, ALP, GGT, bile acids, bilirubin, albumin,
urea, glucose
Renal disease Urea, creatinine, phosphate, SDMA, urine
specific gravity (SG)
Hypoadrenocorticism Na+ ,K+, urea, cortisol, calcium, glucose
Diabetic ketoacidosis Blood and urine glucose, ketones
Toxaemia due to infection WBC count
Hypercalcaemia Serum Ca2+ (total and ionised)
Hypokalaemia/ hyperkalaemia Serum K+
CNS disease Cerebrospinal fluid (CSF) analysis (possibly)
Dirofilariasis (cats) Heartworm antigen tests (often negative),
eosinophil count
Lead toxicity Blood lead and/or urinary delta-aminolevulinic
acid (δ-ALA)
Hyperthyroidism (cats) Thyroxine (T4)

In conclusion

Vomiting is a common clinical sign in small animal practice. Causes range from being
relatively clinically innocuous and transitory to being an indication of serious primary or
secondary GI disease.

A logical approach to assessing the patient that presents with the problem of vomiting is
important to ensure that the problem and system are defined correctly so that diagnostic
and treatment plans are rational and justifiable.

Clinical pathology will often progress understanding of secondary GI disorders but is not
usually particularly helpful in primary GI disorders where imaging of the GI tract is often
more diagnostically useful.

8
 INSIGHTS IN TO CANINE OCULAR HEALTH: NAVIGATING
KERATOCONJUNCTIVITIS SICCA, CORNEAL ULCERS AND GLAUCOMA
CHALLENGES

Dr.S.Anoop, MVSc, PhD, Postdoc

Professor
Department of Surgery and Radiology,
College of Veterinary and Animal Sciences,
Mannuthy, Thrissur, Kerala.

Keratoconjunctivitis sicca (KCS) or Dry eye, is a very common ophthalmic affection which
many a times go undiagnosed. KCS is one of the main risk factors for other serious ophthalmic
conditions like corneal perforation and subsequent complications. KCS is an inflammatory
condition of the cornea and conjunctiva, subsequent to a defect in the precorneal tear film (PTF).
KCS is categorized by tear film deficiency as Quantitative KCS, which is a decrease in the aqueous
component of the tear film as measured with the Schirmer tear test (STT) and Qualitative KCS,
which is a decrease in the lipid or mucin components of the tear film and is characterised by a
decreased tear film breakup time (TBUT). This article provides an insight on the pathophysiology,
causes, diagnosis, and medical and surgical management for this condition
Pathophysiology of KCS
Normal PTF is has a thickness of around 3 microns and is composed of aqueous, lipid, and
mucin layers. Tear film deficiencies may lead to chronic inflammation of the ocular surface and
conjunctival epithelium and make it prone to keratomalacia and corneal perforation. Chronic
surface irritation may result in conjunctival hyperemia, squamous metaplasia of the surface
epithelium, hyper keratinization of the surface epithelium and thickening of the corneal epithelium.
Inflammatory cells and blood vessels may enter the corneal stroma and may deposit melanin
pigment and leads to the development of corneal melanosis.
Quantitative KCS
The most common cause of development of quantitative KCS is immune-mediated lacrimal
adenitis. A transient decrease in tear production may be caused by general anesthesia and topical
or systemic administration of atropine also. Other reasons are chronic severe conjunctivitis,
canine distemper, idiopathic, hereditary and congenital alacrima. Prolonged use of medications
like Etodolac and Sulfa-derivative may also cause development of KCS.
Clinical Signs
Thick, adherent mucopurulent discharge, Conjunctivitis, Blepharospasm, Dry, lusterless
corneal appearance, Ulcerative keratitis, Corneal pigmentation, neovascularization, and
keratinization.
Diagnosis
 KCS is diagnosed after consideration of history of previous drug administration,
vaccinations, and surgical procedures. Perform a complete ophthalmic examination in all dogs
presented with clinical signs or disease progression.
Schirmer Tear Test (STT): This test is the gold standard of quantitative KCS diagnosis.
Schirmer tear test 1 (STT1) is performed without application of topical anesthetic agents and
measures both basal and reflex tear production. Normal tear production in dogs is 15-25 mm/min.
SST 2 measures the basal tear production alone and is performed after topical
desensitization of cornea with a topical anaesthetic which help to block the reflex tear production.
Qualitative KCS
The etiology of qualitative tear film deficiency is not completely understood. Chronic
blepharitis with inflammation of meibomian gland can lead to decreased production of the lipid
layer which may promote evaporation of tear film. Infectious causes of blepharitis include
Staphylococcus, Candida, and Malassezia species. Decreased goblet cell density and subsequent
mucin layer deficiency are caused by chronic conjunctival inflammation secondary to infectious
or immune-mediated diseases.
Diagnosis
If qualitative KCS is suspected, perform a STT to rule out quantitative aqueous deficiency.
STT results will be normal in patients with qualitative KCS.
Perform Tear Film Break Up Time (TBUT) to assess for deficiency in the PTF’s mucin
component. Apply 1 drop of fluorescein stain to the eye, hold the eyelids open. Under cobalt-blue
illumination, examine the cornea with an ophthalmoscope or a slit lamp biomicroscope. Note how
many seconds it takes for dark spots to appear as the PTF “breaks up” the fluorescein layer. A
normal TBUT is ≥ 20 seconds. Animals with quantitative tear film deficiencies may often have a
TBUT of < 5 seconds, which indicates an unstable PTF.
Medical management of KCS
Primary medical therapy of both quantitative and qualitative KCS consists of tear
stimulants and tear substitutes. In most patients with KCS, topical therapy is required indefinitely
and clients should be educated about the necessity of lifelong therapy.
Tear Stimulants
1. Cyclosporine A (CsA): Cyclosporine is an immunomodulator that blocks normal production
of interleukin-2, in the lacrimal gland and allows normal production of tears. Cyclosporine also
has an anti-inflammatory action and it decreases corneal pigmentation, normalizes goblet cell
mucin secretion, and stimulates tear production. Topical preparations cyclosporine is effective for
tear stimulation and reducing inflammation. CsA is available as 0.2% ophthalmic ointment and
0.05% eye drops.
2. Tacrolimus: Tough Tacrolimus has a similar mechanism of action; it is more potent compared
to CsA. Tacrolimus is generally available as 0.03% ophthalmic aqueous suspension. Prolonged
treatment may be needed before considering treatment a failure. Tacrolimus not only increase the
tear production, it decreases clinical signs, such as corneal pigmentation associated with chronic
KCS.
3. Pilocarpine: It is a Parasympathomimetic drug which stimulates the parasympathetic nervous
system. It is used to stimulate tear production in cases of neurogenic KCS. It is available as 2%
eye drops.
Tear substitutes
Artificial tear solutions commonly contain 0.1% to 1.4% polyvinyl alcohol. Cellulose-
based solutions/gels and viscoelastic products have slower evaporative loss than artificial tear
solutions. Hydroxypropyl methyl cellulose, Carboxy methyl cellulose and hyaluronate are
examples of cellulose-based solution and viscoelastic products.
Artificial tear formulations containing petrolatum, mineral oil, or lanolin are the most
viscous products and provide long-term lubrication and are best suited for patients with lipid layer
deficiencies and lagophthalmos which promote evaporative tear loss.
A severe, mucopurulent discharge indicate secondary bacterial infection which necessitates
the use of antibiotics. Generally, use a broad-spectrum ophthalmic antibiotic eye drop. Anti-
inflammatory therapy may be useful if the conjunctival inflammation is severe and occluding
lacrimal excretory ducts. Corticosteroids can be used for a short period taking precaution because
dogs with KCS may develop ulcerative keratitis, infection, and keratomalacia. If a patient with
KCS has copious mucopurulent discharge, 5 % N-acetylcysteine is often recommended.
Surgical management of KCS
If there is no response with medical management, surgical treatment for KCS can be
considered. The surgical options are
Parotid duct transposition: The parotid salivary gland duct and papilla are dissected free of the
oral mucosa, mobilized, and transposed to the inferior cul-de-sac. Open and closed methods have
been described.
Labial Salivary gland transplantation: The transplantation of salivary glands to the eye serves
as a substitute for restoring tear volume in patients with severe dry eye disease. The principle
behind this technique is that the lacrimal gland and salivary glands share similar acinar-ductal
organization with only minor differences in the nature of secretions.
Stem cell therapy: The aim of mesenchymal stem cells in the treatment of dry eye is to regenerate
lacrimal gland to repair the corneal, conjunctival, and other damage caused by inflammation, and
to restore tear film stability.

Corneal Ulcers
Corneal ulceration is a break in the corneal epithelium and can have a variety of etiologies,
including trauma, entropion, ocular foreign bodies, and dry eye disease.
Canine Corneal Anatomy and Physiology
The average canine cornea is 0.62 mm thick. It consists of 5 layers: the anterior epithelium,
Basement membrane, the stroma, Descemet’s membrane, and the endothelium. It is covered by
the tear film. The primary role of the tear film is to provide nutrition and oxygen to the cornea.
The corneal epithelium is made of stratified, nonkeratinized squamous cells and its purpose is to
provide a barrier against chemicals, water, and microbes. The epithelium is hydrophobic and
therefore, fluorescein stain does not adhere to it. The stroma is composed of fine, paced collagen
fibers. It is avascular and produces growth factors, extracellular matrix components, and kinases.
The stroma is hydrophilic and therefore, fluorescein stain adheres to it when there is a break in the
epithelium.
Descemet’s membrane is the basement membrane of the posterior epithelium. It is
composed of collagen fibers produced by the endothelial cells that lie below it. Descemet’s
membrane also repels fluorescein stain. An ulcer that completely penetrates the stroma is called a
descemetocele. Descemetoceles are often described as “halos” or “donuts,” as the stroma on the
sides of the ulcer take up stain and the deep center does not.
The endothelium is a single cell layer. It cannot regrow. The endothelium keeps the excess
fluid out of the cornea through sodium–potassium pumps.
Types of Corneal Ulcer
Simple Superficial Ulcers
Simple, uncomplicated ulcers are superficial, only affect the epithelium, and should heal
in 5 to 7 days with or without medical intervention if no complicating factors such as infection or
mechanical irritation are present. Immediately after the injury to the corneal epithelium, epithelial
cells start to migrate to the defect. New cells slide over in a leap frog fashion and as the new
epithelium is loosely attached, an E-collar is recommended until the ulcer heals completely.
Antibiotics and E-collar use should be continued until the cornea is stain negative in FDT.
Stromal Ulcer
As the corneal stroma is well innervated, stromal ulcers can be painful and need systemic
pain medications. Systemic NSAIDs can help with pain as well as any reflex uveitis that may occur
secondary to the ulcer. Topical atropine may also be used to relieve ciliary spasm if reflex uveitis
is present. Usually, one dose is enough.
Descemetoceles and Perforations
Ulcers deep up to Descemet’s membrane are called descemetoceles. When the ulcer
penetrates Descemet’s membrane, the cornea will get perforated. Aqueous humor may leak out
and the hole and may get plugged by either the iris or a fibrin clot. If the eye still has a positive
dazzle response, vision might be able to be saved. Surgical intervention is a must to save the globe.
Disorders Associated with Corneal Ulceration
Entropion, or the inward rolling in of the eyelids, may cause chronic corneal ulceration due to the
eye lashes constantly rubbing the delicate cornea.
Abnormal eyelid hairs such as trichiasis, distichia and ectopic cilia can also cause chronic corneal
ulceration. Distichia are hairs that erupt from the meibomian gland openings along the eyelid
margin.
Tumors of the eyelid may also cause corneal ulceration by constantly rubbing the cornea. Most
canine eyelid masses are benign but continue to grow over time.
Ulcers Due to Chronic Corneal Exposure
Constant corneal exposure due to the inability to close the eye lids completely can lead to
the development of corneal ulcers. Brachycephalic dogs are more prone to corneal ulcers than
breeds with other skull conformations as they are often exophthalmic as well as lagophthalmic.
Ulcers Due to Tear Film Abnormalities
Both qualitative and quantitative tear deficiencies contribute to the development of canine
corneal ulcers. Quantitative tear deficiency, better known as keratoconjunctivitis sicca (KCS), is
more commonly recognized than qualitative tear deficiency.
Spontaneous Chronic Corneal Epithelial Defect
Indolent ulcer and Boxer ulcer are common names for spontaneous chronic corneal
epithelial defect (SCCED). A hyalinized membrane which is formed over the stroma, prevent
epithelial cells from adhering and the ulcer from healing. To allow epithelial cells to adhere, the
membrane must be debrided. These ulcers can be difficult to treat until they are correctly
diagnosed. They will not heal without surgical intervention.

Glaucoma
Glaucoma is a neurodegenerative disease with an elevation in intraocular pressure (IOP).
In clinical practice, glaucoma is caused by drainage disturbances, while cases of increased
production are not recognized.
Production and drainage of aqueous humor
Aqueous humour is transparent fluid produced in the ciliary processes, from where it flows
into the posterior chamber and through the pupil into the anterior chamber. After circulating in the
anterior chamber and supplying the metabolic requirements of the lens and cornea, this fluid exits
the eye through the iridocorneal angle which is spanned by pectinate ligaments. Aqueous humor
may also exit the eye through an unconventional pathway called Uveoscleral pathway.
Classifying glaucoma
Glaucoma may be classified in one of two ways:
 Based on the cause, glaucoma can be classified as primary and secondary. In primary
glaucoma, outflow problems are due to genetic abnormalities in the drainage angle while
secondary is due to another ocular disease.
Glaucoma can also be classified according to the state of the drainage angle as open angle
or narrow or closed angle. Primary glaucoma is extremely rare in cats.
Primary open angle glaucoma
Primary open angle glaucoma (POAG) is an inherited disease commonly seen in beagles,
in which it was shown to be an autosomal recessive disorder. The filtration angle and pectinate
ligaments are normal in dogs with POAG. The disease is chronic in nature, and the IOP increases
slowly over many months or years. Although the dog may be presented with buphthalmos or even
with secondary lens luxation, vision frequently is retained in advanced stages of this disease.
Primary narrow and closed angle glaucoma (Goniodysgenesis)
Here, a developmental abnormality results in the formation of dysplastic pectinate
ligaments, which can be seen as sheets of tissue spanning the drainage angle.
Secondary glaucoma
In the case of secondary glaucoma, IOP rises due to obstruction of aqueous humour outflow
subsequent to another ocular disease, most commonly one of the following:
Lens luxation. Lens in the eye serves as a barrier against forward movement of vitreous. Lens
luxation (whether anterior or posterior) may allow vitreous humor to move into the anterior
chamber and obstruct the outflow. If the lens luxation is anterior, fluid outflow will be further
impeded by the physical presence of the lens in the anterior chamber.
Uveitis. In these patients, the inflammatory material in the anterior chamber can obstruct the
iridocorneal angle. Uveitis can lead to the formation of adhesion between the iris and the lens or
cornea and there by obstructing aqueous humor outflow.
Intraocular tumor. Tumors can cause glaucoma by inducing uveitis. Neoplastic cells can obstruct
the filtration angle, or if the tumor is large enough, it may physically compress the angle.
Diagnosis
Tonometry (measuring IOP)
Normal IOP in canines ranges from 15 to 25 mm Hg. The IOP measurement should be similar in
both eyes. Differences of more than 10 mm Hg between eyes may be suggestive of glaucoma.
Gonioscopy (examining the iridocorneal angle)
It is important to examine the filtration angle to determine the risk of glaucoma in breeds
with goniodysgenesis. Gonioscopy is performed using goniolens that is placed on the cornea. The
lens refracts outgoing light and allows visualization of the entire angle to classify its state.
 In dogs with unilateral glaucoma, the disease may be secondary; or it can be a primary
disease, as one eye is frequently affected before the other. If unilateral primary glaucoma is
suspected, gonioscopy is mandatory.
Clinical signs
Pain. Glaucoma is a painful disease and it may be expressed as blepharospasm or as general
depression.
Buphthalmos. Glaucoma may cause an increase in the size of the globe, resulting from stretching
of the collagen fibers of the cornea and sclera.
Congestion of blood vessels. The eye will appear red due to congestion of episcleral vessels
Corneal pathology. Elevated IOP damages the corneal endothelium, which is responsible for
maintaining corneal dehydration, resulting in edema. Stretching of the corneal fibers due to
buphthalmos may cause rupture of the endothelial basement membrane. These ruptures are called
striate keratopathy and are pathognomonic for glaucoma.
Pupils. In early stages of the disease, the pupil may be dilated slightly with sluggish response. In
advanced stage of glaucoma, the pupils will be dilated and nonresponsive.
Lens. The lens may luxate (or subluxate) due to stretching and tearing of the zonules.
Retina, optic nerve and vision. Glaucoma will cause atrophy of the ganglion cell layer and other
inner retinal layers. The effect of elevated IOP may be seen ophthalmoscopically as cupping of the
optic disc in the retina. Because of the damage to the retina, the patient will suffer progressive or
acute loss of vision, which may lead to complete blindness.
End-stage glaucoma. Subsequent to chronic IOP elevation, the ciliary body may undergo atrophy,
causing decreased aqueous production and lowering of pressure and atrophy of the eye called
phthisis bulbi.
Medical therapy
Osmotic diuretics
These drugs are not used for long-term treatment of glaucoma and they serve for emergency
lowering of IOP in patients with acute attacks. The most commonly used drug in this category is
intravenous mannitol administered slowly at 1 to 2 g/kg over 30 minutes; water is withheld for
three to four hours.
Carbonic anhydrase inhibitors
Carbonic anhydrase is a key enzyme in the production of aqueous humor and, therefore,
its inhibition will result in lower production and decreased IOP. The topical form of the drug like
dorzolamide and brinzolamide is administered twice a day.
Prostaglandin analogues
 These drugs act by increasing the unconventional outflow. These drugs are most effective
in dogs because their effect is independent of the state of the angle. These drugs are ineffective in
cats because cats lack the receptor, and these drugs are contraindicated in all patients with uveitis.
Latanaprost, travaprost and Bimatoprost are administered once or twice a day.
Topical miotics
These drugs increase drainage of aquous humour by opening the iridocorneal angle by the
contraction of the iris and ciliary muscles. The most commonly used drug in this category is
pilocarpine 1% to 4%, applied two to three times a day.
Beta-blockers
Sympatholytic drugs reduce aqueous production by reducing blood flow to the ciliary body.
Drugs in this category include timolol, levobunolol and betaxolol, which are administered once or
twice daily. A preparation containing a combination of timolol and dorzolamide is commercially
available and is very much effective.
Surgical treatment
Surgery to increase aqueous humor to decrease aqueous production through partial
destruction of the ciliary body, using laser or cryotherapy. Trabeculectomy can be performed to
increase the drainage of aquous humour
Patient welfare requires removal of this eye through enucleation. Owners of dogs with
primary glaucoma may be offered to provide a more cosmetic appearance.
References
Herring IP, Pickett JP, Champagne ES, Marini M. Evaluation of aqueous tear production in dogs
following general anesthesia. J. Am. Anim. Hospital Asso. 2000; 36(5):427-430.
Sanchez RF, Mellor D, Mould J. Effects of medetomidine and medetomidine-butorphanol
combination on Schirmer tear test 1 readings in dogs. Vet Ophthalmol 2006; 9(1):33-37.
Martin CL, Kaswan R. Distemper-associated keratoconjunctivitis sicca. J. Am. Anim. Hospital
Asso. 1985; 21(3):355-359.
Westermeyer HD, Ward DA, Abrams K. Breed predisposition to congenital alacrima in dogs. Vet
Ophthalmol 2009; 12(1):1-5.
Morgan RV, Abrams KL. Topical administration of cyclosporine for treatment of
keratoconjunctivitis sicca in dogs. J.Am.Vet. Med. Asso 1991; 199(8):1043-1046.
Berdoulay A, English RV, Nadelstein B. Effect of topical 0.02% tacrolimus aqueous suspension
on tear production in dogs with keratoconjunctivitis sicca. Vet Ophthalmol 2005; 8(4):225-232.
Hendrix DVH, Adkins EA, Ward DA, et al. An investigation comparing the efficacy of topical
ocular application of tacrolimus and cyclosporine in dogs. Vet Med Inter 2011; 2011:487592.
Smith EM, Buyukmihci NC, Faryer TB. Effect of topical pilocarpine treatment on tear production
in dogs. J.Am. Vet. Med. Asso. 1994; 205(9):1286-1289.
Rhodes M, Heinrich C, Featherstone H, et al. Parotid duct transposition in dogs: A retrospective
review of 92 eyes from 1999-2009. Vet Ophthalmol 2012; 15(4):213-222.
Packer RM, Hendricks A, Tivers MS, Burn CC. Impact of facial conformation on canine health:
brachycephalic obstructive airway syndrome. PLoS One 2015;10(10):e0137496.
Maggio F, Bras D. Surgical treatment of canine glaucoma: filtering and end-stage glaucoma
procedures. Vet Clinic North Am Small Animal Pract 2015(6):1261-1282.
Jack, Candyce M., and Patricia M. Watson. Veterinary Technician’s Daily Reference Guide:
Canine and Feline. 2003. 2nd ed., Ames, Iowa, Wiley Blackwell, 2008.
 AVIAN ORTHOPAEDIC SURGERY
Dr. Nihar Jayakar, B. Sc (Micro), B. V. Sc & AH, M. V. Sc.
Pawprints Veterinary Clinic, Mumbai, India

As avian veterinarians, we are often called upon to treat avian orthopaedic

problems. Some occur as the result of trauma (ceiling fan injuries, flying into a
window or mirror, or getting stepped on), others occur from nutritional
imbalances, and others may occur as a result of genetic or developmental
problems. Fortunately, our training in mammalian orthopaedics will give us a
good base for approaching correction of orthopaedic problems, as the main
principles are the same. Most of the orthopaedic techniques developed for
mammals can be applied to birds, taking into account the anatomical differences
in avian species, and whether or not the bird can have flight restored.

Bird patients bring with them a range of challenges, in terms of size,

pneumatised bones,
thin cortices, brittle bones, compound fractures or metabolic bone disease.

The aim of orthopaedic surgery, in any animal, is to attempt to return a ‘broken’

animal to normalfunction. In some cases, this may not be possible, practical, or
even necessary. Injured wild birdsand sporting birds must be returned to normal
function; failure to do so in an injured wild birdwill make release back to the
wild impossible. In comparison, pet parrots do not need to search forfood or
need to fly, and more adventurous techniques can be considered, even though
they may notgive a ‘perfect’ result.

LAME BIRDS

It is uncommon for bruising or a sprain to cause lameness that lasts long enough
for the bird to bebrought to the veterinarian. Only make this diagnosis if you are
sure that other causes of lamenesshave been ruled out. Never jump to
conclusions or think that a single problem is the whole answer.
The bird may have an obvious injury or cause of lameness but always examine
the rest of the bird.Long term captive birds are often nutritionally deficient and
newly imported birds, young birds, orwild birds can be affected by infectious
diseases that can make the bird clumsy and more likely toinjure itself.
Birds will be brought by clients in cages, traveling boxes, jessed and on the fist,
or loose and
unrestrained. However, all birds should be restrained and under control whilst in
the waiting room.

A full clinical history should be obtained:

• Species, breed, sex, and age;
• Length of time in owner's possession, wild caught or captive bred and who
bred thebird, or where it was purchased;
• Diet and housing;
• How did the lameness occur: observed traumatic event, sudden or insidious
onset.
• Sudden onset lameness in a growing bird might still be a reflection of a
long‐standinggrowth problem.
• Record which limb(s) is involved.

Whilst taking a history from the owner watch the bird. Note abnormal behaviour
‐ is the wing
placement normal or does it favour one leg? Owners frequently refer to a bird
having a dropped
wing, this just means that its wing is ‘hanging’ or held in the wrong position
If possible, examine the bird without restraint. This is easy in trained falconry
birds or pet
parrots. Observe the whole bird at rest, as it may not be possible to perform a
full clinical
examination easily.
Catch the bird: use a towel and veterinary common sense. It is vital to avoid
further injury to thelimb. It is a two persons job to examine a conscious bird.
First of all, carry out a general clinical examination to assess the bird’s state of
health. Lie a
bird of prey on its back on a towel and use this to cover the bird's head so that it
cannot see.
Parrots can be held and assessed but usually need a general anaesthetic for a full
examination.
Examine the affected limb and compare with the normal limb. Birds are very
strong and it may not bepossible to ascertain the full extent of the injury. Great
care must be taken not to exacerbate thedamage especially if the limb has a
fracture(s). The signs of a fracture are similar to those inmammals: disability,
deformity, crepitus, swelling.

Pain is usually a less obvious sign.

Also look for:
• Damage to the integument, traumatic or pathological;
• Site of fracture;
• Note whether the fracture is:
• Compound
• Close to a joint or has joint involvement
• How did the fracture occur? Consider trauma, pathological fracture due to
neoplasia,
• metabolic bone disease, osteomyelitis (in particular M avium). If it arose
subsequent to trauma, have other structures also been traumatized? Which bone
is affected? Compound or closed, avian bones have a wide medulla and thin
cortex (in order to minimise weight, in order to maximise flight ability). Avian
bones are brittle, they are surrounded by only a small amount of soft tissue,
hence many fractures are compound. The soft tissues, especially of the wing are
prone to desiccation. If compound, how contaminated or devitalised is the
potential surgical site? Is there significant soft tissue damage? Is nerve and
vascular supply intact? Does the fracture involve a joint or is it close to a joint?
After due consideration, if the case is to be treated, rather than euthanised, the
condition of the bird must be assessed. Many birds which have undergone
sufficient trauma to fracture bones will at the same time have suffered
considerable other soft tissue damage. Pre-anaesthetic screens should be
performed and supportive care administered if appropriate. Fluid imbalances
must be corrected, the patient stabilised, analgesia and antibiotics administered,
prior to surgery.

Are there any neurological deficits? If it cannot move the limb, can it feel the
extremity?
Pinching involving a finger nail will nearly always elicit a response ‐ if it cannot
feel this you
should worry. Some birds do not respond on day 1 so if it cannot feel try again
tomorrow.

Place the bird in a warm, dark cardboard box and, if thin, feed an appropriate,
high‐energy food 30minutes later. Critical Care Formula is good but if the bird is
unwell beware of it refluxing up the oesophagus and down the trachea. If it is
collapsed, an IV bolus of glucose salinewould be better.

Do not perform surgery on injured wild birds for the first 24 hours unless there
are special
reasons. First aid is of greater benefit. A good proportion of injured wild birds
will die in the
first 24 hours due to their illnesses no matter what one does; hasty surgical
interference will
make the numbers greater.

Examination of a conscious bird will allow diagnosis of only a proportion of the

causes of
lameness. It is often possible to diagnose fractures and dislocations but minor
fractures and
injuries to joints and their associated structures can only be assessed by
examining the
unconscious bird.

General anaesthesia and examination of the unconscious and relaxed bird,

followed by radiography ismandatory in all cases where the cause of lameness is
serious, equivocal, and persistent, or wherethere is a fracture or dislocation.

The next step is radiography: whole body ventrodorsal and lateral views, then
specific limb
radiographs. Comparable radiographs of the contralateral limb are often useful if
only to help theowner understand what the normal view looks like. It is also
useful to make a ‘library’ of normalviews of common species which can be used
in a similar manner. Always attempt two views, which maybe difficult for elbow
and carpus. However, there are cases where the bird will have to be heldusing
leadgloves with the radiologist near to the primary beam. Birds with joint
injuries may needradiographs with the joint under strain.

ANATOMY & PHYSIOLOGY

The bones of flighted birds are unique in that they have evolved some pneumatic
bones that are hollow and contribute to the bird being light enough to fly. The
bones of the pelvic girdle, some ribs, the humerus and the femur all are
pneumatic, and contain large air-filled medullary canals that are involved with
the respiratory cycle during flight. The bones of birds are relatively brittle and
have thin cortices. They also contain more calcium than mammalian bone,
which tends to make them more brittle and prone to developing multiple
fractures at one site. The distal portion of the leg, below the tibiotarsus, has very
little soft tissue covering bone, and the proximal half of the humerus also has
little soft tissue covering bone, so fractures in these areas are often open and
comminuted. When a pneumatic bone is fractured, often subcutaneous
emphysema occurs, but it usually resolves within a day, without treatment.

Avian orthopaedic techniques have advanced remarkably over the last years.
Orthopaedic techniques developed for other species have all been proved to be
applicable in avian fracture stabilization. The principles of fracture stabilization
are the same as those defined for mammals. Deciding on a method of fracture
repair will depend on several factors, including what the bird's function will be.
Wild birds destined to be released must be able to fly, catch prey and perch
normally. Breeder birds must have enough limb function to successfully
copulate. Pet birds may do well after limb amputation as a salvage procedure.

Primary or secondary bone healing may occur. Primary bone healing can occur
with rigid stabilization and minimal fracture gap, however most avian fractures
heal by secondary or callus healing. This occurs because of larger fracture gaps
or micromotion across the fracture site. Endosteal callus production provides
major and early support for fracture healing.

Avian bones usually heal faster than mammalian bones. Simple, closed
fractures, such as a midshaft tibiotarsal fracture, when properly splinted, will be
clinically stable within two to three weeks, however a callus may not be visible
radiographically for three to six weeks. If a fracture site feels stable on
palpation, it may be advisable to remove fixation devices, if warranted, even if a
callus is not visible on radiographs.

Non-unions may occur in birds, and the principles for treatment are the same as
for mammals. Other complications may interfere with healing, including
osteomyelitis. Birds with osteomyelitis may not show clinical signs of systemic
disease, however, the white blood cell count is usually elevated. Non-unions
may benefit from autogenous bone grafting.

PRINCIPLES OF FRACTURE REPAIR

In comparison with mammals, the bones of the thoracic and pelvic limbs of
birds are very strong fortheir weight. The structure of the avian bone causes
fracture repair problems that are somewhatdifferent to those encountered in
mammals.

The bones of the pelvic and thoracic limbs are most commonly repaired after
fracture. Fractures maybe simple, greenstick, comminuted or compound; they
are usually caused by trauma but may be causedby infection, neoplasia or
metabolic disease. Therefore all fractures must be assessedradiographically as
well as by clinical examination. It is advisable to radiograph the whole birdas
well as the fracture site. Many injured birds have more than one problem.

The aims of fracture repair are to aid healing by promoting the formation of an
intact, strong
bone, with no involvement with the surrounding structures. These aims are
complicated by a numberof factors:

The rate of healing of avian bone is very rapid, and in wild birds a significant
amount of scar
tissue and bony callus can form in seven to 10 days. This can happen before the
injured wild birdis presented for treatment. Some birds recover with no
intervention.

Many fractures are commuted and the bone has broken into a large number of
splinters that may bedifficult or impossible to reconstruct.

Greenstick and folding fractures are frequently seen at the distal femur, mid
todistal‐tibiotarsus, and mid‐tarsometatarsus, however because they are usually
caused by nutritional
osteodystrophy they are invariably multiple and involve other areas of the body
too. This can causemajor complications. If the fracture is new the bird must have
vitamin D and calcium
supplementation, if possible, for 24‐48 hours prior to surgery.

External immobilisation of the limb above and below the fracture site will
immobilise the joints.In many cases this would allow scar tissue to form around
the joint and permanently reduce theability of the joint to function. Even joints
that are uninvolved with the fracture can be affectedin this manner.
Immobilisation may also allow callus to incorporate other moving tissues,
e.g.flexor tendons in the tarsometatarsal groove or synostosis formation between
the radius and ulna.
Immobilisation of joints must therefore be avoided if at all possible. Robert
Jones bandages areeven more inappropriate for birds than they are for dogs and
cats.
A large number of fractures are compound, especially in injured wild birds. The
protruding bone isusually desiccated and dead. The exposed medullary cavity is
a portal of entry for bacteria, andoccasionally fungi or foreign bodies. The bone
that is dead or going to die must be removed: userongeurs. The medullary cavity
must be picked clean if possible: lavage usually tends to washmaterial deeper
into the cavity where it is trapped by the internal struts. Lavage is
alsocontraindicated in pneumatised bones. Dead tissue surrounding the fracture
site should also bedebrided and irrigated with normal saline.
Purulent material in birds is solid and does not flow; the provision of drainage in
cases where pusis present is ineffective. Repaired compound fractures should be
radiographed weekly during thehealing process and purulent material should be
removed surgically when it forms.

Assessment for fracture repair must take into consideration the future function
of the bird.

APPROACH TO AVIAN ORTHOPAEDIC CASE

This requires initial consideration of the following key factors:

• is it a wild or a captive bird,
• is complete repair and return of normal function possible,
• and what degree of functional disability is acceptable for the species and
individual bird to
live a compassionate future life?

ANALGESIA

Non‐Steroidal Anti‐Inflammatory Drugs are now routinely used to alleviate pain

in veterinary andhuman medicine and surgery.

Carprofen : 2 – 10 mg/kg
Meloxicam : 0.5 – 1 mg/kg
Tramadol : 5 – 30mg/kg

METHODS OF FRACTURE REPAIR

Treatment
The aims should then be to: -
• Treat contaminated or infected wounds.
• Preserve soft tissues, if necessary by applying splints or other dressings. In
view of the
extreme fragility of avian skin, and the small volume of soft tissue, special care
is required
in many cases to prevent desiccation of muscle and tendon tissues.
• To realign fractures or replace luxations.
• To rigidly stabilise the fracture site, preventing any movement or rotation, this
may require
a combination of surgical techniques together with a full understanding of the
husbandry of
the bird, such that it may be properly controlled during its convalescent period.
• Maintain full early function of all joints and tendons.
• Return the limb to full normal function, without adversely affecting the healing
process as
quickly as possible.
• An important point to remember is that wing amputee male birds are highly
unlikely to
ever successfully copulate. Leg amputee birds over 150g, almost inevitably
develop
bumblefoot or arthritis in their remaining foot sooner or later.

SURGERY

It is the author’s experience that all such orthopaedic cases should have surgery
delayed by
24 hours. In the interim, desiccation and further trauma should be prevented.
The bird should bestabilised with fluid therapy, analgesia, antibiosis,
parasiticides if necessary, and nutritional
support.Timing and method should always be considered on an individual cases
basis, decisionswill verydepending on the nature and life style of the bird, let
alone the fracture and the state of theproximate tissues.

CHEMICAL RESTARIN &ANAESTHESIA

Butorphanol :1 mg/kg + Midazolam : 0.5mg/kg IM

Diazepam : 0.05 – 0. 5 mg/kg IV – can be used Intranasally followed by
Isoflurane Gas Anaesthesia @2%
Midazolam : 0.1 – 2 mg/kg IM, IV – cam also used Intranasally @ 2mg/kg
followed by Isoflurane Gas Anaesthesia @2%
Ketamine : 10-25 mg/kg + Acepromazine : 0.5 – 1 mg/kg IM higher end of
doses for birds<250gms
Ketamine : 5 – 30 mg/kg + Diazepam : 0.5-2 mg/kg –IV use lower end of
range.
Ketamine :10- 40 mg/kg + Midazolam 0.2- 4mg/kg SC, IM
Ketamine : 10 – 30 mg/kg + Xylazine 2-6 mg/kg higher end of doses for birds
<250gms

Authur prefers Midazolam+ Isoflurane Combination

METHODS OF FRACTURE REPAIR

Always consider the bird’s welfare and do not attempt surgery unless the
alternate leg can copeduring the recovery phase.

• External coaption (splints, extension splints, bandages etc.)

• Internal fixation (pins, wire, cement, etc), surgical intervention and trauma
should be
minimized.
• External fixation (half or full pin, with lateral stabilising bars).
Case and method selection should be made in consideration of the degree of
perfection that thatspecies requires in order to survive happily in the wild, or if a
captive bird, for it to still be afunctional bird for the owner in relation to its
current or potential future uses.

To prevent scarring and adhesions the limb must be allowed to move as soon as
possible during thehealing period. The fracture must therefore be rigidly
supported but the joints allowed to workfreely. It is useful to keep the birds
restrained by their husbandry rather than by physicalmethods.

There are many factors to consider when choosing a method of fixation to repair
a fracture. The patient's role (pet, breeder, wild bird), the function required of
the injured limb, the type of injury, the location of the injury and the age and
weight of the bird all should be considered when choosing a method of repair.
The anatomy of the injured area should be studied, including review of the
surgical approaches, with special attention paid to the arteries, veins, nerves,
tendons, ligaments and muscles in the area. Fractures to the wing require special
attention, as flight feathers are attached to the periosteum of the ulna and major
metacarpus. If the periosteum is elevated during surgical manipulation, the
follicles may become damaged, resulting in deformed feathers or feather cysts.

Pneumatic bones require special care, as well. During surgery, it is very

important that no fluid be allowed to enter the proximal fracture segment, as this
may result in aspiration pneumonia, air sacculitis or asphyxiation.

If there is any evidence of injury to the skin near a fracture site, the fracture
should be considered open, even if no evidence of infection is present.

Young birds may be presented with healing or healed folding fractures as a

result of nutritional deficiencies, most commonly metabolic bone disease. This
is most often observed in African grey parrot babies, Psittacus
erithacuserithacus, that are from the second, third or fourth clutches of the
breeding season. If the hen is on a nutritionally marginal diet, she will become
depleted of her calcium stores in her bones, and will be unable to pass adequate
calcium to her eggs. As these baby birds grow, their leg bones will not be able to
support their body weight and folding fractures and bowing of long bones may
occur. If a baby bird tries to support itself partially by leaning on a wing, the
wing may also become deformed. Healed fractures in baby birds may be better
off left alone, as significant bone remodeling may occur as weight bearing
occurs, and the leg may be quite functional as is. If tendons are incorporated into
the callus, some loss of mobility of joints distal to the fracture may occur.
However, attempting surgical correction in these cases is often unrewarding and
is unlikely to restore normal mobility. Young, rapidly growing baby birds heal
very quickly, regardless of the method of fixation employed.

EXTERNAL COAPTATION

The use of bandages, splints or slings often work well for fracture fixation, and
is the least expensive way to stabilize fractures. Splints work very well for
tibiotarsal fractures in birds that weigh less than 200 grams, and are particularly
well suited to stabilize fractures in small birds where tiny bones make internal
fixation almost impossible. Splints also are indicated to stabilize fractures due to
metabolic bone disease, since soft bone may not hold internal fixation devices.
Splints can also be used when the risk of anaesthesia or surgical correction is too
great, in certain cases.

Splints can often be applied using manual restraint, if the bones do not need to
be manipulated extensively, although general anaesthesia will allow for greater
muscle relaxation and will prevent pain sensation.

The different techniques for splinting bones of the pelvic and thoracic girdles
have been well described in the avian literature. As in other species, the joints
above and below the fracture must be immobilized for adequate stabilization.
White cloth tape works well for tibiotarsus fractures, however since the hip joint
cannot be immobilized adequately, splints are ineffective for femoral fractures.
In small birds, less than 200 grams, tape alone, crimped after application with a
haemostat along the caudal surface, will be sufficient to immobilize fractures.
Larger birds will benefit by having wooden applicator sticks, tongue depressors,
aluminium rods or other material incorporated into the splint to add support.
SAM splints also work well to make a strong, lightweight support to immobilize
fractures. Splints must be as light in weight as possible. White tape can be used
to immobilize the entire wing, so tape splints work very well for most fractures
of the thoracic limb, especially in the smaller birds. By immobilizing the wing in
its normal anatomical resting position, the bones will usually be pulled into
proper alignment, resulting in adequate healing for most pet birds. Care must be
taken when applying a splint to the body to immobilize the wings, as the
bandage must not prevent normal respiration, nor can it impede normal crop
function.

The use of splints may result in poor alignment, joint ankylosis, tendon
contracture or entrapment within the callus or shortening of the bone may occur.
For pet birds, splinting will often result in adequate fracture repair for those sites
amenable to external coaptation.

INTERNAL FIXATION

When function is of utmost importance, internal fixation will provide the best
chance for proper anatomic alignment. Internal fixation requires general
anaesthesia, so the patient must be stabilized, hydrated and able to withstand the
procedures.

Intramedullary pins are the most common type of internal fixation. Pins do not
counteract rotational forces or shear forces, and the cortices of avian bones are
quite thin so they don't provide much purchase to hold IM pins. Additional
methods of internal fixation may be utilized in addition to the IM pin to help
counteract rotation and shear forces. Cerclage and hemicerclage wires, external
fixators or stack pinning may all be employed. Cross pins may be used to
stabilize metaphyseal fractures.

Orthopaedic wires may be used, especially in small birds, however, they must
not be used as a sole method of fixation because they are not stable against
bending forces.

EXTERNAL SKELETAL FIXATION (ESF)

The Kirschner-Ehmer splint is the most well known ESF, however, many types
of K-E type biphasic fixators have been devised, using acrylic cement columns
in place of the stainless steel connecting bars and clamps utilized by the
Kirschner-Ehmer splint. K-wires, Steinmann pins, hypodermic needles, spinal
needles, threaded fixation pins and half-pins have all been employed to transect
both cortices of the fractured segments of bone. ESF devices are usually well
tolerated by birds, and do not interfere with joint function, which allows for
early return to function. This is very important, especially in birds that are
destined to be released back to the wild. Latex tubing, drinking straws and
Penrose drains may be used to hold pins in place. The hollow tubes are filled
with non-sterile PMM or dental acrylic cement, and the pins are stabilized once
the cement has cured. Hexcelite or epoxy resin may also be used for the
connecting system, especially in small birds. K-wires can also be used for the
connecting system, with each fixation pin glued to the K-wire connecting bar,
using epoxy.

Bone plates can be used in birds, and are best utilized to repair fractures in
ratites or the larger flighted birds. Screws used in conjunction with plates must
be inserted in a different manner than that used in mammals, due to the thin
cortices of avian bone. IM PPM may be used to improve screw purchase in the
bone. Some form of external coaptation must be used for at least 24 hours after
bone plate application to help reduce soft tissue swelling. Plates need not be
removed.

The Doyle technique was developed to apply compression pressure at the

fracture site, which aids in bone healing. This technique combines IM support of
the Rush technique with external fixation. Dental impact rubber bands are used
to apply compression at the fracture site and to improve rotational stability. This
is a lighter system than traditional ESF devices, as K-wires are adequate for
most avian fractures. This technique can also be applied to repair of the beak
and fractures of the mandible, when combined with acrylics.
HYBRIB FIXATOR (ESF-IM tie-in)

As mentioned above, this is the newest and most widely recommended

technique for manyavian fracture cases. Any device inserted should promote
load sharing, as healing progresses, partsof the fixator may be removed, a
process referred to as dynamic destabilization.The technique has been present in
various forms for a number of years. It was refined andfurther developed, as an
answer to providing longitudinal and rotational stability tohumeral fractures,
without having to resort to total wing fixation. With good fixation and
goodoverall vascular condition at the fracture site, healing will often be achieved
in 2.5 - 3.5 weeks.However, on many occasions when vascular function is
impaired, or there is significant traumarelatedtissue damage, full repair may take
several weeks. Loosening of pins should not occur, andthe use of positive profile
pins greatly assists in prevention.In simplistic terms, a single IM pin is placed
along the full length of the bone, but avoidingany damage to or full functioning
of the joints. External fixator pins are then placed in safe sites(to avoid major
blood vessels and nerves or contusion of tissues in subsequent limb
movements),with at least two the other side of the fracture, spread out as far as
possible along the length of thebone. The free end of the IM pin is bent through
90º and attached to a bar which in turn joins withall the external fixator pins,
there by linking IM and ESF.

LUXATION

Luxation usually occur as the result of trauma, and coxofemoralluxation are one
of the more commonly seen injuries. Elbow luxation usually occur in raptors
from trauma during flight. To successfully correct a luxation, reduction should
take place as quickly as possible to minimize the formation of periarticular
fibrosis.

LIMB DEFORMITIES

Baby birds may develop spraddle or splay leg. This may occur as a result of
parents sitting too tightly on the babies, from inadequate substrate in the nestbox
or brooder or as a result of genetic or nutritional problems. As soon as a problem
is discovered, correction should be attempted. Small, heavy bodied babies, such
as rose-breasted cockatoos, tend to develop spraddle leg, and should be placed in
a small, deep container that will keep the legs underneath the baby. Hobbles,
foam saddles, braces, splints and other methods of support may be employed to
correct splay legs. Placing the baby in a deep cup with a rough surface that
allows a foot hold is important. In some cases, the digital flexor tendons may be
displaced, and correction of these cases is more challenging. Osteotomies may
be used in some cases to correct angular bone deformities.

BEAK REPAIR
Birds may suffer from traumatic injury to the beak and underlying structures, or
they may develop mandibular prognathism or lateral deviation of the rhinotheca
(scissors beak), which may be congenital defects. The application of
rhamphorthotic devices, using wire mesh, wires and dental acrylic may be used
to redirect the growth of abnormal beaks. Mandibular fractures may be repaired
using stainless steel wires, mesh splints or dental acrylic. These fractures are
difficult to manage, as osteomyelitis, non-union, tissue avulsion or avascular
necrosis may occur.

Scissor beak
this is a common finding in young macaws, although it can seen in manyspecies.
This condition is easily recognized. The key is that correction must be effected
before thebird’s beak becomes hardened. Initially coping and physiotherapy may
be tried, but if not effectivewithin 14 days, a dental acrylic ramp should be
created. This is fixated on the lower beak, on theside to which the top beak
deviates. In this way, as the beak closes, the top beak hits the ramp andis pushed
back towards the center. Placing any rigid structure on a flexible beak, means
theprosthesis will come off within 10 days, warn the owner of this. Typically, 10
days correction issufficient to resolve the problem.

Bragnathism
this is where the top beak closes inside the lower beak. Again,physiotherapy can
be tried initially. If the problem does not resolve, then an extension will need
tobe created to the tip of the top beak, so that as it closes, the beak is pulled
forward. Again within10 days the beak will correct – so long as correction is
attempted before the beak has becomehardened.

Developmental Problems
Rickets is still common and is always associated with a Ca:P:D3 imbalance. The
bonesaffected will be dependent on the age of the chick at the time of
deficiency. Chicks may hatch andbe deficient. This occurs if the hen laid a
deficient egg, as a result of dietary (or ultraviolet light)deficiency, renal or
parathyroid disease. These chicks are weak, may have a defective
hyoidapparatus, and have swollen epiphysis. Bowing is most often present in the
tibiotarsus at the levelof the fibular crest, although in severe cases, the femur,
ulnar, radius, humerus, ribs and pelvis maybe affected. Cases with marked
clinical signs are generally hopeless. Others may have less severesigns which
may comprise tarsal valgus or varus, tibial head dyschrondoplasia, or
longitudinalrotation around the length of the tibiotarsus.Long bone deviations
should be corrected as soon as possible. When very young and thebones are still
soft, this is best achieved with closely applied aluminium finger splints.
Theseshould be applied under GA. The clinician must be mindful of the very
fast growth rates achievedat this stage of life, and such splints will need to be
changed every 2-3 days. Typically, 1-2 changesare all that are required, as bone
healing is rapid. Growth restriction (through controlled foodintake), Ca & D3
supplementation is crucial. Once splints are applied, the chick must be
restrainedso that undue pressures do not develop at the end of the splint (this is
not uncommon). Youngchicks may be suspended in a plastic box filled with
wood shavings, until such age as they attemptto crawl out of this all the time.
Slinging or suspending a slightly older parrot is another option,although not all
parrots will tolerate this.If a juvenile bird is presented with deviations of long
bones (distal tibiotarsus is one of thecommonest sites), then all bones should be
assessed in relation to their longitudinal alignment andcorrect alignment.
Surgery is typically indicated, but before embarking on this one must assesshow
many bones will require correction, and if any can be performed simultaneously.
One shouldconsider the welfare aspects to the bird of repeated surgeries, the
likely final outcome and the costsbefore one commences.

Xrays of young birds may prove confusing and difficult to interpret. The
epiphysis arecartilagenous, and do not become radiolucent until growth has
stopped at which point theymineralize. The distal tibiotarsus and proximal
tarsometatarsus may look as though they have amammalian growth plate but it is
in fact only the tarsal bones giving this deception.Tarsal varus or valgus, may
also occur after damage to the growth plate of one of themetatarsae, but not the
others. Treatment comprises removal of the damaged cartilage, correctionof the
angulation of the bone and restraint in a cast for 10 days.Osteoarthritis is rare in
birds, usually following chronic inflammatory joint disease causedby untreated
conditions such as femoral head fractures, pins left in joints or developmental /
growthabnormalities. If mal-alignment is present, then one should consider if
this should be corrected.

Metabolic Bone Disease

this is caused by an abnormality in the Ca:P:D3 content of thediet. This may
relate to renal damage of the hen, lack of UV light for the parents, incorrect
diet(too much muscle and no bone in a raptor, or too many pulses and protein in
a psittacines). Thefaster the bird is growing, the more critical is the correct ratio.
At all times grow (especially largelong legged birds) very slowly. If a chick is
presented with MBD, internal fixation is not possibleas the bone is so soft.
Instead, external splints and if necessary slinging the bird, to prevent
weightbearingon legs, can be done, but beware weight-bearing on flexible ribs
with the effect of cardiaccompression. Correct the diet (Ca:P:D3), slow down
the rate of growth and assess the whole body.

Splay leg
This is caused when birds grew up nesting on a smooth surface. If detected
early,using tape hobbles, rearing in a round bottomed bowl, or taping legs inside
a drinking cup, i.e.anything to get the legs back into a biological position, will
effect normality, so long as long bonegrowth has not finished. If the bones have
finished growing, the only option will be multipleosteotomies and de-rotation. In
such cases the bird’s welfare needs to be carefully considered.

BONE HEALING
• In correctly aligned and opposed bones, repair is by endosteal callous.
• If not rigidly fixed, periosteal callous will also form.
• Stable, properly aligned fractures, heal more rapidly than in mammals typically
being fully
stable in 3 - 4 weeks.

PHYSIOTHERAPY

Regardless of the method of repair employed, it is very important that the avian
patient begin some type of physical therapy as soon as possible, to prevent joints
from freezing and loss of range of motion. When a bird is to be re-released into
the wild, the sooner that some exercise can be begun, the better.

Conclusions
Avian orthopaedics present a unique challenge to the avian practitioner, but with
a good knowledge of bone repair techniques in mammals and an understanding
of the anatomical and physiological differences in avian patients, repairs can be
rewarding and successful.

References and Further Reading

BUSH M, MONTALI R J, NOVAK G R, JAMES A E (1976): The healing of
avian fractures. A histologic
xeroradiographic study. J Am Anim Hosp Assoc;12: 768-773.
BENNETT RA. Orthopedic Surgery. In: Altman R B, Clubb S L, Dorrestein G
M, Quesenberry K. eds.
Avian Medicine and Surgery. Saunders, Philadelphia. 1997; 733-766.
CARPENTER, J W (2018). Exotic Animal Formulary, Fifth Edition
COLES B H (1996). Diseases of the Wing. In :Manual of Psittacine Birds. Eds.
N A Forbes, M C Lawton &
P H Beynon. BSAVA. Cheltenham.
HARCOURT-BROWN, N H (1994). Diseases of the Pelvic Limb of Birds of
Prey. FRCVS Thesis. RCVS
Library.
HARCOURT-BROWN, N H (1996). Diseases of the Leg. In :Manual of
Raptors, Pigeons and Waterfowl.
Eds. N A Forbes, N H Harcourt-Brown & P H Beynon. BSAVA, Cheltenham.
HESS, R E (1994). Management of Orthopaedic Problems of the Avian Pelvic
Limb. Seminars in Avian and
Exotic Pet Medicine, 3, 2, 63-72. Saunders. Orlando.
HOWARD, D J AND REDIG, P T (1993). Analysis of avian fracture repair :
implications for captive and
wild birds. Proceedings Association of Avian Veterinarians Annual Conference.
AAV. Lake Worth, Florida.
HOWARD, D J AND REDIG, P T (1994). Orthopaedics of the wing. Seminars
in Avian and Exotic Pet
Medicine. 3, 2 51-62. Saunders. Orlando.
MARTIN, H D, BRUEKER, K A, HERRICK, D D AND SCHERPELZ, J
(1993). Elbow luxations in raptors
: A review of eight cases. In :Raptor Biomedicine. Eds. P T Redig, J E Cooper, J
D Remple, D B Hunter.
University of Minnesota Press. Minneapolis.
OROSZ, S E, ENSLEY P K, HAYNES C J (1992). Avian Surgical Anatomy :
Thoracic and Pelvic Limbs.
Saunders, Philadelphia.
REDIG, P T (1996). Avian Emergencies. In :Manual of Raptors, Pigeons and
Waterfowl. Eds.
N A Forbes, N H Harcourt-Brown and P H Beynon. BSAVA, Cheltenham.
REDIG PT (2000). Trauma-related medical conditions. In :Avian Medicine. J
Samour (ed). Mosby, London.
 Purr-fectly Informed: Navigating Feline Gynaecology
Dr. C. Jayakumar, Ph.D
Associate Professor & Head
Dept. of Animal Reproduction, Gynaecology & Obstetrics,
CVAS, Mannuthy, Kerala Veterinary & Animal Sciences University

Unlike unplanned reproduction, which contributes to the widespread issue of

unwanted cats, deliberate breeding typically produces well-cared for and highly
valued pets. In order to successfully breed cats in a cattery, it is crucial to have
knowledge about the female's reproductive cycle, behavior, and management.
Improper management can often be the sole cause of infertility. When choosing
breeding animals, traits such as health, temperament, and reproductive performance
play a significant role. However, the extensive use of certain popular males has
resulted in a high level of inbreeding in several cat breeds. If there are too few
individuals that meet the requirements for breeding, negative effects associated with
inbreeding may occur. Inbreeding reduces genetic variability and increases
homozygosity, which negatively impacts reproductive performance. Therefore,
breeding should involve not only the "best" individuals but also those that are "good
enough" to maintain genetic diversity within the breed.
Housing of breeding cats
The number of cats in a cattery can differ based on location and breed, but it is
recommended to have an average of three to five intact females per cattery.Larger cat
groups can lead to increased stress among the felines and make it challenging to
control infections.It is advisable for catteries with many cats to maintain smaller
groups of three or four cats to easily manage treatment during disease outbreaks,
while keeping stress levels low.
Seasonality
The cat is known for being seasonally polyoestrous and a long-day breeder,
with the queen cycling during longer day lengths and ceasing cyclicity when the day
length is short.The effect of seasonality diminishes or disappears near the
equator.To induce and maintain cyclicity, the queen needs at least 2 months of
exposure to 14 hours of artificial lighting. However, if the lighting duration is reduced
to 8 hours, cyclicity will stop and the queen will enter an anoestrus period.Unless
interrupted by pregnancy, pseudopregnancy, or illness, queens undergo oestrous
cycles repeatedly during a breeding season. Queens living together may experience
synchronized estrous cycles, with longhair breeds being more affected by daylight
duration compared to shorthair breeds. Insufficient light exposure can lead to irregular
estrous cycles in indoor cats, so breeding catteries should ensure 12 to 14 hours of
daylight or artificial light daily to promote regular cycles.
The queen is an induced ovulator and ovulates after coitus.Spontaneous
ovulation may occur in approximately one-third of cats, and its incidence increases
with body weight.Factors affecting spontaneous ovulation are not clearly known, but
it is more common in cats housed within the visual, olfactory, and auditory presence
of an intact male.In one study, the incidence of spontaneous ovulation was 0-22%
before the addition of a male, compared to 33-57% after a male was housed in a
separate cage within the room.
Puberty
Queens typically experience their first oestrus between 5 and 9 months of age,
although the onset can vary significantly from 3.5 to 18 months due to factors like
breed, season, and body condition. Shorthair breeds tend to reach puberty earlier than
longhair breeds, with Persian and related breeds possibly not experiencing their first
estrus until 18 months or older, and not reaching sexual maturity until 2 to 3 years of
age. The average body weight at puberty is around 2.3 to 3.2 kg, which is
approximately 80% of the adult body weight, with shorthair breeds like Siamese and
Burmese potentially reaching puberty at a lower body weight.
Stages of feline oestrous cycle
The reproductive cycle of a cat can be categorized into proestrus, oestrus, interoestrus,
anoestrus, and dioestrus phases.
Proestrus
Cats commonly do not display proestrus because of its brief duration, usually
less than 24 hours, and subtle behavioral cues. During the proestrus phase, female cats
engage in affectionate behavior by rubbing their head and neck against objects. Some
queens may also experience a minor discharge from their vulva and increased
frequency of urination. Although male cats may show interest in the queen during this
time, she will not be ready for breeding. Proestrus is characterized by follicle growth,
rising oestrogen levels, and thickening of the vaginal epithelium in preparation for
estrus. Vaginal cytology during proestrus shows less than 50% cornified cells, with
predominantly small to large and intermediate cells.
Oestrus
 The duration of oestrus can range from 2 to 19 days, with an average of 5.8 ±
3.3 days. Mating might impact the length of estrus, although conflicting evidence
exists regarding this. A queen in estrus will exhibit specific behaviors such as
crouching with front legs pressed to the ground, back in lordosis position, and tail
turned to one side to present the vulva. Queens in oestrus may roll or thrash on the
floor and vocalize to attract males. They might also display restlessness, poor appetite,
and increased affection towards their caretakers. The behavioral signs of oestrus
typically appear after the start of the oestrous phase. By day 4 and day 6, there is a
gradual increase in the number of queens displaying these signs. If mating happens
before the follicles mature, ovulation is unlikely to take place.
During estrus, vaginal cytology will show an increase in >75% cornified
epithelium, with intermediate cells still visible. Complete cornification, as seen in
dogs, may not reach 100%. The nucleus of cells becomes pyknotic during estrus, but
typically does not disappear entirely. Red blood cells are rarely seen in vaginal
cytology, unless due to mucosal irritation during swab collection. Neutrophils are
uncommon but may briefly appear as the queen transitions into interestrus.
Interoestrus
If ovulation does not occur, the interoestrus phase will follow oestrus in cats,
with an average length of 8-9 days varying among individuals. During interoestrus,
dominant follicles will undergo atresia and oestradiol levels will decrease, leading to a
decrease in vaginal cytology to <50% cornified epithelial cells, mainly containing
parabasal and intermediate cells. However, cornified epithelial cells may still be
present during interoestrus, but will be less than half of all cells. While one set of
follicles is decreasing, the next wave of follicular development is already in progress,
transitioning interoestrus back into oestrus.
Dioestrus
Unlike rabbits, queens vary in the number of copulations needed to induce
sufficient LH release and ovulation. The occurrence of ovulation is influenced by the
number of matings within a short time frame. Most queens will ovulate after four or
more copulations. LH release sufficient to induce ovulation requires several days of
oestradiol priming, typically by the third or fourth day of estrus. Ovulation typically
occurs within 36 hours after mating, if preovulatory follicles are present. All oocytes
are released simultaneously. The queen enters the diestrus phase after ovulation takes
place. During the luteal phase, active corpora lutea are found on the ovaries and the
queen experiences increased levels of progesterone.
Anoestrus
Anoestrus refers to the lack of cycling activity, which can occur naturally
during periods of shorter daylight. The impact of the season on the duration of
anoestrus decreases closer to the equator. It is important to note that individual
variations are quite common in this regard.
Pseudopregnancy
If the queen mates and ovulates without conceiving, it results in
pseudopregnancy lasting around 40-45 days, shorter than a real pregnancy. During
pseudopregnancy, progesterone levels rise and peak like in pregnant queens, but then
decline steadily after day 30 until reaching baseline at around 40-41 days post-mating.
The average time to the next estrus after progesterone decline is 17 days ± 4 days.
Mating with a sterile or subfertile tom can also lead to pseudopregnancy.
Determining whether ovulation happened or not in the Queen
The duration of the non-receptive phase in a queen can indicate her ovulation
status. If the time between heat behaviors is 10 days, it means the queen did not
ovulate. On the other hand, if this period lasts for 40-50 days, it suggests that the
queen ovulated but did not conceive. Another way to determine ovulation is by testing
the queen's serum progesterone levels 5-7 days after mating. If the progesterone level
is below 2.0 ng/ml, it indicates failed ovulation, whereas an elevated level (>2.0 ng/ml)
suggests successful ovulation.
Breeding Management
Before breeding, ensure all animals are current on vaccinations, deworming,
and preventive healthcare. Vaccinations should be given at least 2–3 weeks before
mating, avoiding during breeding and pregnancy. Cats should be separated based on
breeding status: pregnant queens together, nonpregnant queens apart from pregnant
animals, and lactating queens with kittens separated. Queens should be 12–15 months
old before breeding, as fertility declines around 3.5–4 years. When breeding naturally,
take the queen to the tom's location, exposing her during heat or confirmed estrus.
During oestrus, the queen can be introduced to the male for 1-2 days for
mating, followed by separation to determine an accurate queening date. Monitoring
breeding activity is crucial, and if natural heat detection is not possible, the queen can
be left with the male for an extended period, typically at least 2 weeks. Close
observation of the pair for breeding activity or fighting is necessary, and if fighting
occurs, they should be separated for a few days before trying again or until vaginal
cytology indicates oestrus. Behaviors exhibited by the queen post-mating, such as
rolling, rubbing on objects, and grooming the vulvar area, serve to verify successful
intromission. After being together, a serum progesterone concentration >2 ng/ml 3-4
days post-mating can confirm ovulation, allowing the queen to return to her housing.
If the concentration is <2 ng/ml, mating may not have occurred, or the queen was still
in early oestrus with immature follicles. In such cases, the queen should be returned to
the male for another attempt.
Pregnancy
Progesterone levels, produced by the corpora lutea and placenta, sustain
pregnancy but decrease as parturition approaches in cats. Basal levels may not return
until after birth, making progesterone concentrations unreliable for predicting
parturition. Prolactin levels rise around day 35 of pregnancy and play a crucial role in
sustaining the pregnancy by supporting the corpus luteum. Inhibition of prolactin
using a dopamine agonist leads to abortion. Relaxin concentration, secreted by the
fetoplacental unit, rises between days 20-25 of gestation. Starting from day 29, a
relaxin test designed for dogs can be utilized to accurately diagnose pregnancy in cats.
Abdominal palpation is most effective for diagnosing pregnancy between days 21 and
25, but becomes challenging after day 35 when the uterine swellings merge.
Ultrasound is a more commonly used method that can provide information on the
viability of the fetuses. The gestational chambers can be seen from day 10, while fetal
heart activity becomes visible between days 16 and 17. Prediction of parturition in
cats is based on DBP = (ICC [mm] – 62.03)/1.1 and DBP = (BP [mm] – 23.39)/0.47,
where DBP is Days before parturition ICC is Inner chorionic cavity diameter and BP
is Fetal Biparietal Diameter.The level of accuracy is contingent upon the gestation
period, and declines as it approaches its end.
Parturition
The average gestation period for pet cats is around 65 days, with most births
(95-97%) happening between 61 and 70 days, and a range of 57-72 days. The average
length of parturition in is 16.1 ± 14.3 hours, with a range of 4 to 42 hours.
Occasionally, a queen will deliver live healthy kittens over 2 to 3 days, which stresses
the importance of understanding the wide range of normal parturition lengths in this
species before intervening.
Dystocia
Of all causes identified, the most common cause of feline dystocia reported in
the literature is primary uterine inertia. Uterine inertia may be primary (failure to start
synchronous uterine contractions) or secondary (uterine fatigue). Obstructive dystocia
may result from inadequate size of the maternal birth canal due to bony or soft tissue
impingement on the canal, from intrapartum uterine torsion or rupture, or from large
fetal size (often associated with small litter size) or fetal deformity /monstrosity.
Diagnosis of failure to progress while in labor is based on the duration of the first and
second stages of parturition. Because most queens deliver their kittens over a period
of several hours, a 4-hour course of labor before the first kitten and 2-hour course
between kittens should be allowed. Partial expulsion of a fetus is a common problem
experienced by queens during parturition; digital manipulation and delivery following
vaginal lubrication usually are successful. Diagnosis of intrapartum maternal
compromise often is associated with failure to progress in labor when uterine rupture
or uterine torsion is present.
Medical Management
If there is no obstructive cause of dystocia and the dam and fetuses are in good
condition, ecbolic drugs can be used for treatment. Oxytocin can be administered
intramuscularly to increase uterine contractions, with initial doses of 0.1 IU/kg
recommended. For cats, the dosage can be increased up to 0.5-2 IU. Alternatively,
oxytocin can be administered intravenously at lower doses by adding it to intravenous
fluids and giving it slowly. Administration may be repeated after 30 mins, but further
administrations should be avoided to minimize the risk of uterine hyperstimulation
and placental detachment, although this risk is reduced with lower doses.
Administering intravenous 10% calcium gluconate slowly at a rate of 0.2
ml/kg, is an option, but it should be avoided in patients with compromised cardiac
function. Another option is to administer it subcutaneously, diluted in saline.
Hypoglycemia and hypocalcemia are not commonly observed in queens with dystocia.
Medical treatment for dystocia is generally less successful in queens compared to
bitches, achieving success in only about 30% of cases.
Management of Infertile queen
Failure to ovulate despite mating: After a single mating, only half of the cats
may ovulate, and it is possible that multiple matings are necessary for queens to fully
express their ovulatory potential. Not only the number, but also the frequency of
copulations ensure ovulation. Moreover, sufficient oestrogen priming for several days
is essential before copulation can induce an LH surge and ovulation. This is typically
reached 3rd or 4th day of oestrus. A highly effective breeding method includes
breeding the queen three times per day, with a four-hour interval, during the
second and third days of estrus. This protocol has demonstrated a success rate of
inducing ovulation in over 90% of queens. Alternatively, a successful breeding
scheme permits the pair of cats to breed freely for short periods throughout the
initial three days of estrus.
In all infertile queens, blood progesterone concentration is to be measured
after the last observed mating, typically 5-7 days later. If the concentration remains
low (⩽1-2 ng/ml), it indicates that ovulation has not occurred. In such cases,
assistance is required to induce ovulation during the next heat cycle, either through
mechanical or hormonal means. Ovulation can be induced by performing five vaginal
stimulations of 3-5 seconds each, using a regular cotton swab, at 30-minute intervals
during the peak of oestrus. Alternatively, a single injection of hCG@75-100 iU/cat iM
or gonadorelin@25-50 μg/cat iM can be administered on the day the queen is
presented to the male, ensuring successful ovulation induction.
Primary anoestrus: When a female fails to show the first estrus by the age of
24 months, it is referred to as primary anoestrus. It can occur for various reasons, both
internal and external, and it is crucial to thoroughly investigate the history of queens
experiencing this condition. Factors such as housing and husbandry should be taken
into consideration. Lack of social interaction with other cats, inadequate lighting in
the breeding facility, a body weight below 2.3 kg (or higher in larger breeds), or
excessive stress can potentially delay the onset of puberty. Stressors have the potential
to impact ovarian function and disrupt estrous cycles in cats. Common stressors found
in catteries consist of regular exhibition and travel, overcrowding, drastic temperature
changes, and negative social interactions. In order to stimulate puberty, it may be
necessary to improve poor environmental conditions. The use of supplemental
lighting is essential. Additionally, a comprehensive clinical examination is necessary
to rule out any anatomical or genital abnormalities.
Nutrition: Frequently attributed to infertility in cats is nutrition, but the
impact of nutrition may be exaggerated, as most commercial pet foods are adequately
balanced. However, certain nutrients like taurine, arachidonic acid, polyunsaturated
fatty acids, and copper can influence reproductive performance in cats. These
essential nutrients are typically included in commercial feline diets.
Secondary anoestrus: Characterized by extended periods between heat cycles
or irregular estrous cycles, and it is more prevalent in female cats compared to
primary anestrus. It’s to be differentiated from interoestrus in cats by examining
vaginal smears, with anoestrus showing mostly parabasal or intermediate cells, while
cycling queens with silent oestruses will have 20-30% cornified superficial cells.
Reasons for lack of oestrus in adult queens include ovulation without pregnancy
leading to pseudopregnancy, ovarian luteinised cysts, or ovarian tumors secreting
progesterone that blocks the cycle. To address complete anoestrus in a queen, it is
advisable to conduct blood progesterone assays and ultrasound examinations of the
ovaries before attempting to induce oestrus. It is important to regularly assess and
adjust daylight exposure, and it can be advantageous to house anoestrus queens with
those in regular oestrous cycles. It is not typically necessary to use hormonal
induction for estrus in queens. Various protocols utilizing FSH or PMSG have been
outlined for inducing estrus in queens.
CEH-Pyometra is frequently seen in cats that have undergone multiple
instances of spontaneous ovulation or unsuccessful matings, resulting in extended
progesterone secretion and endometrial growth without conception. Incidence is more
common after 7 years of age. The presence of CEH can be easily identified through
the use of ultrasound imaging. Degenerative changes in the uterine tissues associated
with CEH create a favorable environment for uterine infections to develop.
Opportunistic bacteria from the vagina are able to multiply within the uterus as a
result of decreased local immunity. Treatment includes aglepristone at a dosage of 10
mg/kg subcutaneously on days 1, 2, and 7, with a potential fourth dose on day 14 if
needed. Additionally, administer a broad-spectrum antibiotic. Dinoprost at a rate of
0.1 mg/kg, administered subcutaneously every 12 to 24 hours for a duration of 3 to 5
days. And OHE are other options.
Mucometra as a cause of infertility is occasionally encountered with an
excess buildup of mucus secretions from the endometrial glands, reaching up to 500
ml in the uterine cavity, probably, due to congenital defects.The only available choice
is an ovariohysterectomy.
Fibroepithelial hyperplasia, a condition that depends on progesterone,
characterized by the growth of epithelium, myoepithelium, and fibroblasts, leading to
the enlargement of one or more mammary glands. It can occur during pregnancy,
especially in young queens, or in the non-pregnant luteal phase, following ovulation-
inducing treatments or progestin therapy. In fibroadenomatous tissue, there is a
notable expression of IGF-1 and receptors for progesterone and growth hormone. The
severity of the condition varies, with some cases showing mild swellings while others
may progress to mastitis and abscess formation. Diagnosis is typically made based on
history and clinical signs, with the condition often being a one-time occurrence but
can also recur. Aglepristone, a progesterone receptor blocker, is typically
administered at a dose of 10 mg/kg subcutaneously on the first two days of treatment,
followed by weekly administration for a period of 3-4 weeks, which is generally
sufficient. Another treatment option is ovariohysterectomy.
References
Bailin, H.G., Thomas, L., Levy, N.A. 2021. Retrospective evaluation of feline
dystocia: clinicopathologic findings and neonatal outcomes in 35 cases (2009-2020).
JFMS. 24: 344-350
Fontbonne, A. 2022. Infertility in queens- Clinical approach, experiences and
challenges. JFMS. 24: 825–836
Holst, B.S. 2022. Feline breeding and pregnancy management - What is normal and
when to intervene. JFMS. 24: 221–231
Johnson, A.K. 2022. Normal feline reproduction- The Queen. JFMS. 24: 204-211.
Kutzler, M.A. 2007. Estrus induction and synchronization in canids and felids.
Theriogenology, 68: 354-374.
 Challenges in Canine High Risk Pregnancy - The Way Forward
Dr. C. Jayakumar, Ph.D
Associate Professor&Head
Dept. of AnimalReproduction, Gynaecology&Obstetrics,
CVAS, Mannuthy, KeralaVeterinary&AnimalSciencesUniversity

The primary objective of a breeding program is to ensure the birth of healthy

offspring. However, the mortality rate among newborns after normal delivery in dogs can
range from nine to 26 percent, increasing to 30 to 40 percent in cases of complicated
births.The method of delivery significantly influences the mortality rate of newborns in dogs,
with studies showing a rise in mortality following complicated births. This high mortality rate
can have a substantial economic impact on commercial breeding programs.Breeders now aim
for high conception and pregnancy rates, along with increased survival rates of offspring,
surpassing standard parameters. Managing parturition is labor-intensive and can lead to
criticism of veterinary obstetricians due to reduced puppy survival rates.Many veterinary
hospitals lack the resources for continuous monitoring, making it crucial to closely monitor
the health of birthing dogs to detect any potential issues early on. Understanding the
challenges of parturition is essential for effective whelping management.
Dilemma of parturition management
Bitches in the advanced stages of pregnancy, where only the dates of mating are
known, pose a significant challenge and account for the majority of requests for parturition
management. Veterinary obstetricians lack precise and objective timing criteria to safely
intervene in the obstetric care of these bitches.Premature delivery of puppies leads to fatal
outcome for the puppies and potential danger of excessive uterine haemorrhage.
Luteolytic cascade in pregnant dogs
Dogs stand out among domestic species due to their unique reproductive evolution.
When it comes to the regulation of corpus luteum, dogs have distinct mechanisms compared
to other domestic animals.In the dog, the lack of an acute luteolytic mechanism in the
absence of pregnancy results in prolonged regression of the corpus luteum. In contrast to non-
pregnant dogs which lack endogenous PGF2α secretion by the uterus, the utero-placental
unit of pregnant bitches secretes PGF2α that leads to pre-partum luteolysis. It originates
predominantly from the microsomal compartment of foetal trophoblast cells in the placenta,
and triggers contractility of the myometrium and apoptosis of luteal cells.
Gestation length
The gestation period in female dogs typically ranges from 57 to 72 days starting from
the day of breeding. Monitoring serum P4 levels is crucial for identifying the LH surge,
ovulation, and predicting the due date. An increase in serum P4 levels precedes the luteal
phase, with a P4 level >1.5 ng/mL signaling the LH peak. Ovulation usually takes place
around 48-60 hours post-LH peak, leading to a pregnancy duration of approximately 63 days
(62-64 days).
Duration of second stage
The length of the second stage of labor was found to have the greatest impact on the
survival of puppies, regardless of the type of obstetrical assistance provided, with a notable
rise in stillbirth rates as labor extended beyond four hours.Positive outcomes for both the
mother and puppies were observed when labor lasted less than 12 hours, highlighting the
importance of timely obstetrical intervention for puppy survival. Puppies had a significantly
higher chance of survival when obstetrical assistance was initiated within the first 6 hours of
the second stage of labor, emphasizing the critical role of timely medical or surgical
interventions in cases of dystocia for the well-being of both the mother and offspring.
Foetal lung maturity
The short duration of pregnancy in dogs means that fetal growth mainly happens in
the final third of gestation, emphasizing the importance of full fetal maturity before delivery
for survival. Ensuring fetal lung maturity is crucial for the survival of puppies outside the
uterus. Understanding the safe timing for intervention, accurately predicting the delivery date,
and confirming imminent labor in the preparturient period can all aid in effectively managing
the birthing process in dogs.A feature that accounts for more than 60 per cent of neonatal loss
in canines is respiratory distress syndrome (RDS) or hypoxia. The condition is attributed to
impaired surfactant production by type II pneumocytes. Type I and type II pneumocytes
develop in the canalicular phase between 48 and 57 days of pregnancy. The saccular phase,
the phase in which the production of surfactant may occur probably between 57 to 60 days in
the dog. So, from day 58 onwards, dogs could be theoretically ready for extra uterine life.
The alveolar phase occurs during the neonatal period. Foetal maturity in canines was
achieved at 59 days post ovulation in the female foetus and by 60 days in the male foetus.
High risk pregnancies
Some dogs have a higher prevalence of maternal and foetal perinatal morbidity or
mortality than that of the general obstetrical population and are considered to be having high
risk pregnancies. History of previous dystocia and litter loss in previous whelping, advanced
maternal age, stress to the dam or foetus, an unusually long gestation, singleton litters, low
fecundity with three or fewer foetuses, high fecundity with eight or more foetuses, caesarean
section, brachycephalism, pelvic fracture, metabolic disorders, vaginal strictures are factors
contributing to high risk pregnancy. In high risk pregnancies, decision making at parturition
is challenging. Owners with experience of bitches with dystocia and related puppy mortality
demand timeous intervention. Some owners are along distance away from veterinary care and
fear the extended transit time may compromise the litter in case of dystocia. In addition, after-
hour veterinary facilities available to clients may not be adequately equipped to appropriately
deal with dystocia cases or to perform a CS. Enhancing maternal, foetal, and perinatal health,
maintaining lactation, and maximising the survival of pup are the goals of managing high-risk
pregnancies, which includes an elective caesarean section or medical induction of whelping.
In order to ensure successful outcome, it is essential to make sure that the foetus has
accomplished, but not exceeded its required gestational age before delivery.
Parturition induction in the bitch
An optimal protocol should facilitate the birthing process efficiently, maintain a
consistent and predictable timeframe for induction, ensure acceptable expulsion times, inter-
pup intervals, and total whelping duration, have no adverse effects, be safe for both the
mother and her offspring, not interfere with lactation, colostral transfer, placental separation,
uterine involution, future fertility, and be effective across all dog breeds.Dopamine agonists
are not useful for the induction of parturition due to the extended interval and unpredictability
of treatment to onset of parturition.
Antiprogestins
Anti-progestins like mifepristone and aglepristoneare synthetic steroids which bindto
P4 receptors with high affinity, inhibiting P4 from executing its biological effects. Anti-
progestins are useful in various P4-dependent conditions in canines such as pregnancy
termination, induction of whelping as well as the medical treatment of
pyometra.Antiprogestininduced parturition in the dog may or may not require ecbolic
support. If antiprogestins are administered prior to the precursor formation, ecbolic support
will be required and conversely, if administered closer to normal expected parturition date,
none is required. When ecbolic support was required in antiprogestin induced parturition, it
was successfully achieved using either oxytocin almost hourly or prostaglandins once or
twice.
Baan et al. (2005) examined the effectiveness and safety of aglepristone,for inducing
whelping on day 58 of gestation. They found that whelping occurred within a relatively short
and predictable timeframe, with an average of 41 hours (range 32-56 hours) after the first
administration of aglepristone.
Fieni and Gogny (2009) utilized aglepristone to induce whelping on day 60 after the
estimated LH surge and administered oxytocin at regular hourly intervals until the final
puppy was delivered. The combination of oxytocin and aglepristone successfully induced
parturition. Fontbonne et al. (2009) successfully performed whelping induction by
administering aglepristone at a dose of 15 mg/kg body weight on days 59-61 post-estimated
ovulation, followed 24 hours later by subcutaneous administration of oxytocin at a dose of
0.15 IU/kg every two hours.
Abhignya (2014) reported that a combination of mifepristone @ 5mg/kg body
weight twice daily on two consecutive days and natural PGF2α at the dose rate of 0.1mg/kg
body weight twice daily for two consecutive days could induce whelping efficiently.
Jayakumar et al. (2017) reported that oral administration of mifepristone in late
gestation @ 5mg/kg body weight twice daily resulted in induction of whelping between 44
and 49 hours after the first dose of mifepristone with no side effects and pups were relatively
healthy. Anti-progestins were involved in stimulation of ACTH and cortisol production
through partial blocking of the glucocorticoid receptors that triggered foetal lung maturity
and improved the pup survival.
Raheema (2018) stated that combination of oral administration of mifepristone @
5mg/kg body weight (BW) twice daily for two consecutive days, in association with anterior
vaginal administration of 400μg misoprostol, 24 h following the first dose of mifepristone
proved to be a better choice for whelping induction in canine high-risk pregnancy.
Ayana (2023) reported that the incorporation of misoprostol in the mifepristone-
based whelping protocol at four-hour intervals @ 5 mg/kg body weight after onset of cervical
relaxation until completion of whelping enhanced the puppy outcome compared to the
induction protocol without any ecbolics.
Caesarean Section
Cesarean sections are common in small animal practice, with a high percentage of
dystocia cases in dogs requiring surgical intervention, often on an emergency basis.Planned
cesarean sections in dogs are preferred over emergency ones to reduce complications, but
timing is crucial to ensure puppy survival and avoid lung immaturity issues.The criteria for
determining the timing of elective cesarean sections in dogs involves monitoring serum
progesterone levels, which can be challenging due to the need for repetitive measurements
over several days, potentially impacting live birth rates and neonatal survival.
Emergency Caesarean Section
In small animal practice, emergency cesarean sections are frequently performed, with
approximately 60 to 80 percent of dystocia cases in dogs requiring surgical intervention. Out
of all cesarean sections, about 58 percent are done on an emergency basis. However, it is
important to note that emergency cesarean sections pose a significant risk to both the mother
dog and the puppies. Mortality rates can be as high as 20 percent for the puppies and 1
percent for the mother dog, especially in certain breeds such as French Bulldogs, Boston
Terriers, Chihuahuas, and Pugs, which are predisposed to complications. The main cause of
puppy death in these cases is hypoxia, which occurs due to prolonged labor, placental
separation, and difficulties in the birth tract caused by factors like malpresentation and large
litter sizes.
Elective CaesareanSection
In the case of high risk pregnant dogs, a properlyplanned elective CS is considered to
be a safe, effectiveand justified intervention. Planning CS in the dog is crucialbecause early
intervention can lead to reduced puppysurvival due to lung immaturity.
Using the signs of parturition to time elective CS in the bitch is problematic-fetal
distress or -demise may occur in some bitches before the first signs of parturition, resulting in
reduced survival of the offspring in such elective CS. Because the behavioral signs associated
with early stage 1 of parturition may be variable, cervical dilatation offers a reliable and
objective indicator of onset of the first stage of parturition. Cramer and Nothling (2017)
evaluated the temporal relationship between the decrease in the plasma P4 levels and the time
of cervical dilatation (TCD) which correlated to the onset of stage one of parturition in the
preparturient period in the context of planning when to perform elective caesarean sections. If
the P4 level was below 2.73 ng/ml, there was a 99 per cent probability of reaching TCD
within 48 h and if the level was below 1 ng/ml, there was a 100 per cent probability of
reaching TCD within 24 h.
The criteria mooted fordetermining the timing of elective cesarean and
ensuringdelivery of mature puppies was a dip of serum progesteroneto values below 2 ng/ml.
However, theprocedure requires repetitive measurements of serumprogesterone over several
days to identify the decline to 2ng/ml. In a clinical setting, such diagnostic support couldbe
challenging and could lead to foetal distress during thewaiting period resulting in reduced
live birth rate or survivalof the distressed neonates following CS.
 Preparturient CS may reduce the prevalence of parturient fetal demise and stillbirths
in pregnancies destined for CS delivery. The time of day during which CSs are performed
influences the proportion of still born fetuses because a full staff complement during normal
working hours helps maximize puppy survival. These arguments form the basis for planning
elective CS as preparturient CS occurring at a fixed date and time before the onset of
parturient cervical dilatation, in bitches where a CS is unavoidable. Planned preparturient CS
obviates the need for after-hour interventions and allows for timeous delivery of the puppies
potentially reducing the prevalence of fetal compromise and still births.
In conditions when the day of LH surge or ovulation is known, planned cesareans can
be safely performed after Day 63 following the LH surge. Planned C‐section after an accurate
determination of ovulation and using aglepristone as a primer is a safe procedure for bitches
and their offspring. Ovulation was considered to occur when progesterone plasma level was
approximately 6 ng/ml. Levy et al. (2009) reported that elective CS, one to two days before
the expected date of parturition (61 d after ovulation), with previous aglepristone
administration (21.3 ± 1.2 h) was safe for neonates and the dam, provided that ovulation had
been previously determined very accurately. Bonte et al. (2017) administered aglepristone
subcutaneously (15mg/kg bwt) on days 61 to 62 after ovulation and CS was performed 18 h
later. Roos et al. (2018) performed elective CS on day 60, 61 and 62 after ovulation with
aglepristone priming on the previous day. Aglepristone was injected subcutaneously @ 5–15
mg/kg (average of 11.1 mg/kg),in late afternoon in dogs with progesterone value greater than
2 ng/ml and the surgical procedure was performed the following morning (17–19 hr after the
injection).
A decrease in serumprogesterone below 2ng/ml by day 63 post-ovulation wasnot a
prerequisite for safe maternal and neonatal outcomesfollowing elective CS in dogs. A good
neonatal outcome could be obtained with prepartum P4levels between 2.0 to 3.71 ng/ml also.
Identification of type II pneumocytes onlung samples of neonates indicate that foetal lung
maturityis complete by day 63 after ovulation in canine fetuses andelective CS could be
successfully attempted without the aidof any priming agents (Sophia, 2020).
Forseberg (2015) opined that treating pregnant dogs with methylprednisolone or
dexamethasone 0.5, 1 or 2 mg/kg body weight preferably, 24 to 48h or at least 1h pre-surgery
augmented foetal lung maturation.Regazzi (2017) reported that prenatal administration of
betamethasone (0.5 mg/kg b.wt. of betamethasone acetate or phosphate) on day 55 post-
ovulation in canines revealed structural pulmonary maturation and concurrently an
improvement in clinical condition of neonates. Hence favorable neonatal outcome at day 58
could be attributed to betamethasone treatment.
Cramer and Nothling (2019) considered elective CS as ‘parturient’ if performed when
the cervix is open and the bitch is in labour or ‘pre-parturient’ when performed before the
onset of labour, while the cervix is closed and suggested that in high risk pregnant dogs, pre-
parturient caesarean section could be scheduled and safely performed on day 57 after onset of
cytological dioestrus with puppy survival rates of 99 percent.
Conclusion
 High-risk pregnancies in canines present significant challenges that necessitate
careful management to ensure the well-being of both the mother and the
puppies.Veterinary assistance may be required during labor and delivery to address
complications like dystocia, potentially involving medical induction or cesarean
section.Early planning and proactive management are crucial, starting with breeding
management, to increase the likelihood of a successful outcome for both the mother and
her litter.Medical induction of whelping with progesterone receptor antagonists can be a
life-saving measure that reduces risks and complications associated with cesarean
sections.Despite all these arguments in favour of CS for the bitch, the veterinary
obstetrician should only concede to CS where there is a medical emergency or plan
elective CS in only those bitches belonging to an obstetric population with a known
increased obstetric risk relative to bitches in general.
References
Abhignya, K. 2014. A clinical study on induction of parturition in female dogs. M.V.Sc. thesis,
Karnataka Veterinary, Animal and Fisheries Sciences University, Bidar, 93p.
Ayana.C.I. 2023. Induction of whelping with a combination of Progesterone receptor antagonist and
prostaglandin E1 analogue. M.V.Sc thesis, Kerala Veterinary and Animal Sciences
University, Pookode, 164p.
Baan, M., Taverne, M.A.M., de Gier, J., Kooistra, H.S., Kindahl, H., Dieleman, S.J. and Okkens, A.C.
2005. Induction of parturition in the bitch with the progesterone- receptor blocker
aglepristone. Theriogenology. 63:1958–72.
Bonte, T., Del Carro, A., Paquette, J., Charlot Valdieu, A., Buff, S. and Rosset, E. 2017. Foetal
pulmonary maturity in dogs: Estimated from bubble tests in amniotic fluid obtained via
amniocentesis. Reprod. in Domest. Anim. 52: 1025-1029.
Cramer, K.G.M. and Nöthling, J.O. (2019). Curtailing parturitionobservation and performing
preparturientcesareansection in bitches. Theriogenology. 124: 57-64.
Fieni, F. and Gogny, A. 2009. Clinical evaluation of the use of aglepristone associated with oxytocin
to induce parturition in bitch. Reprod. Dom. Anim. 44: 167-169.
Fontbonne, A., Fontaine, E., Levy, X., Bachellerie, R., Bernex, F., Atam‐Kassigadou, S., Guffroy, M.,
Leblond, E. and Briant, E. 2009. Induction of parturition withaglepristone in various sized
bitches of different breeds. Reprod. Domest. Anim. 44: 170-173
Jayakumar, C., Chinnu, A.V., Amritha, A. and Unnikrishnan, M.P. 2017. Challenges in management
of canine high-risk pregnancies with single pup syndrome. Indian J. Canine Pract. 9: 22-26.
Raheema, S. 2018. Induction of whelping in canine high-risk pregnancies with small litter size using
progesterone receptor antagonist and prostaglandins. M.V.Sc thesis, Kerala Veterinary and
Animal Sciences University, Pookode, 104p.
Regazzi, F. M., Silva, L. C. G., Lúcio, C. F., Veiga, G. A. L., Angrimani, D. S. R., Kishi, D. and
Vannucchi, C. I. (2017). Influence of prenatal maternal corticosteroid therapy on clinical and
metabolic features and pulmonary function of preterm newborn puppies. Theriogenology, 97,
179–185.
Roos, J., Maenhoudt, C., Zilberstein L., Mir, F., Borges, P., Furthner, E., Niewiadomska, Z.,
Nudelmann, N. and Fontbonne, A. 2018. Neonatal puppy survival after planned caesarean
section in the bitch using aglepristone as a primer: A retrospective study on 74 cases. Reprod.
Domest. Anim. 53: 85–95.
Sophia X. 2020. Maternal and neonatal outcome following elective caesarean section in dogs based
on progesterone levels. M.V.Sc thesis, Kerala Veterinary and Animal Sciences University,
Pookode, 152p.
 ANGIOTENSIN RECEPTOR - NEPRILYSIN INHIBITORS (ARNIs), A
POTENTIAL GAME CHANGER IN THE MANAGEMENT OF CHRONIC
HEART FAILURE IN DOGS
Dr.K.Jeyaraja, Ph.D.
Professor,
Dept.of Veterinary Clinical Medicine,
Madras Veterinary College, Chennai

Chronic heart failure is a progressive condition seen commonly in dogs due to an

underlying heart disease. Decreased systolic function is well reported in dogs with acquired
cardiac diseases which are often accompanied by diastolic dysfunction also, thus reducing the
contractility of the heart. With ever upgrading therapeutic protocols, prognostic implication
of the therapy for chronic heart failure is being improved. Digoxin was the earlier drug used
in its management however with the introduction of ionodilator, ACE inhibitors, diuretics
combination the condition is being more effectively managed with reversal seen in few cases.
The never-ending quest to improve the quality of treatment has paved light on
Angiotensin Receptor Neprilysin inhibitors (ARNI), a new class of drug. It was approved for
usage by USFDA and few publications till date reported its superiority in the management of
heart failure in human patients when compared to ACE inhibitors and ARB’s alone.
The maladaptive RAAS plays a key role in the pathophysiology of heart failure, and
its blockade with ACE inhibitors or ARBs or mineralocorticoid receptor antagonists (MRA),
alone or in combination has proven efficacy in the reduction of morbidity and mortality
(Ames et al. 2019). In patients with poor cardiac output, the RAAS initially acts as a
compensatory neurohormonal response to increase systemic vascular resistance and blood
volume. The increased production of renin stimulates conversion of angiotensinogen to
angiotensin I, which is converted to angiotensin II by ACE. The cardiovascular effects of
angiotensin II, the major final mediator of RAAS was known to be elicited through
interaction with angiotensin II type 1 (AT1) and angiotensin II type 2 (AT2) receptors
(Lemarie and Schiffrin, 2010). The pathological effects of angiotensin II are thought to be
primarily caused by stimulation of the AT1 receptor, whereas stimulation of the AT2 receptor
is linked to positive effects like decreased cell proliferation, induction of apoptosis, and
vasodilation through increased nitric oxide and bradykinin production. Angiotensin II's
pathogenic effects include vasoconstriction and stimulation of aldosterone secretion, which
results in salt and water retention. In the long term, activation of the RAAS contributes to the
progression of HF through its deleterious effects on cardiac remodeling, particularly left
ventricular hypertrophy and fibrosis, and by a reduction in diuresis and natriuresis,
contributing to volume overload.
The natriuretic peptide (NP) system is another compensatory mechanism activated in
heart failure. There are 3 NPs that play a key role in heart failure: atrial NP (ANP), brain or
B-type NP (BNP), and C-type NP. In heart failure, fluid overload causes increased atrial
pressure, which in turn stimulates the release of ANP from the cardiac atria, (Hori et al.,
2011) and increased filling pressures stimulate the left ventricle to release BNP (Volpe,
2014). These ANP and BNP released from myocardium also has diagnostic importance
(Oyama and Singletary, 2010). These natriuretic peptides increase natriuresis and diuresis,
and prevent cardiac hypertrophy and fibrosis. In addition, NPs also produce direct
vasodilation along with inhibitory effect on RAAS, thereby reducing systemic vascular
resistance and arterial pressure (Volpe et al. 2014). Neprilysin, also known as a neutral
endopeptidase, is the enzyme responsible for the breakdown of these natriuretic peptides and
a variety of other substances, including angiotensin I, angiotensin II, amyloid β protein,
substance P, and bradykinin.
ARNi is a combination of angiotensin receptor blocker sacubitril and neprilysin
inhibitor i.e. valsartan. This combination is designed to address the above mentioned two
pathophysiological process involved in heart failure i.e., activated RAAS and increased
destruction of natriuretic peptides i.e., ANP and BNP.
Sacubitril acts by preventing the breakdown of endogenous vasoactive peptides,
including natriuretic peptides (ANP, BNP, and CNP), thereby enhancing their activity. This
facilitate their sustained action resulting in natriuresis, diuresis, vasodilatation, inhibition of
fibrosis and cardiac remodelling.
Valsartan, an angiotensin receptor blocker effectively decrease vasoconstriction and
aldosterone production, and increase natriuresis by blocking vascular and adrenal AT1
receptors (Mehta, P.K. and Griendling, 2007). This blockade at AT-1 receptor levels also
effectively counteracts the angiotensin produced through alternate pathways. During
angiotensin receptor blockade, angiotensin II (Ang II) concentrations are increased due to
lack of feedback inhibition of renin production, and Ang II may exert favourable or
unfavourable effects through non-AT1 receptors.
Sacubitril if administered alone will result in enhanced angiotensin II levels apart
from natriuretic peptides. This increased angiotensin II if unaddressed will contribute to the
enhanced maladaptive action on the failing heart. Hence, sacubitril will be combined with
ARB valsartan to effectively block angiotensin II at AT-1 receptors.
 Image source: Volpe, 2014.

In canine practice few trials were done on mitral valve disease, cardiorenal syndrome
and all the trials yielded superior results in their management (Sabbah, et al. 2017, Newhard,
et al. 2018) along with significant reduction of aldosterone (Mochel et al. 2019). It was also
found to induce cardiac reverse remodelling and improved metrics of systolic and diastolic
function in heart failure with reduced fractional shortening (Martens et al. 2018).
Paradigm-HF trial conducted by Mc Murray et al. (2014) comparing enalapril with
ARNi in heart failure patients with reduced ejection fraction revealed reduced risk of death
and hospitalisations in patients treated with sacubitril/valsartan. Significant improvement of
left ventricular systolic function along with decreased markers of renal injury was also
reported in experimental cardiorenal syndrome in dogs (Sabbah, et al. 2017).
Sacubitril/Valsartan was also found to reduce urinary aldosterone creatine ratio (Uald:c) with
significant reduction of LA/Ao in dogs with myxomatous mitral valve disease (Newhard, et
al. 2018). The enhanced natriuretic effect produced through ARNi usage and thus improved
hemodynamics will significantly reduce the dose of diuretics needed in the protocol
(Vardeny, et al. 2019). Recent study by Sun et al. 2022 revealed the superior effect of
sacubitril/valsartan in left atrial reverse remodelling in heart failure patients compared with
ACE/ARB’s.
Sacubitril/valsartan also promote higher levels of Ang1-7 peptide and other
alternative angiotensin peptides like Ang1-5 through higher pooling of AT-II (as ACE
inhibition not seen angiotensin II production continues). These alternative peptides are having
potential natriuretic, vasodilatory and cardioprotective effects (Larouche‐Lebel et al. 2021).
Thus apart from blocking the pathophysiological process also promotes beneficial effect of
these peptides.
Recent study in TANUVAS on ARNi in chronic heart failure due to canine dilated
cardiomyopathy revealed its higher efficacy and early resolution of clinical signs as well as
superiority in improving cardiac indices compared to enalapril. Reverse remodelling was also
seen in majority of the cases treated with this drug.
Thus ARNi is a new dimension in the management of chronic heart failure
contributing to early resolution of clinical signs, increased survivability and better cardiac
reverse remodelling. Extensive multicentre studies are recommended to assess its
effectiveness in various other cardiac diseases involving cardiac remodelling and RAAS
activation.

Ref:
1. Ames, M.K., Atkins, C.E. and Pitt, B., 2019. The renin‐angiotensin‐aldosterone
system and its suppression. Journal of veterinary internal medicine, 33(2), pp.363-
382.
2. Hori, Y., Yamano, S., Kanai, K., Hoshi, F., Itoh, N. and Higuchi, S.I., 2011. Clinical
implications of measurement of plasma atrial natriuretic peptide concentration in dogs
with spontaneous heart disease. Journal of the American Veterinary Medical
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 ESSENTIALS OF ANAESTHETIC PRACTICES IN DOGS AND CATS IN THE INDIAN CONTEXT

Dr. S. Senthil Kumar, M.V.Sc., Ph.D., FISVS,

Professor and Head
Department of Veterinary Surgery and Radiology
Veterinary College and Research Institute
Tamil Nadu Veterinary and Animal Sciences University
Salem – 636 112

INTRODUCTION
Anaesthesia is a carefully conducted concerto of medications, meticulously orchestrated
to ensure the safety and comfort of our animal companions during medical interventions.
Anesthesia acts as a compassionate shield, cloaking pets in a temporary slumber, and
safeguarding them from the physical and emotional trauma of procedures. Without the gentle
embrace of anesthesia, the surgical requirements would be excruciating sufferings for pets.
Anesthesia is not a one-size-fits-all melody. Each pet requires a customized score. Age, species,
breed, and individual health factors all influence the anesthetic cocktail. Meticulously tailored
drug combinations and dosages ensure the safety and efficacy of the procedure for each
patient. Anesthesia, though often shrouded in mystery, is a vital pillar of veterinary care. It
allows treating pet patients effectively, alleviating their suffering, and improving their quality of
life. By understanding the importance and appreciation of the skill involved in anaesthesia,
veterinary procedures can be approached with greater confidence, safety and ease. In the
diverse landscape of India, the practice of anaesthesia in small animals presents unique
challenges and opportunities. This lecture aims to explore the essential principles and practices
of anaesthesia, tailored to the specific needs of dogs and cats in the Indian context. By
understanding the nuances of anaesthesia administration, monitoring, and recovery, we can
optimize patient outcomes and enhance the veterinary experience for both animals and their
caregivers.

PREMEDICATION
Premedication is a critical step in preparing dogs and cats for anaesthesia, focusing on
anxiety reduction, smooth induction and recovery, and effective pain management. In India,
where options like morphine or methadone are not routinely used in small animal practice,
alternative agents such as butorphanol and buprenorphine are common choices for opioid
analgesia. For dogs, acepromazine provides sedation and anti-anxiety effects, alongside alpha-2
agonists like xylazine for additional sedation and muscle relaxation. In cats, acepromazine
serves as a sedative, and opioid analgesics like butorphanol and buprenorphine offer pain relief,
with alpha-2 agonists such as dexmedetomidine aiding in sedation and depth of anaesthesia.
Tailoring premedication to the specific requirements of each animal, considering factors like
age, weight, and health status, ensures a safe and effective anaesthetic experience. This
personalized approach minimizes postoperative pain, reduces the risk of emergence delirium,
and supports a smoother recovery process for both canine and feline patients.
COMMONLY USED PREMEDICANTS
Atropine Midazolam
Category: Anticholinergic Category: Benzodiazepine
Dose and Route: Dogs - 0.02-0.04 mg/kg, Dose and Route: Dogs - 0.2-0.4 mg/kg, Cats
Cats - 0.04-0.06 mg/kg, IM, IV - 0.2-0.3 mg/kg, IV, IM
Onset: <5 minutes Duration: 1-2 hours Onset: <5 minutes Duration: 15-60 minutes
Indication: Bradycardia, decrease in Indication: Sedation, anxiolysis
salivation. Contraindications: Respiratory depression
Contraindications: Tachycardia, glaucoma
Acepromazine
Glycopyrrolate Category: Phenothiazine
Category: Anticholinergic Dose and Route: Dogs - 0.01-0.05 mg/kg,
Dose and Route: Dogs - 0.01-0.02 mg/kg, Cats - 0.05-0.1 mg/kg, IM
Cats - 0.005-0.01 mg/kg, IM, IV Onset: 30-60 minutes Duration: 4-8 hours
Onset: <15 minutes Duration: 4-6 hours Indication: Sedation, anti-anxiety
Indication: Bradycardia, decrease in Contraindications: Seizure-prone animals
salivation.
Contraindications: Tachycardia, glaucoma Butorphanol
Category: Opioid Analgesic
Xylazine Dose and Route: Dogs - 0.2-0.4 mg/kg, Cats
Category: Alpha-2 Agonist - 0.2-0.4 mg/kg, IM, IV
Dose and Route: Dogs - 0.5-1.1 mg/kg, Cats Onset: 15-30 minutes Duration: 4-6 hours
- 0.5-1.0 mg/kg, IM Indication: Pain management
Onset: 5-15 minutes Duration: 30-60 Contraindications: None listed
minutes
Indication: Sedation, muscle relaxation Buprenorphine
Contraindications: Cardiovascular disease Category: Opioid Analgesic
Dose and Route: Dogs - 0.01-0.02 mg/kg,
Dexmedetomidine Cats - 0.01-0.02 mg/kg, IM, IV
Category: Alpha-2 Agonist Onset: 30-60 minutes Duration: 6-12 hours
Dose and Route: Dogs - 2-10 mcg/kg, Cats - Indication: Pain management
5-10 mcg/kg, IM Contraindications: Respiratory depression
Onset: 10-15 minutes Duration: 30-120
minutes. Indication: Sedation, analgesia Meloxicam
Contraindications: Cardiovascular disease, Category: NSAID
bradycardia Dose and Route: Dogs - 0.1 mg/kg, Cats
(oral) - 0.05 mg/kg, Cats (SC) - 0.1 mg/kg,
Diazepam SC, PO
Category: Benzodiazepine Onset: 30-60 minutes
Dose and Route: Dogs - 0.2-1 mg/kg, Cats - Duration: 24 hours
0.5-2 mg/kg, IV, IM Indication: Analgesia, anti-inflammatory
Onset: <5 minutes Duration: 15-60 minutes Contraindications: Renal or gastrointestinal
Indication: Sedation, muscle relaxation disease, pregnancy
Contraindications: Respiratory depression
 Drug Dose Body Total quantity Concentration Volume to be
(mg/kg) weight required (mg) available (mg/ml) injected (ml)
(kg)

Atropine 0.02 10 0.2 0.6 0.33

Atropine 0.04 10 0.4 0.6 0.67
Atropine 0.02 10 0.2 1 0.20
Atropine 0.04 10 0.4 1 0.40
Glycopyrrolate 0.01 10 0.1 0.2 0.50
Diazepam 0.1 10 1 5 0.20
Diazepam 0.5 10 5 5 1.00
Midazolam 0.1 10 1 1 1.00
Midazolam 0.5 10 5 1 5.00
Midazolam 0.1 10 1 5 0.20
Midazolam 0.5 10 5 5 1.00
Xylazine 0.5 10 5 20 0.25
Xylazine 1 10 10 20 0.50
Butorphanol 0.1 10 1 1 1.00
Butorphanol 0.2 10 2 1 2.00
Butorphanol 0.1 10 1 2 0.50
Butorphanol 0.2 10 2 2 1.00
Acepromazine 0.04 10 0.4 10 0.04

INDUCTION OF ANAESTHESIA
The induction of anesthesia is a critical step to ensure a smooth transition into
unconsciousness before surgical procedures. Careful consideration must be given to the
animal's health status, age, and breed when selecting agents for induction to minimize risks and
ensure optimal outcomes. In India, commonly used induction agents for dogs and cats include
thiopental, ketamine, propofol, tiletamine zolazepam, and etomidate. Thiopental is known for
its rapid onset and short duration of action, making it suitable for quick induction. Ketamine
provides reliable anesthesia, while propofol offers rapid onset and smooth recovery. Tiletamine
zolazepam provides balanced anesthesia and muscle relaxation, and etomidate is valued for its
cardiovascular stability. Precautions during induction include monitoring vital signs closely,
ensuring proper dosing based on the animal's weight, and being prepared to manage any
potential complications that may arise during the process.
Thiopental
Category: Barbiturate
Dose and Route: Dogs - 10-20 mg/kg, Cats - 5-10 mg/kg, IV
Onset: <30 seconds
Duration: Short
Indication: Rapid induction of anesthesia
Contraindications: Cardiovascular instability

Ketamine
Category: Dissociative Anesthetic
Dose and Route: Dogs - 5-22 mg/kg, Cats - 5-15 mg/kg, IM, IV
Onset: 1-2 minutes
Duration: 10-20 minutes
Indication: Analgesia and anesthesia
Contraindications: Increased intracranial pressure

Propofol
Category: Intravenous Anesthetic
Dose and Route: Dogs - 2-6 mg/kg, Cats - 4-6 mg/kg, IV
Onset: <1 minute
Duration: Short
Indication: Smooth induction and recovery
Contraindications: Respiratory depression

Tiletamine Zolazepam
Category: Dissociative Anesthetic
Dose and Route: Dogs - 5-10 mg/kg, Cats - 3-5 mg/kg, IM
Onset: 2-5 minutes
Duration: 30-60 minutes
Indication: Balanced anesthesia, muscle relaxation
Contraindications: Liver disease

Etomidate
Category: Imidazole Derivative
Dose and Route: Dogs - 0.2-0.4 mg/kg, Cats - 0.2-0.3 mg/kg, IV
Onset: <1 minute
Duration: Short
Indication: Cardiovascular stability during induction
Contraindications: Adrenal insufficiency

Please note that the doses and details provided for premedicants and induction agents
are general guidelines and may vary based on individual animal factors such as weight, health
status, and specific circumstances. It is essential to carefully assess each patient and tailor the
dosing regimen accordingly to ensure safe and effective anesthesia induction.
Drug Dose Body Total quantity Concentration Volume to be
(mg/kg) weight required (mg) available (mg/ml) injected (ml)
(kg)

Ketamine 5 10 50 50 1.00
Ketamine 10 10 100 50 2.00
Propofol 2 10 20 10 2.00
Propofol 4 10 40 10 4.00

TOTAL INTRAVENOUS ANAESTHESIA (TIVA) FOR ANAESTHETIC MAINTENANCE IN DOGS

Total Intravenous Anaesthesia (TIVA) involves the continuous administration of
intravenous drugs to maintain general anaesthesia throughout a surgical procedure. TIVA is
commonly utilized in veterinary practice due to its advantages, including precise control of
anaesthetic depth, rapid recovery, and minimal impact on organ function. Butorphanol
provides analgesia and sedation during TIVA, reducing the requirement for other anaesthetic
agents. It acts on opioid receptors in the central nervous system, producing analgesia and
sedation without causing significant respiratory depression. Lidocaine provide analgesia and
stabilizes cardiac rhythm, reduces the requirement for anaesthetics, minimizing the risk of
cardiac arrhythmias and decreasing anaesthetic-induced myocardial depression. It achieves this
by blocking sodium channels, thereby reducing neuronal excitability and conduction velocity.
Ketamine contributes to anaesthetic maintenance by inducing a dissociative state characterized
by profound analgesia, amnesia, and catalepsy. It acts as an NMDA receptor antagonist,
inhibiting excitatory neurotransmission and producing a dissociative anaesthetic state. The
combination of butorphanol, lidocaine, and ketamine in TIVA provides balanced anaesthesia
with analgesia, sedation, and amnesia while minimizing the need for inhalational anaesthetics
and opioid analgesics. This approach results in smoother recoveries, reduced postoperative
pain, and improved patient outcomes.

BUTORPHANOL
Butorphanol is a synthetic opioid analgesic with sedative properties, commonly used to
provide intraoperative analgesia and reduce the requirement for other anaesthetic agents.
Dosage for TIVA maintenance: 0.1-0.4 mg/kg/hour IV infusion.
 Butorphanol can be administered as a continuous IV infusion diluted in an appropriate
solution, such as saline or lactated Ringer's solution, using an infusion pump to maintain a
constant plasma concentration.

LIDOCAINE
Lidocaine is a local anaesthetic agent with antiarrhythmic properties, commonly used to
stabilize cardiac rhythm and reduce anaesthetic requirements during surgery.
Dosage for TIVA maintenance: 3-6 mg/kg/hour IV infusion. A loading dose of lidocaine
(0.5 to 1 mg/kg) is required to achieve the desired effect.
Lidocaine is administered as a continuous IV infusion diluted in a solution (e.g., saline)
and delivered using an infusion pump to maintain a stable plasma concentration.
KETAMINE
Ketamine is a dissociative anaesthetic agent with analgesic properties, commonly used
to induce and maintain general anaesthesia.
Dosage for TIVA maintenance: 5-15mg/kg/hour IV infusion.
Ketamine is administered as a continuous IV infusion diluted in a solution (e.g., saline)
and delivered using an infusion pump to maintain a stable plasma concentration.

Close monitoring of the patient's vital signs, including heart rate, respiratory rate, blood
pressure, and oxygen saturation, is essential during TIVA to ensure the adequacy of anaesthesia
and detect any adverse effects promptly. Individual patient factors, such as age, breed, health
status, and concurrent medications, should be considered when determining TIVA dosages and
adjusting infusion rates.

ANALGESIC ADJUNCTS
USE OF LOCAL ANAESTHETICS
A simple application of local anesthesia in a testicular block involves injecting a drug
directly into the testicle, allowing it to travel to the spermatic cord. This helps reduce pain
during the procedure and afterward when the cord and associated blood vessels are surgically
manipulated. The amount of anesthesia used can vary, with typically 0.2 to 2.0 ml of 2%
lignocaine administered per testicle, adjusting the dosage based on the size of the dog or cat.
Intraperitoneal lavage with lignocaine is a technique used during ovariohysterectomy (spaying)
in female dogs to desensitize the serosal surfaces within the abdominal cavity, including the
ovarian and uterine tissues.
Lignocaine Dosage: Dogs: 4-6 mg/kg; Cats: 2-4 mg/kg
Dilution: Mix lignocaine with an equal volume of sterile saline.
(Prepare a solution consisting of 2.5 ml of 2% lignocaine and 2.5 ml of saline per 10 kg of
the animal's body weight).
The lignocaine-saline mixture is instilled into the abdominal cavity either immediately
after the abdominal wall is incised or just before abdominal closure. This technique helps
reduce pain and discomfort during and after the surgical procedure, making it more
comfortable for the animal.

SPLASH BLOCK
 A splash block technique involves saturating the surface with bupivacaine before closure
in order to enhance postoperative analgesia. This technique is commonly employed in surgical
procedures to provide extended pain relief in the postoperative period. Bupivacaine is a long-
acting local anesthetic that works by blocking nerve impulses, thereby reducing the sensation of
pain in the affected area.

INHALATION ANAESTHESIA
Inhalation anesthesia involves the administration of volatile anesthetic agents through
the respiratory tract. These agents are rapidly absorbed into the bloodstream and cross the
blood-brain barrier to produce their anaesthetic effects. Inhalation anesthesia is one of the
oldest and most widely used forms of general anesthesia, and it remains a safe and effective
way to induce and maintain anesthesia for a wide range of surgical procedures. Inhalation
anesthesia is an indispensable tool in veterinary practice, playing a crucial role in ensuring the
safety, comfort and successful outcome of more complicated, delicate and time consuming
surgical procedures performed on animals. Nevertheless, while inhalation anesthesia offers a
multitude of advantages, it is not without its intricacies, and several challenges are faced when
administering it. The successful understanding and application of inhalation anesthesia in
veterinary practice require a commitment to continuous learning, collaboration, and adherence
to best practices. With the right knowledge, equipment, and protocols in place, veterinarians
can overcome the intricacies, ensuring the well-being of their animal patients and the success
of their practice. Proficiency in the operation and maintenance of anesthesia machines and
associated equipment is essential for the safe and effective administration of inhalation
anesthesia in animals. Insufficient expertise can lead to complications and in severe cases, it
may jeopardize the animal's life. Regular equipment maintenance is imperative to prevent
breakdowns or malfunctions during procedures involving anesthesia machines and associated
equipment. Familiarity with the anaesthetic machine's built-in safety features, including alarms
and fail-safes, is essential for promptly addressing potential issues. Although anesthesia
machine operation might seem intricate initially, a strong comprehension of its fundamental
principles simplifies the procedure, yielding significant advantages for veterinarians and their
animal patients. This knowledge not only streamlines the inhalant administration but also
improves the surgeon's capacity to perform surgical procedures more efficiently and with
increased ease.

ANESTHETIC MONITORING
Monitoring anesthesia is of paramount importance to ensure the safety and well-being
of the animals undergoing surgical or medical procedures. Comprehensive monitoring involves
assessing various physiological parameters, including heart rate, cardiovascular function,
respiratory function, oxygenation, ventilation and ECG. Monitoring heart rate provides insights
into the cardiovascular status of the patient. Significant changes in heart rate can signal
potential issues such as arrhythmias, cardiac stress, or hypovolemia. Sudden elevation in heart
rate or respiratory rate may indicate inadequate analgesia during surgical intervention.
Continuous monitoring of blood pressure is essential to detect changes in perfusion, which can
indicate inadequate oxygen and nutrient supply to vital organs. Monitoring respiratory rate and
quality helps ensure that the patient is adequately ventilated. Oxygen saturation (SpO2)
monitoring is crucial for assessing the adequacy of oxygen in the blood. A sudden drop in
oxygen saturation can be an early warning sign of respiratory compromise. Capnography
measures the carbon dioxide concentration at the end of each exhalation. It provides
information about the patient's ventilation and helps detect potential issues like airway
obstructions or malpositioned endotracheal tubes. Assess mucous membrane color, which
should be pink and moist, to gauge circulation and oxygenation. Breathing pattern and effort
should be monitored to ensure it is regular and unlabored. Rapid or shallow breathing could
indicate respiratory distress. Muscle relaxation should be assessed and it gives inference on the
adequacy of anaesthetic depth for the surgical intervention. Electrocardiography (ECG) allows
for continuous monitoring of the heart's electrical activity. Detecting arrhythmias or
irregularities is critical to prevent complications. Monitoring helps anesthetists adjust the depth
of anesthesia as needed, avoiding over dosage or under dosage of anesthetic agents. This
ensures that the patient is neither too deeply anesthetized nor inadequately sedated.
Continuous monitoring allows for the early detection of any issues, enabling prompt
intervention. This is crucial in preventing anesthesia-related complications and ensuring patient
safety. Comprehensive monitoring during anaesthesia contributes to safer and more successful
surgical procedures, ultimately leading to better outcomes.

ANESTHETIC RECOVERY
The anesthetic recovery phase is a critical period that requires careful monitoring and
management to ensure the patient's safety and well-being. Anesthetic recovery is a vulnerable
period where dogs and cats are regaining consciousness and control of their bodily functions.
Ensuring a smooth and uneventful recovery is essential for their safety. Continuous monitoring
during recovery allows for early detection of complications or adverse events, enabling
immediate intervention if necessary. Post-operative pain management often begins during the
recovery phase. Proper pain control enhances the dog's comfort and aids in a smoother
transition from anesthesia. Continue to monitor heart rate, respiratory rate, and oxygen
saturation. These parameters provide insights into the dog's cardiovascular and respiratory
function. Hypothermia is a common concern during anesthetic recovery, and preventing it is
crucial for the dog's comfort and recovery process. Dogs are susceptible to hypothermia during
recovery due to the effects of anesthesia. Monitor their body temperature and take steps to
maintain warmth. Ensure that the recovery area is warm. Use heating pads, warm blankets, or
heated cages to maintain a comfortable ambient temperature. The administration of warmed
intravenous fluids helps in maintaining the dog's core body temperature. Covering the dog with
snug, dry blankets or materials designed for insulation minimize the heat loss. Particular focus
should be placed on areas prone to losing heat, like the extremities. Ensure the dog stays dry,
as damp fur can greatly increase heat loss.

CONCLUSION
In conclusion, establishing a robust anaesthetic protocol for dogs and cats is imperative
to uphold the safety and welfare of these animals. Through meticulous selection of
premedication and induction agents, diligent monitoring of vital signs throughout the
anaesthetic period, and attentive postoperative care, veterinary practitioners can effectively
mitigate the inherent risks associated with anaesthesia. By prioritizing these measures, we not
only enhance patient safety but also optimize surgical outcomes, underscoring the critical role
of meticulous anaesthetic management in veterinary practice.
 Lumbar spinal disorders

Dr. S. Ayyappan
Professor and Head ( Retd)
Department of Veterinary surgery and Radiology
Madras Veterinary College
Chennai-7
E mail ID: jujus61@hotmail.com

Abstract
The most common causes of naturally occurring acute spinal cord injury involving the
lumbar spine in the dog are intervertebral disc herniation from degeneration of the
intervertebral discs, and exogenous trauma from road traffic accidents. The neurologic
manifestations of acute spinal cord injury in dogs are dependent upon the region of the spinal
cord affected. Signs may range from neck or back pain to complete paralysis and loss of
autonomic functions such as loss of bowel and bladder control. Currently practiced medical
therapies are aimed at controlling secondary injury mechanism that occur secondary to the
primary cause of the injury. Surgical therapies are aimed at correcting the primary cause of
the injury. Prognosis of the case depends on the severity of injury and the time of
intervention.

Key words: Spinal cord, disc, decompression, myelography, trauma,fracture

Introduction

The ability to initiate and coordinate movement depends on the flow of information
between the brain and the skeletal muscles of the body and limbs. The pathway that unites the
brain and the skeletal muscles is divided into two parts:

* Communication between the brain and the spinal cord (Upper motor neuron).
* Communication between the spinal cord and the skeletal muscles (Lower
motor neuron).

All areas of the spinal cord contain both white and grey matter. However, there are
two areas of the spinal cord grey matter that have specific importance in relation to limb
function. These are called the cervical and lumbar intumescence.

The cervical intumescence is present between C6 and T2. The lumbar intumescence is
present between L4 and S2. This area gives rise to the lower motor neurons to the hindlimbs.

The effect of location of spinal cord injury in the lumbar spine on limb function

Lesion T3-13 L4-S3

Forelimbs Normal Normal
Hindlimbs UMN LMN
Causes of spinal cord dysfunction

The list of possible causes of spinal cord dysfunction is lengthy. These can be broadly
listed using the `DAMNIT' mnemonic degenerative, autoimmune, metabolic, nutritional,
neoplastic, infectious, inflammatory, idiopathic, traumatic and toxic. The majority of spinal
patients present as a result of spinal cord dysfunction arising from intervertebral disc disease
(IVDD).
Pathophysiology
Spinal cord trauma may be direct or indirect. Spinal cord injury secondary to vertebral
fracture may be direct from penetration or tearing of the spinal cord. Other types of vertebral
fracture or intervertebral disc herniation cause indirect trauma by concussive and
compressive injury. Direct trauma and concussion of the spinal cord acutely damages
meninges, blood supply and neural tissue (primary injury). Following primary injury, a
cascade of vascular, biochemical and cellular events results in additional secondary injury to
the cord. Slowly compressive injury mainly results in white matter pathology with lesions
ranging from demyelination to severe malacia.
Clinically, the severity of neurological deficits correlates with the severity of the
spinal cord damage. First loss of conscious proprioception is observed. Then, there is the
progressive loss of motor function, superficial pain and finally deep pain sensation. Patients
also may become incontinent.
Following a severe concussive injury, spinal cord damage may continue in cranial and
caudal direction and results in ascending-descending diffuse myelomalacia. Following a
thoracolumbar disc herniation, this may clinically be characterized by systemic signs of
toxemia, a flaccid abdomen, the level of “cut-off” of the cutaneous trunci reflex response
migrating cranially, a shift from upper motor neuron to lower motor neuron signs in the rear
limbs, progressive involvement of the forelimbs, and eventually respiratory paralysis and
death..

EMERGENCY MANAGEMENT OF SPINAL INJURY

Once the neurological assessment has been made, opioids can be administered as an
analgesic. Methylprednisolone sodium succinate or prednisolone sodium succinate is the
treatment of choice. The protocol is 30 mg/kg IV bolus, followed by a 15 mg/kg holus 2
hours later. Additional 15 mg/kg IV bolus doses are continued every 6 hours for 24 hours.
Starting treatment > 8 hours after spinal trauma is detrimental by causing inhibition of
neuronal sprouting and neuronal glucose uptake. Cimetidine and misoprostol have been used
for treatment of gastric ulceration. However, this treatment remains questionable and is
not recommended.
Decompression usually is accomplished with a hemilaminectomy or a dorsal laminectomy
Herniated disc material and hematoma should be removed to further relieve spinal cord
compression. Durotomy permits evaluation of the cord for myelomalacia and relieves the
intramedullary compression. Irrigation of the spinal cord with normothermic or chilled saline
may protect against sequels of intraoperative spinal cord trauma and decreases the amount of
free radical mediated lipid peroxidation catalysts. The healing of the spinal cord may be
augmented with the application of an oscillating field stimulator.
IVDD:
Hansen type I disk degeneration

Occurs primarily in chondrodystrophic breeds of dogs. Chondroid metaplasia (more

collagen, less, proteoglycans, less water) of the nucleus pulposus and weakening of
the annulus fibrosus begin at 2-9 months of age. The herniated disk material causes
signs of acute, compressive myelopathy. Dogs often show clinical signs of acute disk
herniation at 3-6 years of age.

Hansen type II Disk degeneration

Occurs in nonchondrodystrophic dogs, including large breeds. Fibroid metaplasia

occurs within the disk and leads to protrusion or bulging of the disk. The result is a
chronic, slowly progressive myelopathy in older dogs (5-12 years of age).

Hansen type III

Low volume high velocity disc

Grading system for neurologic signs

Increasing severity with higher number:

Grade 1 - spinal pain; Grade 2 - mild ataxia (proprioception deficits), Grade 3 - severe ataxia,
no weight bearing. Grade4-Loss of deep pain and bladder and faecal control

Clinical signs in a dog with thoracolumbar disk herniation

The forelimbs and cranial nerves are normal. The hind limbs show signs of upper motor
neuron disease. Depending on the severity and chronicity of the herniation, the hind limbs
may be paretic or paralyzed. If ambulatory, the patient is often ataxic and has hyperreflexic
femoral and patellar reflexes. Other signs might include focal hyperpathia along the spine,
bowel or bladder dysfunction, reluctance to jump or climb stairs, crying in pain, and an
arched back (kyphosis).

Common sites for Thoracolumbar disk herniation: T11-12 to L1 - 2

Radiographic findings of intervertebral disk herniation

Narrowing or wedging of an intervertebral disk space, change in shape of the intervertebral

foramen at the site of the herniation, narrowing of the space between facets, mineralized disk
material visible in the spinal canal

Medical therapy for disk herniation

The most important part of medical therapy is strict confinement. Analgesics and anti-
inflammatory medications are often given but may have minimal effect on the disease.

Maintain systemic blood pressure and oxygenation, decompression of the spinal cord, and
stabilization, if indicated. Use hypertonic saline iv
For paralyzed patients, care should include prevention of decubital ulcers

SPINAL FRACTURES/LUXATIONS
Nonsurgical management
Strict cage rest for 4-6 weeks, back braces or body casts, cessation of steroids, use of
analgesics and serial neurologic examinations (determination warrants reevaluation, with or
without surgery).

Surgical techniques for stabilization of vertebral fractures-luxations.

Pins and polymethyl methacrylate, Pins and wires, vertebral body plating, External fixators,
pedicle screw fixation and spinous processes plating

Spinal radiography and myelography

Plain radiography

Plain radiography should always be performed prior to the use of myelography. At

least two views of an area are required to evaluate the radiographic anatomy and thus
visualise the presence or absence of plain radiographic pathology in that area.

Myelography
Myelography is a positive contrast radiographic technique. The contrast agent is introduced
into the subarachnoid space, where it mixes with the cerebrospinal fluid..
Myelography permits the delineation of the following types of lesions affecting the spinal
cord:
*Extradural Compression, Intradural - Extramedullary compression (IDEM) and
Intramedullary compression.

However, MRI remains the gold standard for evaluation of spinal cord disorders

Surgical and non-surgical management outcome

Non-surgical Surgical
management management
Success rate 70% 95%
Recurrence rate 50% <50%
Predictability of recovery Low High
Requirement for confinement Strict confinement for 6 Minimal
weeks or more
Ease of performance of Some techniques may be Safe to perform
physiotherapy hazardous

Spinal surgical techniques can be divided into decompressive and non-decompressive

surgical techniques. It should be noted that a surgical technique might only be described as
decompressive if it removes the compressive mass. Making a hole, however large, in the
spinal canal does not relieve compression on the spinal cord.
TECHNIQUES

1. Fenestration

2. Ventral slot

3. Laminectomy

4. Hemilaminectomy

5. Foramenotomy (mini - hemilaminectomy)

6. Distraction fusion technique

Apart from fenestration, the surgical techniques are named after the route of access to
the spinal canal. The word "lamina" describes the vertebral arch. The suffix "ectomy' means
to cut out or remove. Thus "laminectomy" means to cut out or remove the vertebral arch. If
the lateral part of the lamina (wall”) including the articular facets is removed, this is a
hemilaminectomy. If the dorsal aspect (or the roof) of the lamina is removed, this is a dorsal
laminectomy. If the intervertebral foramen is merely enlarged without removing the articular
facets this is termed a mini-hemilaminectomy or a foramenotomy. The word `fenestration'
comes from the French for window, fenetre, and refers to the surgical technique of cutting a
window in the intervertebral disc in order to remove the nucleus The ventral slot procedure is
used in the treatment of cervical disc disease only.

Spinal surgical equipment

Spinal surgery requires certain specific equipments which is listed below: Rongeurs for
making access to the spinal canal, high - speed air drill and burrs for making access to the
spinal canal through thick bone, periosteal elevator to permit retraction of soft tissues with
minimal haemorrhage and curettes to remove disc material from the spinal canal and from the
spinal canal and from the disc itself.

NURSING THE SPINAL PATIENT

Problems associated with urinary management

This is probably the most problematic nursing challenge. Failure to manage bladder
dysfunction may lead to urine scalding of the skin, cystitis, bladder over - distension (leading
potentially to long - term urinary dysfunction) and inadvertent bladder rupture during manual
expression. Urine `scalding' can be avoided by emptying the bladder two to three times daily.
Manual expression is always preferable to catheterization. The latter has an increased risk of
inducing cystitis as a result of the mechanical irritation of catheterization and the difficulty in
performing the procedure in a completely sterile way.
Problems associated with recumbency
Many spinal patients are temporarily recumbent. This may be paraplegia (hindlimbs
only) or quadriplegia (all four limbs affected). The paraplegic patient may be able to
voluntarily, alter position within certain limits and will be able to sit up unassisted. However,
the quadriplegic patient will be entirely dependent upon assistance for even the most minor
postural changes.
Pressure - related injury
As a result of prolonged focal contact with a non - deforming surface, the local blood
flow to the contact area of skin and the subcutaneous tissues is reduced. Ultimately, if the
contact is unchanged, the skin will die and a non - healing wound will develop. This tends to
occur over bony prominences such as the greater trochanter, acromial processes, lateral
epicondyle of the elbow and stifle and the distal fibula. Pressure sores are much easier to
prevent than they are to treat. There are four main aspects to the prevention of this problem:
Prevent prolonged recumbency in one position, use well - padded bedding, be attentive to
bladder management and groom the patient at least once daily.
Hypostatic pneumonia
This also develops as a result of failing to change the patient's position regularly. It
generally results from prolonged unilateral recumbency. One position should not be
maintained for more than four hours. Coupage or manual percussion of the chest wall with a
cupped hand may reduce the accumulation of airway secretions and may be beneficial in
these patients.
Problems associated with the non - surgical management of high `movement risk'
patients.
All patients with neurological deficits resulting from spinal cord dysfunction will
benefit greatly from physiotherapy and assisted walking. The danger of performing many of
these techniques in dogs with conservatively managed disc disease or spinal fracture will
often preclude their use. In general, the only safe activities for these patients are massage of
the limbs, grooming and passive flexion - extension of the limb joints.

In general, the technique of assisted walking uses a towel or blanket placed under the
abdomen in order to elevate the hindlimbs from the ground or to provide support in the case
of patients that have begun to weight bear on the limbs.
IVD Extrusion IVD Protrusion

Myelographic study showing Extradural compression

Pre and post op imaging –Lumbar vertebral body plating
Pre and post op imaging and intraoperative image of segmental spinal stapling-cat
Pre and post op imaging and intraoperative image of segmental spinal stapling-pup
 LUMBOSACRAL SYNDROME
Dr. S. Ayyappan
Professor & Head (Retd.), Dept of Veterinary Surgery and Radiology,
Madras Veterinary College, Chennai
Correspondence: jujups61@hotmail.com

Lumbosacral syndrome, also known as degenerative lumbosacral stenosis, is a

complex and multifactorial degenerative disease primarily affecting middle-aged to older
large-breed dogs, with a higher incidence in males. This syndrome is characterized by a
variety of clinical signs and is often managed through surgical intervention. This paper aims
to provide an in-depth understanding of lumbosacral syndrome by addressing its anatomy,
causes, clinical manifestations, diagnostic methods, and treatment options.
Learning Objectives:
1. Understanding the Basic Anatomy: To comprehend the anatomical aspects of
lumbosacral syndrome, including the conus medullaris and the cauda equina. This knowledge
is fundamental to understanding the condition's pathophysiology.
2. Recognizing the Causes: Exploring the various factors that contribute to
lumbosacral syndrome, such as lumbosacral stenosis, degenerative changes in the
intervertebral disk and joint, ligamentum flavum hypertrophy, and other structural
abnormalities.
3. Identifying Clinical Signs: Recognizing the clinical signs associated with
lumbosacral syndrome, which can vary in severity. This understanding is crucial for timely
diagnosis and intervention.
4. Learning about Diagnostic Methods: Gaining knowledge of the diagnostic
techniques and tools used to confirm lumbosacral syndrome, ensuring accurate assessment
and differentiation from other conditions.
5. Exploring Treatment Options: Exploring the medical and surgical treatment options
available for managing lumbosacral syndrome, with a focus on improving the quality of life
for affected animals.

Anatomy:
The lumbosacral region is characterized by the termination of the spinal cord, known
as the conus medullaris, and the presence of the cauda equina. The cauda equina comprises
spinal nerves that extend within the lumbar and sacral vertebral canal, specifically ranging
from L7 to the coccygeal nerve roots. Importantly, the vertebral column is longer than the
spinal cord, potentially leading to issues in this region.
Causes:
Lumbosacral syndrome can result from various factors, including:
• Lumbosacral stenosis, characterized by the narrowing of the vertebral canal at the
lumbosacral joint.
• Degenerative changes in the intervertebral disk or joint, leading to structural issues.
• Hypertrophy of the ligamentum flavum.
• Telescoping of S1 into L7.
• The presence of transitional vertebra.
• Hypertrophy of articular processes.
Clinical Signs:
Clinical signs of lumbosacral syndrome can range from mild to severe. Mild signs
may include low back pain, tail elevation, difficulty in sitting and climbing, hyperesthesia,
and pruritus. In more severe cases, clinical signs may manifest as pelvic limb paresis, low tail
carriage, muscle atrophy, fecal and urinary incontinence, self-mutilation,
pseudohyperreflexia, absent hock flexion, and dragging or scuffing of toes.
Diagnosis:
Diagnosis of lumbosacral syndrome involves recognizing transitional vertebra and
various clinical signs associated with the condition. It is crucial to differentiate lumbosacral
syndrome from other conditions, such as hip issues or iliopsoas problems, to ensure accurate
diagnosis.
Conservative treatment of lumbosacral disease

Strict rest with leash walks only for 6-8 weeks. Minimal controlled activity is warranted to
provide physically therapy. Passive and active pelvic limb physical therapy is recommended
for animals with neurologic dysfunction. After the initial 6-8 weeks of limited activity, it is
best to retrain slowly and increase activity over 3-4 months. It is not necessary for animals to
work (jump, climb,), permanent lifestyle restrictions are encouraged

Surgical Approach:
For severe cases of lumbosacral syndrome, surgical intervention is often necessary.
Common surgical procedures include dorsal laminectomy and discectomy, which aim to
decompress the affected area. The choice of surgical approach, whether static (decompression
only) or dynamic (decompression and stabilization), depends on the specific case. Additional
surgical techniques may include LS foraminotomy and distraction fusion.
In conclusion, lumbosacral syndrome is a challenging condition primarily affecting
large-breed dogs. Veterinary professionals must have a thorough understanding of its
anatomy, causes, clinical signs, diagnostic methods, and surgical approaches to effectively
manage and improve the well-being of affected animals. Several references and educational
resources are available to further explore this complex veterinary subject.

Pedicle screw fixation with dorsal hemilaminectomy for a Lumbosacral fracture luxation
MRI of an LS syndrome
 DECODING OF VITAL SIGNS: A COMPREHENSIVE GUIDE TO INTERPRETING HEMATOBIOCHEMICAL
VALUES IN VETERINARY MEDICINE
Dr. Justin Davis K
Assistant Professor
College of Veterinary and Animal Sciences, Mannuthy

In veterinary medicine, haematology serves as a cornerstone of diagnostic evaluation,

offering crucial insights into the health status of animals. The interpretation of laboratory tests in
haematology is paramount, as it forms the basis for understanding an animal's physiological
condition. However, it's essential to acknowledge the inherent variability in laboratory parameters,
necessitating careful interpretation in light of individual patient factors.

Laboratory test results are typically compared to reference ranges established from a population of
healthy animals. It's crucial to recognize that these reference ranges can vary between laboratories
and across different species. Therefore, interpreting haematology results requires diligence and an
appreciation for individual variability.

Haematological analysis is a routine task undertaken by every small animal clinician. It involves
conducting both automated complete blood counts (CBC) and the interpretation of blood smears. By
integrating these results with clinical history, physical examination findings, and biochemical profiles,
clinicians can construct comprehensive differential diagnoses and assess the severity and progression
of disease.

Haematology serves as a valuable diagnostic tool, providing clinicians with essential information to
guide patient management. By analysing parameters such as red blood cell counts, white blood cell
counts, and platelet counts, clinicians can identify abnormalities indicative of various pathologies.

For example, abnormalities in red blood cell parameters may suggest anaemia or polycythaemia,
while deviations in white blood cell counts may indicate infection, inflammation, or neoplastic
processes. Platelet abnormalities can provide insights into haemostatic disorders or underlying
systemic conditions.

Guidelines for Collection and Handling of Blood Samples

Efficient and accurate collection and handling of blood samples are essential for obtaining reliable
haematological results in small animal practice. Here are some important points to consider:

Fasting Period: Whenever possible, fast the animal for at least 12 hours before blood collection.
Lipemia induced by recent meals can lead to haemolysis and compromise sample quality.

Choice of Vein: Preferentially use the jugular vein for blood collection, as it allows rapid and smooth
extraction without the need for repeated suction and release of the syringe plunger. This reduces the
risk of clot formation and haemolysis.

Needle Selection: Use needles of 21 gauge or larger to minimize trauma to blood cells. After
collection, remove the needle from the vein before filling the sample tube to prevent haemolysis.

Avoid Sampling through IV Cannula: Sampling through an IV cannula, especially one through which
IV fluids are administered, can result in sample dilution and compromise accuracy. Additionally,
collapse of the cannula during sampling can hinder rapid collection.
Proper Tube Filling: Fill the EDTA tube to the designated line to ensure optimal anticoagulation.
Overfilling can lead to clot formation, while underfilling may cause crenation of erythrocytes, leading
to inaccurate red blood cell counts.

Sample Mixing: After collection, gently invert the sample tube several times to ensure thorough
mixing of the blood with the anticoagulant. Avoid vigorous shaking, as it can induce hemolysis and
compromise sample integrity.

Identification of Clots: Inspect the sample visually for any visible clots. If clots are present, discard
the sample and collect a fresh one, as results obtained from clotted samples will be inaccurate and
unreliable.

Timely Preparation of Smears: Make fresh blood smears as soon as possible after collection to
minimize changes in cell morphology. Delayed smear preparation can lead to artifacts and distortions
in cell appearance, affecting diagnostic accuracy.

Documentation of Sample Collection: Make a note in the patient's records if the animal struggled
during sampling or if sedation was required. Such information is essential for interpreting any
deviations in haematological parameters and ensuring accurate diagnosis and treatment.

Understanding Red Blood Cell Parameters: Quantitative and Qualitative Aspects

Red blood cell (RBC) parameters in the complete blood count (CBC) provide vital information about
the quantity and quality of erythrocytes circulating in the bloodstream. These parameters,
encompassing both quantitative and qualitative aspects, are essential for diagnosing and managing
haematological disorders effectively.

Quantitative Parameters

Red Blood Cell Count (RBC): This quantitative parameter measures the total number of red blood
cells per liter of blood (x 10^12 /L). A decrease in RBC count often indicates anaemia, while an
increase may suggest polycythaemia or dehydration.

Packed Cell Volume (PCV) or Hematocrit (Hct): PCV represents the percentage of blood volume
occupied by RBCs in whole blood. It offers insights into the erythrocyte mass and oxygen-carrying
capacity. Decreased PCV levels are indicative of anaemia, while elevated levels may indicate
haemoconcentration or polycythaemia.

Haemoglobin (Hb):Haemoglobin concentration in blood, measured in grams per liter (g/L or g/dL),
reflects the oxygen-carrying capacity of RBCs. Similar to RBC count and PCV, decreased haemoglobin
levels are associated with anaemia, while increased levels may suggest polycythaemia or
dehydration.

Qualitative Parameters

Mean Cell Volume (MCV): MCV represents the average volume of individual RBCs and is measured in
femtoliters (fl). It serves as a qualitative parameter indicating the size of erythrocytes. Abnormalities
in MCV can classify anaemias as microcytic, normocytic, or macrocytic.

Mean Corpuscular Hemoglobin (MCH): MCH measures the average amount of haemoglobin per RBC
and is expressed in picograms (pg). It provides qualitative information about the haemoglobin
content of individual cells, influencing their colour and staining properties.
Mean Corpuscular Haemoglobin Concentration (MCHC): MCHC reflects the average concentration of
haemoglobin within RBCs and is expressed in grams per liter (g/L or g/dL). Changes in MCHC levels
can indicate alterations in cellular haemoglobin content, affecting the staining characteristics of
RBCs.

Understanding Red Blood Cell Quantity: Causes and Considerations

Red blood cell (RBC) quantity, reflected in parameters such as RBC count, packed cell volume (PCV),
and haemoglobin concentration, plays a crucial role in assessing the haematological status of
animals. An understanding of the factors influencing RBC quantity, both decreases and increases, is
essential for accurate diagnosis and effective management of haematological disorders.

Reduced RBC Quantity:

Causes:

1. Anaemia: Anemia, a common condition, results from various underlying etiologies such as blood
loss, decreased production, or increased destruction of RBCs.

2. Haemolytic Anaemia: This condition involves the accelerated destruction of RBCs, leading to a
decrease in their quantity within the circulation.

3. Haemolysis due to Poor Handling: Mishandling of blood samples during collection, processing, or
storage can induce haemolysis, resulting in reduced RBC counts.

4. General Anaesthesia (GA) or Sedation: Splenic engorgement, often observed during GA or

sedation, can sequester RBCs, leading to a decrease in their circulating levels.

5. Late Pregnancies: Physiological changes during late pregnancies, including haemodilution and
increased RBC destruction, can contribute to reduced RBC quantity.

Errors:

1. Excessive EDTA from Underfilled Tube: Inadequate filling of EDTA tubes can lead to improper
anticoagulant-to-blood ratio, affecting RBC morphology and count.

2. Dilution from IV Drip: Intravenous fluids administered improperly or excessively can dilute blood
samples, resulting in falsely reduced RBC counts.

3. Clots in Sample: Presence of clots in blood samples can interfere with accurate RBC counting,
necessitating sample rejection and recollection.

4. Inaccurate Hematology Machine: Calibration issues or use of equipment calibrated for human
samples can lead to inaccuracies in RBC quantification.

Increased RBC Quantity:

Causes:

1. Dehydration: Fluid loss due to dehydration results in haemoconcentration, leading to increased

RBC counts and PCV values.

2. Physiological Haemoconcentration: Stress, fear, and exertion can trigger a transient increase in
RBC count as part of the body's adaptive response.
3. Secondary Polycythaemia: Conditions such as hypoxia, congenital cardiovascular abnormalities,
renal neoplasia, hyperthyroidism, or residence at high altitudes can stimulate erythropoiesis,
resulting in secondary polycythaemia.

4. Primary Polycythaemia: Polycythaemia rubra vera, a rare myeloproliferative disorder, involves

abnormal proliferation of erythroid precursors, leading to primary polycythaemia.

Errors:

1. Evaporation: Improper sealing or storage of blood samples can result in evaporation, leading to
falsely increased RBC counts.

2. Note: Certain breeds, such as Greyhounds, may exhibit naturally higher PCV and RBC counts,
which should be considered during interpretation.

Understanding Mean Cell Volume (MCV) and Associated Conditions

Mean Cell Volume (MCV) is a crucial parameter in hematological analysis, providing valuable insights
into the size of red blood cells (RBCs). Variations in MCV, whether increased or decreased, can
indicate underlying conditions affecting erythropoiesis or RBC morphology. Here, we delve into the
significance of MCV alterations and the conditions associated with them.

Terminology:

• Normal MCV: Represents normocytosis, indicating a typical average volume of RBCs.

• Increased MCV: Characterized by macrocytosis, wherein RBCs exhibit larger than normal
volume.
• Decreased MCV: Indicates microcytosis, wherein RBCs are smaller than normal in size.

Macrocytosis:

Macrocytosis, often observed in regenerative anaemia, occurs when reticulocytes, which are larger
than mature RBCs, are abundant in the circulation. However, macrocytosis may not always accurately
reflect regeneration, as marked regeneration is required before MCV is affected. Hence, other
indicators like red cell distribution width and reticulocyte counts are more sensitive markers of
regeneration.

Causes of Macrocytosis:

• Regenerative Anemia: Typically seen due to increased production of larger reticulocytes.

• FeLV: Feline leukemia virus infection may lead to macrocytosis.
• Youth: Neonates may exhibit transient macrocytosis, which normalizes by around two
months of age.
• Familial Macrocytosis: Certain breeds, such as miniature or toy poodles, may have genetic
predispositions to macrocytosis.
• Stomatocytosis: Specific breed-related conditions like stomatocytosis in miniature
schnauzers or malamutes can cause macrocytosis.
• B12/Folate Deficiency: Rarely, deficiencies in vitamin B12 or folate, sometimes triggered by
medications like trimethoprim sulphonamide, can lead to macrocytosis.

Errors Associated with Macrocytosis:

 • Old Sample: Prolonged contact with EDTA in blood samples can cause cells to swell, resulting
in falsely increased MCV.
• Agglutination: Agglutinated cells may be counted as single cells, leading to erroneous MCV
measurements.
• Large Platelets or WBC Counted as RBC: In severe anemia, large platelets or white blood cells
(WBCs) may be mistaken for RBCs, affecting MCV determination.

Microcytosis:

Microcytosis, characterized by smaller than normal RBC size, is commonly associated with conditions
such as iron deficiency or disorders affecting iron metabolism.

Causes of Microcytosis:

• Iron Deficiency: Chronic hemorrhage or inadequate iron intake, particularly in young animals,
can result in microcytosis.
• Congenital and Acquired Portosystemic Shunts: Liver conditions affecting iron metabolism
can lead to microcytosis.
• Familial Microcytosis: Certain breeds, such as Akitas, may have genetic predispositions to
microcytosis.
• Familial Dyserythropoiesis: Genetic disorders like familial dyserythropoiesis in breeds like
English springer spaniels can cause microcytosis.

Errors Associated with Microcytosis:

Red Cell Crenation: Underfilled tubes containing excess EDTA can lead to crenation of RBCs, affecting
MCV measurements.

Hypertonic Fluid: Conditions like azotemia, hyperglycemia, or hypernatremia can alter RBC
morphology, leading to erroneous microcytosis.

RBC Fragments or Platelets Counted as RBC: Presence of RBC fragments or platelets in the sample
may interfere with accurate MCV determination.

Understanding Red Cell Distribution Width (RDW) in Haematology

Red Cell Distribution Width (RDW) is a critical parameter used in hematological analysis to quantify
the variability in the size of red blood cells (RBCs). RDW provides valuable insights into the
heterogeneity of RBC sizes within a blood sample, which can be indicative of various underlying
conditions.

RDW offers a quantitative description of the variation in the size of RBCs present in a blood
sample. It is calculated based on the width of the distribution curve of RBC volumes
measured during haematological analysis. A higher RDW value indicates greater variability in
RBC size, while a lower value suggests more uniformity in RBC size distribution.

Mean Cell Haemoglobin (MCH) and Mean Cell Haemoglobin Concentration

(MCHC)
MCH is calculated as the mass of haemoglobin per average red cell irrespective of the
cell size. (Usually expressed in pg)

MCHC is more useful as it describes the average concentration of haemoglobin per red
cell. It is calculated from the PCV rather than the RCC and therefore takes into account
red cell size (usually expressed in g/dl). We will therefore only consider the MCHC.

Normal MCHC = Normochromasia

Reduced MCHC = Hypochromasia

Hyperchromasia – meaning increased MCHC is a rarely used term because in the vast
majority of cases elevated MCHC is the result of poor sample handling and haemolysis
in vitro. It is therefore usually an artefact. Lipaemia or icterus (or oxyglobin) can elevate
the MCHC. Rarely, very large numbers of spherocytes (in immune mediated haemolytic
anaemia) can elevate the MCHC (because they are small cells which have lost part of the
cell membrane but no haemoglobin )

Causes of Hypochromasia

• Regenerative Anaemia - most common

• Iron deficiency or inefficient iron use
• Rarely – other dietary deficiencies – protein, VitB6 (pyridoxine), copper
• Age – low at birth but normal by 5-6months
• Stomatocytosis (Alaskan Malamute)

Therefore genuine macrocytic hypochromic anaemia is most likely to

be regenerativewhereas genuine microcytic hypochromic anaemia is most likely to
result from iron deficiency.

White Blood Cells (WBC)

The CBC gives an absolute WBC and a differential count. The differential count is
usually expressed as a percentage of leucocytes counted and also as an absolute count of
each cell line. Always base your interpretation of results on the absolute counts. Using
the percentages can cause unnecessary confusion.

Leucocytosis (Increased WCC)

Doesn’t always mean infection! Obviously we will already have looked at the patient and
taken a history which helps us put the list in order of likelihood – A pot-bellied, thin-
skinned, polydipsic middle-aged dog points us in a different direction from a puppy with
persistent pyrexia.

Results from:

• Inflammation - examples of underlying diseases include infection, immune

mediated disease (such as immune mediated haemolytic anaemia), trauma, tissue
necrosis.
 • Epinephrine/Adrenaline induced – fear, stress, struggling on sampling,
exercise.
• Steroid induced- iatrogenic (exogenous glucocorticoids such as prednisolone),
hyperadrenocorticism, stress (any sick animal could potentially produce a ‘stress
leucogram’)
• Neoplasia- tumours cause elevated WBC in a number of ways: (i) Tissue
necrosis- can cause an inflammatory response. (ii)Paraneoplastic response – for
example tumours secreting G-CSF (granulocyte colony stimulating factor) cause a
marked neutrophilia. (iii) Neoplastic transformation of precursors and
uncontrolled production of WBC (leukaemias)
• Immune dysfunction – if WBCs do not function properly more are produced in
an attempt to compensate and control infection.

Orders of magnitude:

1. Neutrophil counts above 30x109/l are not likely to be the result of adrenaline or
steroids alone – look for inflammation, neoplasia or immune dysfunction.
2. Adrenaline induced leucocytosis does not usually exceed 15x109/l in dogs or
20x109/l in cats
3. Extreme WBC counts (100x109/l) are most likely to result from leukaemia

Neutrophils (PMNs)

In general a neutrophilia results from movement of neutrophils into the circulation. This
can result from increased production of neutrophils or from their redistribution.
Neutropenia results from shifting of neutrophils into tissues or reduced production by
the bone marrow.

Left Shiftis an increase in the numbers of immature neutrophils in the circulation. In the
acute phase of inflammation neutrophils leave the circulation and enter affected tissue
(the tissue pool gets bigger). Neutrophils are released from the storage pool in response
to the increased demand and this causes a ‘left shift’ which is an increase in the numbers
of immature neutrophils in the circulation. There is also an increase in mitosis in the
marrow producing more immature neutrophils. These are called band cells and are
recognized by the lack of segmentation of their nuclei.

Regenerative Left Shiftis an increase in the numbers of immature neutrophils in the

circulation, but mature cells still outnumber the immatures.If new neutrophils enter the
circulation more rapidly than they exit into the tissues then a neutrophilia with
a regenerative left shiftresults. Both mature neutrophils and band neutrophils are
increased, but the mature cells outnumber the bands. This is a good thing. It means that
the marrow has had time to respond and most cells being released are adequately
matured.

If there is an overwhelming infection or inflammatory process, neutrophils leave the

circulation more rapidly than they can be replaced. A neutropenia may result or the
neutrophil count may be within the normal range but bands predominate, exceeding the
number of mature neutrophils. Toxic changes to the neutrophils will be seen on a smear
in the form of dohle bodies and foamy basophilic (bluish) cytoplasm.

Degenerative Left Shiftis when immature neutrophils outnumber mature neutrophils.

This is called a degenerative left shiftand is a poor prognostic indicator.If inflammation

is not overwhelming but is persistent then chronic inflammation results.In this situation a
mild to moderate neutrophilia usually persists and there may or may not be a mild left
shift because the bone marrow has had time to catch up with the demand. Although
inflamation is the commonest reason for neutrophilia, drugs below are also responsible
for neutrophilia

• Adrenaline
• Steriods.

Left shift does not occur in these instances.

Neutropenia

Results from overwhelming demand or inadequate production of PMNs.

• Overwhelming infection (accompanied by toxic changes and degenerative left

shift)
• Infectious disease – feline panleucopenia, canine parvo, FeLV
• Iatrogenic – chemotherapy, oestrogen, idiosyncratic drug reactions
• Aplastic anaemia
• Myeloproliferative or lymphoproliferative diseases
• Cyclic neutropenia (rare – grey collies Q12 days lasts 2-4 days)
• Immune mediated neutropenia – extremely rare.

Lymphocytes

B Lymphocytes, T Lymphocytes and Null cells contribute to humoral and cytotoxic

immunity and recirculate from the tissues via the lymphatic system back into the
circulation. B cells and T cells cannot be distinguished from each other on light
microscopy. B cells develop into plasma cells but these are rarely found in the circulation.

Causes of Lymphocytosis

• Adrenaline response (as above – more marked in cats)

• Chronic inflammation infection or immune stimulation ( including post vaccinal)
• Lymphoid leukaemia – the lymphocytosis can be extreme especially with chronic
lymphocytic leukaemia
• Hypoadrenocorticism (mild)

Causes of Lymphopenia

• Acute viral infections

 • Steroid response (lymphopenia is the most consistent of all the steroid induced
changes in leucocyte numbers)
• Depletion of lymph e.g.. Loss into body cavity -chylothorax, or loss of afferent
lymph – enteric pathology such as lymphoma or lymphangiectasia
• Lymphoid hypoplasia – e.g.. combined immunodeficiency in Basset Hounds,
chemotherapy, destruction of lymphoid tissues – multicentric lymphoma

Eosinophils

Circulate for a very short time therefore their normal counts are low in comparison to
neurophils (they spend longer in the tissues). Their main functions are the destruction of
parasites, the damping down of inflammatory responses and regulation of allergic
reactions. Their numbers are reduced in response to steroids.

Causes of Eosinophilia

• Hypersensitivity (allergy) – e.g.. Flea bite hypersensitivity, ‘asthma’, pulomary

infiltration with eosinophilia (PIE)
• Parasitism (doesn’t conisitently cause an eosinophilia) – for example intestinal
parasitism, aelurostrongylus, protozoa
• Idiopathic eosinophilic diseases – e.g. eosinophilic gastroenteritis, eosinophilic
myositis, idiopathic hypereosinophilic syndrome of cats, panosteitis
• Infectious diseases e.g.. FIP
• Neoplasia – mast cell tumours, paraneoplastic eosinophilia, eosinophilic
leukaemia (rare)
• Hypoadrenocortcism

Causes of Eosinopenia are similar to causes of neutrophilia

• Infection/inflammation
• Adrenaline response – acute stress, pain, excitement , exercise
• Steroid response- chronic stress/illness, glucocorticoid administration,
hyperadrenocorticism

Basophils

Are not usually present in significant numbers in the circulation. They function in allergic
reactions and degranulate in a similar way to mast cells. Basophilia rarely occurs without
eosinophilia. (therefore see list above for causes of eosinophilia). There is no such thing
as basophilopenia as numbers are so low in the first place.

Monocytes

Monocytes become macrophages when they leave the circulation and enter tissues where
they phagocytose dead cells or microorganisms. Monocytopenia is of no diagnostic
significance.

Causes of Monocytosis
 • Inflammation especially chronic or pyogranulomatous inflammation (TB/FIP)
• Steroid response- chronic stress/illness, glucocorticoid administration,
hyperadrenocorticism
• Monocytic or myelomonocytic leukaemia (monocytosis likely to be extreme)

Platelets

Thrombocytopenia is generally not severe enough to cause spontaneous haemorrhage

until the count drops below 50x109 /l. If thrombocytopenia is seen on the CBC it is very
important to check this is genuine. First check there are no visible clots in the EDTA
sample then check the feathered edge of the blood smear to see if there are clumps of
platelets here. If no clumps or clots are seen the platelet count can be verified by a
manual count in the monolayer section of the blood smear.Count the number of
platelets present on 10 high power fields (HPF) (oil immersion x 100) then calculate the
mean. An estimate of platelet count can be made by equating each platelet per high
power field to a count of 15-20x109 /l. A normal animal should have more than 20
platelets per HPF. A count of less than 2 per HPF is likely to be clinically significant.
 Therapeutic Management of Complications in Canine Babesiosis

Dr. K Vinodkumar, Asst. Professor, Dept. of Veterinary Epidemiology and Preventive Medicine,
CVAS, Mannuthy, Kerala Veterinary and Animal Sciences University.

Babesiosis is a parasitic infection caused by hemotropic protozoa of the genus Babesia,

belonging to the family Babesiidae, order Ixoplasmida, class Piroplasmea, phyllumApicomplexa,
subkingdom Alveolata, and kingdom Protozoa. In dogs, a large form of Babesiaspp. is
represented by Babesiacanis(intra-erythrocyticmerozoites measure 3–5 µm, which is at least half
the diameter of the erythrocyte). There are three known variants of the organism, which are
presumed to be distinct subspecies: B. caniscanis, B. canisvogeliand B. canisrossi.Small forms
of the disease are represented byBabesiagibsoni, B. conradae, and B. vulpes(merozoites measure
1–3 µm, which represents less than half the diameter of the erythrocyte).Dogs of all ages can be
affected with Babesiaspp., but young puppies are more commonly affected. The incubation
period varies from 10 to 21 days for B. canisand 14–28 days for B. gibsoni. Mortality for
Babesiaspp. infections ranges from 12% for B. rossito approximately 1% for B. vogeli.

The acute form of the disease is manifested by fever, lethargy, hemolytic anemia, and marked
thrombocytopenia. Dogs recovering from an acute infection become carriers of the pathogen, and
the parasitemia persists for at least 38 months. The chronic form is manifested by intermittent
fever, lethargy, and weight loss and it can persist in the body for years. The severe form of
disease is characterised by marked haemolyticanaemia and acid–base abnormalities with
secondary multiple organ failure and complications such as ARF, hepatopathy, hypoglycaemia
,ARDS, IMHA and cerebral pathology.

Pathogenesis

Canine babesiosis can be clinically classified into uncomplicated and complicated forms. An
uncomplicated form of babesiosis is considered to be a consequence of anaemia caused by
haemolysis. Complicated babesiosis may be a consequence of inflammatory mechanisms that
lead to the development of the systemic inflammatory response syndrome and multiple organ
dysfunction syndrome, which are cytokinemediated conditions. Although various mechanisms
have been suggested to cause both forms of babesiosis, recent studies have indicated that much
of the disease process could be explained by host inflammatory responses to the parasite, rather
than the parasite itself.Parasitic infection causes a systemic inflammatory response, which is
considered to be a major aspect of the canine babesiosis pathophysiology and it contributes to a
variety of clinical manifestations. The pathogenesis results from excessive production of
proinflammatory cytokines. The only cytokine identified, associated with B. canisinfection, is
tumor necrosis factor alpha (TNFα), which was found in higher concentrations in dogs with
higher peripheral parasitemia and more severe disease.

Haemato-biochemical Changes

The most predominant feature of babesiosis in infected dogs are haemolyticanaemia and
thrombocytopenia. Multiple causes like extra- and intravascular haemolysis, RBC destruction
due to increased osmotic fragility, shortened life span of RBCs, erythrophagocytosis and
immune-mediated destruction of RBCs because of parasitic antigens, parasite-induced membrane
damage and possibly other membrane-associated antigens leads to anaemia . Impaired
haemoglobin function, oxidative damage, sludging and sequestration of erythrocytes also likely
occur.

Coagulation abnormalities play an important role in the development of complications. A

consequence of the systemic activation of the coagulation system could be disseminated
intravascular coagulation . This complex thrombohaemorrhagic disorder has increased
complexes of thrombin-antithrombin, decreased antithrombin activity, thrombocytopenia and
shortened activated partial thromboplastin time in dogs with B. canis infection. A compensated
form could be present in canine babesiosis. Although almost all infected dogs are presented with
severe thrombocytopenia, none develop haemorrhage. Thrombocytopenia may result from
immune-mediated platelet destruction, platelet sequestration in the spleen, elevated body
temperatures or disseminated intravascular coagulation.

Leucopenia in canine babesiosisis caused by all 3 large species of the parasite; B. canis, B.
gibsoni and B. rossi. The possible causes are formation of platelet-leukocyte aggregates,
sequestration, increasedutilisation and reduced production. One possible mechanism involved in
leukopenia includes the ability of platelets to interact with leukocytes and induce their so-called
˝secondary capture˝. The subsequent neutrophil-endothelial interaction could contribute to the
initial decrease in leukocyte number and also trigger vascular inflammation.
Complications

Systemic inflammatory response syndrome (SIRS) –It is caused by an excessive release of

inflammatory mediators and considered to be a major feature of the pathophysiology of canine
babesiosis. A higher mortality rate is present in dogs that develop severe inflammation than those
with severe anaemia, indicating that the intensity of the inflammatory response is the dominant
mechanism in the outcome of the disease.

Multiple Organ Dysfunction Syndrome (MODS) -Dysfunction of more than two of central
nervous system, hepatic system, respiratory system and locomotors system indicate MODS in
canine babesiosis. The common clinical manifestations of MODS include acute renal failure,
coagulopathy, cerebral babesiosis, icterus and hepatopathy.

Pancreatitis - This was previously referred to as the “gut form” of babesiosis and is associated
with gastrointestinal clinical signs including anorexia, vomiting, diarrhea, melena, hematemesis,
and abdominal effusion
Hepatopathy - This is a complication of babesiosis evidenced by bilirubinemia, pigmenturia, and
icterus, a sign seldom seen in dogs with only hemolysis.
Acute Kidney Injury - AKI is an uncommon complication of babesiosis and typically presents as
anuria or oliguria despite adequate hydration. At necropsy, the kidneys are swollen and dark in
color, with redbrown urine in the bladder.

Cerebral babesiosis - Occurring uncommonly, cerebral babesiosis carries a poor prognosis and is
caused by endothelial damage with subsequent microvascular necrosis, perivascular edema, and
hemorrhage.
Cardiac dysfunction - Cardiac dysfunction in canine babesiosis has traditionally been regarded as
a rare complication, with the majority of lesions reported as incidental findings at post-mortem
examination.
Treatment
Imidocarbdipropionate: It is an aromatic diamidine and is recommended to be used as 4 - 6.6
mg/kg intramuscularly (IM) or subcutaneously (SC) with a repeated dose in 2 weeks in dogs
against B. gibsoni.Imidocarbdipropionate should not be administered intravenously (IV) in dogs.
The adverse effects of this medication include pain during injection and cholinergic effects such
as salivation, drooling, nasal drip or vomiting which can be mitigated by premedicating with
atropine at 0.05 mg/kg.The toxic effects of imidocarb may occur spontaneously from a dose of
10 mg/kg with massive liver necrosis, and nephrotoxicity.
Diminazeneaceturate: It is 4,4′-(diazoamino) dibenzamidinediaceturate which is widely used in
tropical countries as a first-line agent for the treatment of Babesiacanisinfection of dogs, usually
as an intramuscular injection of 3.5 -5mg/kg. It often fails to eliminate B. gibsonifrom affected
dogs and a relapse may occur. Furthermore, diminazene has a narrow clinical safety margin and
can induce fatal nervous complications after 24–48 h of overdose. It has a very narrow
therapeutic range, as the drug is inconsistently cleared and results in possibly high toxicity. Side
effects can cause central nervous system toxicity in dogs, possibly dose related or as a
consequence of repeated administration due to the drug’s prolonged elimination half-life. A
relapse rate as high as 50% has been reported following diminazine treatment.

Combination therapies
Combination of antiprotozoan drug with antibiotic
Atovaquone and azithromycin:.Atovaquone is administered at the extra-label dose of 13.3 mg/kg
per-os (PO) q8h with azithromycin at 10 mg/kg PO once daily both for 10 days for the treatment
of B. gibsoni, B. conradae and B. vulpes (B. microti-like) infections.

Clindamycin alone or in combination with quinine is the treatment of choice for B. microti
infections in humans. A dose of 25–50 mg/kg/d divided every 12 hours for 10 days has been
reported to resolve clinical signs in canine B. gibsoni infection.

Combination of antibiotics

Doxicycline in a dose of 10 mg/kg/day, administered per os (PO) or intravenous (IV);

clindamycin (10 mg/kg PO, twice daily); metronidazole (20 mg/kg (PO), oncedaily).

Doxycycline (7-10 mg PO, twice daily), enrofloxacin (2-2.5 mg/kg PO, twice daily),
metronidazole ( 5-15 mg/kg PO, twice daily in combination for 6 or 12 weeks.

Supportive Therapy
Fluid therapy Uncomplicated babesiosis - Routine fluids can be used for rehydration and
maintenance, since major electrolyte imbalances are unlikely to occur.

Complicated babesiosis - When severe anaemia is present in a patient in shock, blood is the fluid
of choice.A transfusion rate of up to 10 ml kg/ h is recommended for whole blood, but blood
may be administered far more rapidly to shocked animals. Hypertonic fluids are a rational option
in non-hypovolaemic shock, where plasma expansion, rather than fluid replacement, is required.
These fluids include hypertonic (7,5%) saline and colloidal solutions (eg. dextrans and
hydroxyethyl starch [hetastarch]).

Cerebral babesiosis- Hypertonic saline might be considered for resuscitation in dogs with
cerebral babesiosis accompanied by shock, as it prevents an increase in intracranial pressure,
unlike isotonic solutions.

Pancreatitis – Analgesia, nutrition, gastric acid suppression, isotonic fluids.

Pulmonary oedema - Hypertonic fluids might be safer than crystalloids.

Acid-base imbalance - Severe and complicated babesiosis may result in lactic acidosis with
varying degrees of respiratory compensation. Correction of pH should only be attempted in
severe, life-threatening acidaemia (pH < 7,2) with the aim of increasing pH to above 7,2, not of
returning it to normal.Sodium bicarbonate continues to be recommended and administered in
acidaemia.

Disseminated intravascular coagulation - The most important step in the treatment of DIC is
removal of the underlying cause, followed by correction of potentiating problems such as
acidosis, hypoxia and shock. If these measures fail to control bleeding in the hypocoagulable
phase, transfusion of fresh blood or fresh/fresh frozen plasma (starting dose 1 unit plasma [-225
ml]/10-20 kg) is required.

Haematinics (iron, cobalt, copper) - Provide substrate for increased haemoglobin synthesis in
hypochromic anaemia, but it is unlikely that they stimulate erythrocyte production in the absence
of deficiencies.

Vitamins B - Are common adjuncts to the routine treatment of babesiosis. Their main functions
are as cofactors in metabolism and appetite stimulants.
Patient Monitoring

In hospital settings, hematocrit concentration and platelet count can be monitored daily until
improvement is seen.

Continue monitoring for 1-2wk until hematocrit and platelet numbers have normalized.

Serology is not recommended posttreatment, as titers do not necessarily wane after treatment.

If the patient fails to respond favorably to therapy, additional screening for coinfection should be
considered.

Prognostic Markers (WSAVA 2013)

Serum lactate concentrations - Admission lactate > 5 mmol/l is associated with increased
mortality, but lactate > 2.5 mmol/l and/or increase after admission and/or failure to decrease to <
50% of admission value, is strongly predictive of death. Lactate persistently > 4.4 mmol/l
strongly predicts death and lactate > 4.4 mmol/l at 24 hours after admission correctly predicts
death in every case

Clinical collapse - Hypotension is common in babesiosis and is associated with clinical collapse.
Clinical collapse is also associated with hypoglycaemia. This appears to be a very simple and
useful prognostic factor.

Hypoglycaemia - Hypoglycaemia (glucose < 3.3 mmol/l) is present in c. 20% of cases.

Hypoglycaemia is associated with stupor, collapse and miosis, which disappear after dextrose
infusion. Dogs that are collapsed (non-ambulatory) at presentation have an 18-fold increased risk
for hypoglycaemia. Pups less than 6 months of age are at risk of developing hypoglycaemia.

Capillary and venous parasitaemia - Timing, source of blood (venous versus capillary) and
counting method cause large variability in parasite counts. A significant positive correlation
between high parasitemia and mortality has recently been demonstrated.

Serum cortisol and thyroxine concentrations - Dogs that died had a significantly higher median
cortisol concentration (482 nmol/l) than other admitted dogs that survived (150 nmol/l).
Conversely, the total and free thyroxine concentrations in all but one of the dogs that died were
below the limit of detection and significantly lower (2.7 nmol/l and 0.12 pmol/l, respectively)
than in other admitted dogs that survived (7.4 nmol/l and 0.4 pmol/l, respectively).
 Feathers & Health: Navigating
the top Ten Diseases in Pet Birds
Dr. Shiwani Tandel
B.V.Sc& A.H, M.V.Sc, M.Vet Sci (Conservation Medicine.)
 Top 10 diseases/ problems in Birds.
- Chlamydia - Aspergillosis
- Candida - PBFD
- PDD, ABV - Knemidocoptes
- AGY - Paramyxovirus
- Pox - Avian Asthama
Chlamydia: Chlamydia psittaci

1. Eyes- discharge / watering

2. Affects respiratory system, gastrointestinal
system .
3. Primary affected organ is liver.
4. Pathognomonic sign is lime green urates.
5. Affects different species , differently .
6. Carrier species.
7. Treatment- Doxycycline (Rajdox*) liquid.
Sometimes has to be combined with
enrofloxacin.
Mite infection -Knemidocptes
 Treatment for Knemidocoptes
• 1. Ivermectin oral – 3mg: 1 tab crush in 3ml water: take 0.2ml dilute
with 0.8ml and give 0.1ml/ 100 gms body weight.
• Liquid paraffin/ aloe cream/ coconut oil.
• If open wounds to put on antibiotics.
 Aspergillosis: A. fumigatus, A. niger

• Greys are over represented , can also be seen in birds of prey ( kites, falcons)
• Symptoms can be extremely random like inappetence, vomition, respiratory distress may not
always be observed, birds just not doing well, Feather plucking
• Diagnositc modality- Xray, endoscopy.
• Treatment- Itraconzaole - 2-5mg/kg once a day
Fluconazole - 3-5 mg/kg once a day ( long duration and pulse therapy)
• Nebulisation- with Voriconazole.
Aspergillosis continued.
Candida: Candida Albicans

• Primarily seen in parakeets

• Those on a fruit diet.
• Cage hygeine
• Characteristic feature: plaques in the mouth
especially at the commissures of the beaks,
• Line of treatment: Ketoconazole. Itraconazole ( Itraaraj*),
Fluconazole , Terbinafine (Terbiraj*).
Paramyxovirus- Ranikhet
 Paramyxovirus continued
• Seizures, partial paresis, single incident
• Young birds continue to eat.
• Treatment: Anti- inflammatories ( meloxicam), B complex, .
• Homeopathy : Arnica and Hypericum
• Very rarely an antibiotic.
• High morbidity, low mortality.
 Avian Gastric Yeast-
Megabacter ornithogaster
 AGV continued

• Vomiting , greenish stools stuck to the vent.

• Unkempt appearance. Feathers around mouth and head appear quite
hard.
• Bird appears o eat continuously.
• Diagnosis: stools sample/ crop wash.
• Nystatin, Fluconazole and Itrcnazole.
• Improve immunity.
PDD Proventricular Dilatation Disease

• Species: Macaws and parakeets.

• Symtoms: Vomition, constant hunger,
making baby bird noises.
• Diagnostic: X-ray, Lateral and DV
 PDD treatment

• It was earlier confused with Borna virus.

• Anti- inflammatories: Celecoxib, meloxicam.
• Nerve tonics.
• Dietary restrictions.
Egg binding
 Pox
Avipox virus- transmitted by mechanical
vectors and consumption.

Causes:
Dry form- lesions at the muco-cutaneous
junction neck, or the beak, legs, wings.
Diphtheritic form – Upper GI (mouth and
pharynx)and respiratory tract.

Treatment:
Early stages respond to Doxycycline but is
highly transmissible .
 Avian Asthama
Reasons:
• Toxins (agarbatti, Teflon fumes),
• Infections,
• Macaw allergies,
• Ascites,
• Mass effect

Nebulisation and oxygen therapy.

Fluid replacement

Sedation?

Antibiotics?

Air sac canula placement.

 Use of Steroids
• Indicated only to pull through a stressful situation which may involve
pneumonitis . Avoid giving in trauma.
• Start at 0.5ml-1mg/kg. (should be tapered down)
• Nebulize as well with a steroid (Budecort).
• Always give antifungals with or after steroids.
• Use sparingly!
• Try to give the first dose intramuscularly then move to oral.
 Summary
• Diseases are species specific.
• Certain species have a prediliction for certain diseases.
• Confirm the presence of disease with some diagnostic tests.
• Most systemic diseases have certain pathognomonic lesions which
need to be identified.
• Give an anti-fungal treatment with steroids.
• Always hydrate the bird..
• Nebulisation helps in more ways than you may understand.
 Thank you

Phoenix Veterinary Specialty

Email: pvetspecialty@gmail.com
Instagram: @thephoenixvets, @thebirdvet
 Avian emergency
management and critical care
Dr Shiwani Tandel
Phoenix Veterinary Specialty, Dadar, Mumbai.
Email: pvetspecialty@gmail.com
Instagram :@thebirdvet, @thephoenixvets.
Reasons for trauma/ emergency

• Fracture
• Bleeding (toe nail clip, wing clip, feather break)
• Seizures
• Egg binding
• Respiratory distress
• Vomitting
 Trauma and emergency protocols

• Airway, Breathing, Circulation.

• Understand the fluid lost in relation to body weight. 30% of blood volume ( 1/10 of body weight
=Blood volume)
• Address pain: Meloxicam @1mg/kg , Butorphanol
• Sedation if required 1. Isoflurane
2. Butorphanol (1 mg/kg )+ midazolam (1 mg/kg)
• Warmth
 Pain medication
• Regional anesthesia: Lignocaine 2-3mg/kg
• Opioids:
1. Butorphanol (1-2mg/kg); Amazons: (3-6mg/kg) Used to reduce MAC of Isoflurane
2. Buprenorphine -0.1mg/kg- 1mg/kg
3. Fentanyl- 10mg/kg (can cause anxiety for the first few minutes)
• NSAID’s: studies with circulating blood volume not possible since NSAID’s concentrate at inflammatory site.
1. Meloxicam- 0.5-1.5mg/kg wounds, inflammation, FB
2. Celicoxib – 10mg/kg exclusively used for PDD
Orthopedic pain : Tramadol 10-30 mg/kg
Chronic Pain/ neuropathic ; Gabapenetin 3-10mg/kg. generally given to reduce duration of NSAID administration, although never
together
 Fluid administration

• Generally bolus fluids are preferred ; to give 1/3rd of required fluids intravenously
• 100 gms bird – 10ml blood .
: 3ml blood loss is allowed.
(But that does not mean we should give only 3 ml of fluid)
60-100 ml / kg body weight over a period of time
:- 100gms bird needs 6-10 ml fluid over a whole day.
:- therefore 3/4ml intravenously or intraosseus
:- then repeat after 1 hour
Intraosseus catheter placement
 What fluid to give?
• Ringer Lactate or Normal Saline warmed
• Hetastarch or other such plasma volume expanders.
• (General rule of thumb is to give 20% of fluid volume being given at that point of
time.)
• Blood glucose can be measured and is roughly between (200mg/dl- 400 mg/dl)
• If its low then consider giving 10% Dextrose OR 25% Dextrose small bolus. Check
blood glucose after fluids. Check it after 4 hours to see if body maintains.
Ulnar/ Basilic vein wing
Ulnar Vein Blood draw
Bandage figure of 8 wrap
Leg Anatomy and Venipuncture site
 Stabilizing the foot

• Use of local materials like sticks or syringe split lengthwise into two.
• Vetwrap and gauze bandages
 Seizure

• Is it a seizure or is it trembling or shivering . ( Grey parrots- hypocalcemia and

Ringnecks- newcastles)
• Diazepam @ 0.1ml /200 gms intra muscular.
• Understanding the reason for seizures is important.
• Heart disease - May need Furosemide or Blood pressure medicines
(Atherosclerosis)
• May need to be given Diazepam for a few days till the threshold is established.
 Reproductive anatomy of the bird

• The ovary - ventral surface of the cranial ventral surface aspect of the cranial division of the left
kidney
- flattened, yellow and triangular
• Infudibulum
• Magnum- longest and thickest,
mucous secretion at caudal end
• Isthmus
• Uterus
• Vagina
 Egg Binding

• Sedation always.
• Fluids
• Calcium
• Oxytocin
• Manual manipulation: application of KY jelly and liquid paraffin.
• If egg is old, then it may be adhered to the endometrium.
 Upper Respiratory System

• Cere – sexual differentiation

• Nares -
• Operculum
 Respiratory System
• Oral cavity
• Choana

-Choanal papillae (disease, Vit A

deficiency)
• Infundibulum: Connected to
Eustachian tubes: diving birds
• Glottis
• Large trachea compared to mammals
• Epiglottis absent
 Respiratory System

Trachea and syrinx

 Complete rings of trachea

Endotracheal tube selection
Relatively larger than in mammals
Bifurcation is higher in Penguins and
other diving birds
 Syrinx is at bifurcation
Responsible for vocalization
 Species variation
Syringeal bulla in male ducks and
geese
Coiled trachea in swans
2 syrinx in Lyre birds
Respiratory System
Respiratory System
 Respiratory System

• Air sacs
• Variable number
• Psittacines generally have 9
• Very thin and clear when normal
• No diaphragm
• Must be able to move sternum
or will suffocate
Respiratory System

• Lungs
• Minimally expand
• NO alveoli
• Decreasing size of airways
• 1o bronchi
• 2o bronchi
• Parabronchi
• Air capillaries
• 3 microns
Respiration in birds -Inspiration
Respiration in birds- Expiration
 Respiratory System

• Oxygen exhange
• Occurs on both expiration and
inspiration
• About 20% better than
mammals
• Path of air from trachea being
inhaled to being exhaled out
trachea takes 2 cycles
 Respiratory Distress
- In cases where we have diagnosed parenchymal disease – steroid
- Prednisolone or Dexamethasone
• Remember to give antibiotics and antifungals once bird is stable.
• Amoxycillin with clavulanic acid (dose of Amox=100-125mg/kg)
• Fluconazole ( 4-6mg/kg bd in neonates; 10-15mg/kg once a day ) and Terbinafine (5-
10mg/kg bd )
• Always after food or with food and only once the bird is hydrated.
• How to make a nebulizer ?
Air sac canula placement
 Respiratory Distress

• Nebulization / oxygen therapy.

- Nebulisation drug chart included
• Injectible : aminophylline/ terbutaline
- Very rarely furosemide is indicated
- Is it really respiratory disease( abdominal palpation)
 Anesthesia

• From blood draws to surgery

• Either direct gas with face mask.
• Face mask (empty plastic bottles can be fashioned to be used as masks of
different sizes.)
• Isoflurane till effect then generally maintained on low for small procedures
like radiographs or blood draws.
• Longer procedures one can manage blood
 Injectable Anesthesia

• Butorphanol + midazolam (1:1) Depends on kind of bird and BMR

• Butorphanol with Isofluorane to reduce the MAC of Iso.
• Butorphanol + midazolam + Ketamine (I/v keep giving to effect)- i/v only
• Ketamine and Xylazine – recovery is violent
• Always Intubate the bird especially if it has eaten something.
(not necessary to fast small birds)
 Monitoring Anesthesia
• Temperature
• Doppler pulse
• Respiration
• Elevate the head
• I/v access at all times
• Adrenaline, Doxapram
• When the bird stops breathing- deep anesthesia/ pressure on lungs
• 0.5lts bag ambu bag
 Anesthesia
• Do not let the animal be on the spine for too long.
• Procedure should be done in 40-60 minutes.
• Respiration stops before heart.
• Keep the bird warm and hydrated .
• Blood loss > 30% of blood volume may be fatal.
• Use of ICU / heating and oxygenated unit for recovery.
If you want something you’ve never had, you must be willing
to do something you’ve never done.
- Thomas Jefferson.

Phoenix Veterinary Specialty, Dadar, Mumbai.

Email: pvetspecialty@gmail.com
Instagram :@thebirdvet, @thephoenixvets.
 4/24/24

Margie Scherk DVM DipABVP (Feline) hypurr@aol.com

Vancouver, Canada
1

Thank you to

for sponsoring
2

1
 4/24/24

catvets.com

Catfriendly.com

me
t he ho
in
And

What do
cats want
and need?

2
 4/24/24

What cats want & need…provide it in clinic

1. What makes cats content
2. What makes cats stressed
3. What small changes in the practice can make a big difference

What cats want & need…provide it in clinic

1. What makes cats content
2. What makes cats stressed
3. What small changes in the practice can make a big difference

3
 4/24/24

Want
• A safe space
• Multiple and separated
resources
• An opportunity to play and
express predatory behaviours
• Positive predictable interactions
with humans
• An environment that respects
their sense of smell

Need safety
• Safety = being protected from harm or
other danger
• A sense of control and the ability to find
comfort and pleasure
• Their sense of safety comes from
familiarity, control, predictability, and
avoidance or displacement of threats.
• A cat’s coping ability is influenced by the
number of stressors and the exposure
time to them

4
 4/24/24

Try to imagine…
Walking on 4 feet
Jumping 5X your height
Perceiving the world in overlapping clouds of smell
Having much better night vision
Grooming yourself with your tongue
Locating sound by rotating ears
Having poor close-up vision
Having a tail
Scooping food and sucking water
Having whiskers

10

5
 4/24/24

The essence of being a cat

• Territorial Strategy
• Resource based Solve problems
• Use scent for boundaries Tactics
• Avoid contact with threats
• Observe
• Avoid ambush Stay
• Live alone (or in related groups) safe
• Privacy, safety
• Both predator and prey

11

The essence of being a cat

• Resource-based territory

• FOOD, water,
safe sleeping posts,
observation posts,
scratching surfaces,
bathrooms,
sexual partners

12

6
 4/24/24

Bed Water

There is a bed in both the living and There are several water bowls that are
bedrooms which are places the cat in places the cat can readily access.
will want to be with his/her people.

Food
Water Living room and kitchen Hallway

Litter Balcony

Bedroom
Bed
Perch
Scratching Food

Toys Food bowls are placed on a ledge as

well as on the floor in three different
Scratching tree/post
locations.
A tall scratching tree is placed near the window for
Litter
observation. Another is in the hall and a shorter
scratching post is in the living room beside the sofa
which could otherwise be tempting to scratch. Three comfortably sized, clean litter boxes
are placed in quiet, separate locations.

13

Normal feline behaviours

• Play • Scratching
• Investigation • Travelling
• Observation • Scent marking
• Hunting • Eliminating
• Feeding • Resting
• Drinking • Sleeping
• Grooming • Crepuscular schedule

14

7
 4/24/24

Positive vs negative emotions?

ENGAGING Emotions PROTECTIVE Emotions

• Actively seeks out something • Self-protective against perceived
that benefits welfare threats to welfare
• Desire- seeking • Repelling behaviours
• Food • Increase distance from
• Comfort • Decrease interaction with a threat
• Attention

Rodan JFMS 2018

15

How do cats perceive the

world?

16

8
 4/24/24

From Taylor JFMS 2022

17

Smell
• Surface area of the olfactory
epithelium is 20 cm2 vs 2-4 cm2
in humans
• Vomeronasal system that detects
sensiochemicals
• The “smells” of an environment
provide essential survival
information

18

9
 4/24/24

Olfactory communication/signals

19

Olfactory
communication

• Odour marking is critical

long-range communication
• Helps to avoid
confrontation
• Cannot be changed
• Creates spacing

20

10
 4/24/24

21

22

11
 the home entrance to avoid introducing tion can
ease) or scratching
occur. and stress-related cat’s scent (‘olfactory continuity’).
✜ Use synthetic pheromones to reduce
external smells into the home environment.
illness (eg, urinary tract dis-Other considerations
anxiety, and✜increase grooming,
Use synthetic interest
pheromones to in
reduce
ease) can occur.
✜ Homes with outdoor-access flaps in doors
Other considerations
food and appropriate
anxiety, anduse of thegrooming,
increase litterbox.interest
26
in may✜ be at greater
Homes risk of other cats
with outdoor-access flapsorinanimals
doors 4/24/24
✜ Expose newfooditems to the cat’suse
and appropriate scent profile
of the litterbox.26 introducing
may be at external
greater risk scents or gaining
of other access
cats or animals
by rubbing ✜them withnew
Expose a cloth
itemsthat has
to the been
cat’s scent profile intointroducing
the home.externalVigilance combined
scents or gaining with a
access
in contact with the cat’s
by rubbing scent
them glands
with a clothduring
that has been door flap
into thedesigned to be operated
home. Vigilance combinedby withthea cat’s
in contact with
positive interactions withthe cat’s scent
humans, glands during
or spray door flapidentification
implanted designed to bemicrochip
operated byare theways
cat’s
positive
new items with interactions
a synthetic withpheromone.
feline humans, or spray implantedencroachment
of avoiding identification microchip are ways
of unfamiliar
new items with a synthetic feline pheromone. of avoiding encroachment of unfamiliar
✜ Provide scratching areas that allow a cat to scents. Avoid magnet-operated door flaps
✜ Provide scratching areas that allow a cat to scents. Avoid magnet-operated door flaps
since the magnets can attract foreign
since the magnets can attract foreign
materials.
materials.
✜ Scratching
✜ Scratching areas
areasshould
shouldalsoalso bebe available
available
outdoors
outdoors forforscent
scentdeposition.
deposition.
✜ Scent
✜ Scent marking
markingasaswell wellas
as inappropriate
inappropriate
elimination
elimination shouldnever
should neverbe be punished.
punished.3434
✜ Ensure
✜ Ensure thatthat eachgroup
each groupof of cats
cats within
withinthe the
homehomehashasanan opportunityto
opportunity to scent
scent mark
markareasareas
(by scratching and facial rubbing) that
(by scratching and facial rubbing) that
contain their environmental resources.
contain
✜ A cattheir environmental
returning resources.
to a multi-cat home from
b ✜ A cat returning
a visit away mayto a multi-cat
smell different,home from
disrupting
b a visit
the away may smell different,
home environment’s communal disrupting
scent
Figure 13 Facial
rubbing (a) allows a
the profile
home consisting
environment’s communal
of scents scent
from all feline
Figure 13 Facial
cat to deposit its profile consisting
occupants. ofmost
This is scents from
likely all feline
to occur after
rubbingscent
(a) allows
cat to deposit
a
And mark with colony scent
throughout its
a visit to This
its In orderoccupants.
environment.
the veterinarian,
is most likely where smells after
to occur of
scent throughout
to maintain its
scent medications,
a visit antiseptics, cleaners
to the veterinarian, and even,
where smells of
environment. In order
continuity,
to maintain scent
cleaning
avoid
facially
postoperatively,
medications, anesthesia
antiseptics, gases can
cleaners andbeeven,
Courtesy Sarah Ellis detected by other cats. In such cases, cats
postoperatively, anesthesia gases can be
marked
continuity, avoid areas (b).
a cleaningImages courtesy of
facially that previously got along well can display
Sarah Ellis
marked areas (b). detected by other cats. In such cases, cats
Images courtesy of that previously got along well can display
a
Mark territory Sarah Ellis
JFMS CLINICAL PRACTICE 227
to feel safe
and to protect
JFMS CLINICAL PRACTICE 227
resources

23

Mark territory
to feel safe
and to protect
resources

24

12
 4/24/24

From Taylor JFMS 2022

25

Hearing
• Ears swivel independently, sideways and
backwards, to locate prey
• Perceive frequencies between 48 Hz to
85 kHz with the upper ultrasonic range
about an octave higher than we hear
• High frequencies - rodents
• Low frequencies – male voices
• Also perceive sound through their pads
• They hear things we don’t e.g., compact fluorescent light bulbs,
light dimmers, computer and television displays

26

13
 4/24/24

Auditory signals: convey a need to

Increase distance Encourage socialization

• Hiss • Purr
• Open mouth scream • Trill
• Closed mouth wah-wah • Miaow
• Growl • Silent miaow
• Chatter
• Sexual calling

27

From Taylor JFMS 2022

28

14
 4/24/24

Vision
• Geared to hunting
• Wider visual field (200 degrees, vs
human 180 degrees
• Larger proportion of rods to cones
• Detect movement in dim
lighting
• Long pupil and tapetum lucidum
• Red-green colour blindness?
• Colours are less intense

29

30

15
 4/24/24

Hunting
• Near-sighted
• See rapid movement
more readily than slow
movement
• Large, inflexible lens
impairs focusing
• Vibrissae guide to
neck

31

Whiskers
• Cheek vibrissae critical for neck bite
• Detect air movements that could reflect prey or a predator (including
human caregivers)

Hartz.com

32

16
 4/24/24

• When whiskers touch an object, they

form an “S”-shaped bend within the
follicle. By bending into this “S” shape,
the whisker pushes or pulls on sensor
cells, which then send touch signals to
the brain.

Luo PLOS Computational Biol 2021

33

34

17
 4/24/24

From Taylor JFMS 2022

35

Visual communication
Signals
• Medium range
• Limited by vegetation or lack of
light
• Can change rapidly
• Increase distance between cats

popsugar.com

36

18
 4/24/24

Visual communication/signals
Body language
• Arched back
• Crouch
• Tail
• Facial expression
• Ears
• Whiskers
• Pupils

37

38

19
 4/24/24

From Taylor JFMS 2022

39

Touch

40

20
 4/24/24

Tactile signals: friendly

• Rubbing
• Head bunting
• Nose touching
• Kneading, treading
• Grooming each other

41

Tactile signals: unfriendly

• Biting
• Neck bite
• Scratching

Warren Photographic

42

21
 4/24/24

Body language prevents fights & physical harm

43

Can you handle it? Validating negative

responses to restraint in cats
• Assessed licks/minute, ears position, pupil diameter, RR, staying on table
after being released
• “Passive restraint”: can stand, sit, lie down at will with free HL movement
• “Full body restraint”: held on their side with their back against the handler,
while the handler grasps the front and back legs, with a forearm across the
cat’s neck
• With FBR, struggling increased; during restraint, lip licking, RR and pupil
diameter size increased with ears being positioned down to the side or
back and more cats jumped off the table after release

Moody Appl Anim Behav Sci. 2018

44

22
 4/24/24

Touch: Do’s and Don’ts

• Less restraint is more • Avoid:
• Stroke temple and perioral areas • Scruffing
• Clipnosis
• Cover surfaces (tables, cage • Stroking tail base (behind the
floor, floor) with towels or soft neck)
fleece pads.
• Don’t shave whiskers!
• Administer subcutaneous fluids
warmed to body temperature.

veterinarypracticenews.com ingersollanimalhospital.com

45

From Taylor JFMS 2022

46

23
 4/24/24

Taste

blogs.scientificamerican.com

47

What do cats taste?

• Taste salty, sour, bitter and umami
(meaty/amino acids) flavours
• Not sweet
• Tempt with flavourful treats, food, or
Churu
• Size 4 gelatin capsules for bitter or
multiple meds
• Chase meds

fearfreepets.com

48

24
 4/24/24

And then
there are
some crazy
things

feline-nutrition.org Pinterest.ca Boredpanda.ca

49

From Taylor JFMS 2022

50

25
 4/24/24

What cats want & need…provide it in clinic

1. What makes cats content
2. What makes cats stressed
3. What small changes in the practice can make a big difference

51

Barriers: clients, cats, veterinary team

52

26
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Barriers
• “Travel to the practice, the waiting room and
examination itself are the most stressful events for the
cat, with one- third of respondents indicating that
witnessing their cat’s stress discouraged them from
bringing their cat to the practice”

• “The key stress-causing factors that … impair welfare in

the clinical setting were auditory and olfactory
stimulation, lack of analgesia and the use of restraint. “

Rodan JFMS 2018

53

What is ”Stress”?
• A condition in which predictability and control are compromised
• Environmental demand exceeds the natural regulatory capacity

• Stressor = stimulus that induces this state Physical

Social
• Stress response components:
• Physiologic +
• Behavioural +
HEALTH Mental +
• Psychological
Emotional

54

27
 4/24/24

Karagiannis, in Feline Behavioral Health and Welfare, 2016

55

I can’t cope!

56

28
 4/24/24

Stressor stacking
• Number
• Duration of exposure
• “For example, cats may cope with being temporarily confined in their carriers at
home, but when compounded by enforced confinement, fasting, non-consensual
handling, possible pain/illness/discomfort, removal from their territory and
transport, stressor stacking is experienced, often resulting in cats being unable to
cope and consequently showing signs of negative (protective) emotions on arrival
at the clinic. Stressor stacking will continue not only during the cat’s visit (eg, in
response to sample collection, treatments and hospitalisation), but right up until
the cat is settled back at home “

Taylor JFMS 2022

57

Stressor stacking

I can’t cope!

From Taylor JFMS 2022

58

29
 4/24/24

Getting to the clinic

59

Scotty’s experience!

60

30
 4/24/24

Cat carrier training with a cat friendly carrier

catvets.com
From Taylor JFMS 2022

61

From Taylor JFMS 2022

62

31
 4/24/24

Training works

https://bit.ly/3i7YIlN
63

64

32
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Why can cats be hard to work with?

• Self-defensive behaviours Flee
• Easily threatened Freeze
Fight
• Avoid threats

65

Understanding cat
body language

66

33
 4/24/24

Feeling threatened signals: subtle

• Look away
• Slightly lower ears
• Turn head away
• Lean back

67

Feeling threatened signals:

more intense
• Flatten ears
• Lower and curl tail lateral to thigh
• Turn head to side
• Crouch

68

34
 4/24/24

This is an aggressive cat This is screaming cat in clinic

69

70

35
 4/24/24

Feeling VERY threatened signals: extreme

• Roll over
• Show weapons

Not an aggressor

71

Threatening signals
• Approach
• Stare
• Stiffen limbs
• Stiff upright ears turned laterally
• Elevated tail base Aggressor
• +/- mount subordinate

72

36
 4/24/24

What cats want & need…provide it in clinic

1. What makes cats content
2. What makes cats stressed
3. What small changes in the practice can make a big difference

74

From Taylor JFMS 2022

75

37
 4/24/24

From Taylor JFMS 2022

76

From Taylor JFMS 2022

77

38
 4/24/24

78

Handling the uncooperative

self-defensive cat
• How can we minimize threats?
• Threats are multi-sensory
• Sounds
• Sights
• Smells
• Tactile
• Taste

79

39
 4/24/24

Sense Threats Reduce threat

by? ls
e
Smells Dogs, other cats, people, urine, feces, anals, vomit,
blood, disinfectants, alcohol, medication,
Tow
deodorizer candles, aromatherapy, perfumes,
laundry detergent, (Feliway?)
Sounds Dogs, other cats, strange voices, phones, faxes,
computer printers, doors, water, centrifuge,
dishwasher, music, traffic, spritzers/spray bottles,
shushing, stainless steel is loud
Sights Dogs, other cats, strange people, reflections, things
approaching face, bright lights, strange clothing,
masks, gloves, dark sillhouettes, sudden movement
Sensations Cold, wet, slippery, restraint, blood pressure cuff
inflating, needles, being syringe fed, cold SQ
fluids/injections, stinging injections
Tastes Strange diets, medication

Stainless steel anything Leather gloves! Being scruffed/stretched

80

Give cats a safe space

• Cat-friendly
seating area
• Cat-only exam
room
• Cat-only ward
Willows Veterinary & Referral Service Cat Friendly Waiting Area

81

40
 4/24/24

www.vethospital.co.nz

82

Image from Dr Tamara Iturbe Dr Buffington Cat Care-ier cover

83

41
 4/24/24

Respectful
Invite own exploration
Don’t grab, pull, shake or dump handling

84

85

42
 4/24/24

86

Fighting is a last resort and

occurs when escape is
impossible.

87

43
 4/24/24

Getting to know you

• When the cat chooses to approach a person,
longer human–feline interactions occur than
when a person approaches them.
• Give the cat the opportunity to initiate the
interaction
• Encourage this by getting down to the cat’s level a
few feet away from them and extending a soft
(relaxed and gently curved) hand to invite
approach, rather than picking up or restraining
them.
Rodan JFMS 2018

88

How to introduce
yourself to a cat

Rodan JFMS 2022

89

44
 4/24/24

How to pet a cat

you’ve just met

!
e h ead
h in d th
b e
NOT

90

The best place to examine or work with a cat is

where the cat wants to be!

Dr. Mark Peterson

Animal Endocrine Clinic, NY

91

45
 4/24/24

Allow the cat to decide where Examine the reluctant cat in

the exam will take place the bottom of the carrier

92

Positive reinforcement

93

46
 4/24/24

+/- head covered

TOWELS= amazing

www.vetstreet.com

94

What sensory input is threatening?

Sight
Sound
Smell
Touch
Taste

95

47
 4/24/24

SENSE THREATS REDUCE THREAT BY?

Smells Dogs, other cats, people, urine, feces, anal gland Avoid strong disinfectants, let surfaces dry thoroughly; use
secretion, vomit, blood, disinfectants, isopropyl isopropyl alcohol sparingly; have good ventilation; don’t share
alcohol, medication, deodorizer candles, towels; use feline pheromones in rooms, on clothing/hands.
aromatherapy, perfumes, laundry detergent, Exchange one of two towels to preserve own smell. Avoid
(Feliway?) volatile oils. Wash hands between each cat rather than use
hand sanitizer. Vent isoflurane well. Change top between cats?
Sounds Dogs, other cats, strange voices, phones, faxes, Speak quietly, gently; quiet noises through towels – over the
computer printers, doors, water, centrifuge, carrier, around the cat, over the kennel door, on the floor of
dishwasher, music, traffic, spritzers/spray bottles, the kennel, etc. Open products and close cage doors quietly.
shushing, stainless steel is loud Use white noise. Avoid loud music. Use purring, trilling,
chirruping to calm patient.

Sights Dogs, other cats, strange people, reflections, Lower the lights. Minimize sudden, quick movement. Reduce
things approaching face, bright lights, strange visual stimuli with a towel during handling or behind a partly
clothing (lab coats), masks, gloves, dark covered carrier door. Prevent seeing other cats or dogs. Wear
silhouettes, sudden movement street clothing as uniform.

Sensations Cold, wet, slippery, restraint, blood pressure cuff Cover surfaces with towels or soft fleece pads. Use minimal
inflating, needles, being syringe fed, cold SQ but gentle restraint. Warm subcutaneous fluids to body
fluids/injections, stinging injections temperature. Don’t shave whiskers!

Tastes Strange diets, medication Don’t change diets in clinic. Offer palatable foods and treats;
disguise bitter medications; follow medications with a treat.

96

From Taylor JFMS 2022

97

48
 4/24/24

Ideal layout

From Taylor JFMS 2022

98

Smaller space?

From Taylor JFMS 2022

99

49
 4/24/24

100

What sensory input is threatening?

Sight
Sound
Smell
Touch
Taste

What happens when someone reaches in?

101

50
 4/24/24

Danger!

102

Try to avoid taking cats “to the back”

• Cats get acclimated to the exam
room

• Better for the owner to leave

than the cat

103

51
 4/24/24

Try to avoid taking cats “to the back”

Ears Eyes Skin Lab

From Taylor JFMS 2022

104

Sample collection
• Lateral recumbency w front end up
• Medial saphenous vein
• Blood collection
• Catheter placement
• IV med administration
• Lateral saphenous vein
• Lateral cystocentesis
• Blood pressure evaluation

105

52
 4/24/24

106

Why we should change

our clinic culture
Stressful visits do lasting harm
• Caregivers are more stressed when their cats
are stressed…
• …and they may choose to change clinics or
avoid veterinary visits altogether
• Stressful visits are difficult for staff and may
lead to injury
• Stressful visits take a toll on our feline
patients
• The visit may yield less useful diagnostic data
due to stress
shawellnessclinic.com

107

53
 4/24/24

Optimizing the positive

• Carrier training
• Cooperative care
• Cat friendly environment

Rodan JFMS 2018

108

Choice and
control

109

54
 4/24/24

Resources
Meeting unmet needs

www.catvets.com

Catfriendly.com

Ellis JFMS 2013 www.alamy.com

110

Resources

111

55
 4/24/24

Make it safe

• Imagine the experience

from their perspective
• Put yourself in their skin
• Respect sense of smell
• Reduce threats

112

Thank you! Purr…

hypurr@aol.com
113

56
 4/24/24

UNDERSTANDING
FELINE CHRONIC
KIDNEY DISEASES:

What’s New?

Margie Scherk DVM, DABVP (Feline)

Vancouver, Canada

Thank you to

for sponsoring
2

1
 4/24/24

Catvets.com/guidelines

Sparkes JFMS 2016

3

Relationship is critical for successful management

• CKD is common - > 30-40% of elderly cats
• Variable course between individual cats

2
 4/24/24

Lots of Chronic Kidney Diseases

• Chronic tubulointerstitial • Chronic nephrotoxicoses or

nephritis failure to recover from acute
toxicity
• Pyelonephritis
• Chronic glomerulonephritis
• Obstructive nephropathy
• Amyloidosis
secondary to
ureteroliths/nephroliths • Dry FIP: pyogranulomatous
interstitial nephritis
• Hypokalemic nephropathy • FIV
• Polycystic renal disease • Morbillivirus
• Neoplasia (primarily lymphoma) • Leptospirosis
• Hypercalcemia

Relationship is critical for successful management

• CKD is common
• Variable between individual cats – etiology and presentation

End result: chronic tubulointerstitial nephritis

3
 4/24/24

Relationship is critical for successful management

• CKD is common
• Variable between individual cats – etiology and presentation
• Reassessment needed
• Balance treatment with quality of life (QoL) - prioritize

Risk factors for CKD

ü Age
• Breed
• Hypertension
• Cardiovascular disease
• Hyperaldosteronism
• Urinary tract infections
ü Predictive: Distribution of “renal failure” in 2238 cats from 23
VMTH in USA
• Weight loss Lulich, Compendium 1992
• Poor body condition
• PU/PD, elevated creatinine (Cr),
low urine specific gravity (usg)

4
 4/24/24

Prevalence of Chronic Tubulointerstitial Nephritis

• A study undertaken in 1987 classified the morphologic category of CKD
in 74 cats. Fifty three percent were chronic tubulointerstitial nephritis
DiBartola, JAVMA 1987

• What initiates the

lymphoplasmacytic
inflammatory response is
unclear & may not be the
same in all individuals.

• Aim: to identify lesions best correlated w renal function

• Two 1st opinion practices – over 18 years – 80 cases
– Necropsies with current biochemistries
– 8 cats had specific diseases
• Cortical interstitial fibrosis correlated best w the severity of azotemia,
hyperphosphatemia, & anemia
• Proteinuria was associated with both interstitial fibrosis & glomerular hypertrophy
• Hypertension is associated with glomerulosclerosis and hyperplastic
arteriolosclerosis

Chakrabarti Vet Path 2012

10

5
 4/24/24

Risk factors for CKD

Progression Survival & quality of life
• Azotemia • Proteinuria
• Metabolic acidosis • Hyperphosphatemia
• Anemia • Hypertension

11

History & Clinical Presentation

• Anorexia/inappetence
• Nausea/vomiting
• PU/PD
• Constipation
• Dehydration
• Lethargy, social apathy
• Oral ulceration/dropping food/salivating
o gno monic
h
• Weight loss
ar e not pat
igns
• Anemia
Clinical s

12

6
 4/24/24

Senior cat preventive care & disease screening

Mature cat Senior cat

[6-10 years] [11 years +]
Consultation &
comprehensive physical
examination including Once per year Every 6 months
blood pressure
assessment
Serum chemistries, CBC,
Once per year Every 6 months
total T4, UA
Survey radiographs - Once per year

13

Diagnostics

1. Blood pressure should be measured in all cats with kidney disease and
renal function should be assessed in all hypertensive cats.
2. Cats that go out, should be FIV tested as a significant relationship
exists between FIV and CKD.
3. Proteinuria is common in FIV-infected cats, more frequent screening
for CKD might be justified in FIV-infected cats.

Paepe JFMS 2013

14

7
 4/24/24

Imaging
• Imaging may help reveal a cause • No correlation between
that affects treatment. ultrasonographic findings
and degree of renal
dysfunction.

15

Why Stage?
• Staging facilitates therapeutic choices
• Important to establish diagnosis of cause of renal disease in early stages
(1 & 2)
– Specific therapy

Human staging

16

8
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17

IRIS staging of renal disease

Stage I Non-azotemic renal II Mild renal III Moderate renal IV Severe renal
disease azotemia azotemia azotemia/ “chronic
renal failure”
Creatinine: mg/dL < 1.6 mg/dl 1.6 – 2.8 mg/dl 2.9 – 5.0 mg/dl > 5.0 mg/dl
(mmol/L) (<140 mmol/L) (140-249 mmol/L) (250-439 mmol/L) (> 440 mmol/L)
SDMA: ug/dl < 18 18-25 26-38 > 38
Clinical signs None +/- inappetence, Usually inappetence, Uremia, clinically ill
weight loss, PU/PD weight loss, PU/PD
Progression Stable for long periods Stable for long periods May progress Fragile
of time of time
Therapeutic goals Identify and treat Identify and treat Modify progression: Ameliorate uremic
specific primary specific primary pethelpful.com
phosphorus signs: protein
kidney disease (e.g., kidney disease (e.g., restriction, omega 3 restriction, anti-
acute pyelonephritis, acute pyelonephritis, fatty acids? emetics, fluidtherapy,
nephrolithiasis) nephrolithiasis) erythropoietin,
appetite stimulation,
www.our-happy-cat.com www.pethelpful.com
dialysis, etc.
Proteinuria classify classify classify classify
BP classify classify classify classify

18

9
 4/24/24

Fasting and well hydrated

iris-kidney.com
19

Creatinine
• Marker only, not made by kidney

• Longitudinal increases in serum creatinine (> 27 μmol/L, 0.3 mg/dl)

within the normal range can suggest declining kidney function (as
opposed to laboratory variation)

• Serum creatinine values must always be interpreted in light of changes

in muscle mass and hydration status

20

10
 4/24/24

Stage 1 Stages 2-4

• Usg < 1.035 while dehydrated • Stages 2-4: Based on ↑ creatinine
prior to increased Creatinine levels in HYDRATED cat
• Usg > 1.040 but has • Stage 2: Cr may be high “normal”
– Pyelonephritis, because is insensitive screening test
– Abnormal shape or size • Cr is affected by:
– Painful kidney(s) – Muscle mass
– Abnormalities on renal imaging, – Renal blood flow:
– Abnormal renal biopsy results • Dehydration
• Uncontrolled hyperthyroidism

21

Do you use SDMA here?

• What is SDMA?
• Symmetric dimethylarginine (SDMA) is an amino acid that is produced
via breakdown of proteins by most cells in the body at a constant rate
• It is eliminated primarily by renal clearance and represents a potential
biomarker for diagnosing and monitoring CKD
– It measures GFR

G Grauer ACVIM 2015 presentation:

Reassessment of "Normal Values” in Dogs and Cats with CKD

22

11
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What does SDMA do?

• Renal biomarkers

GFR Glomerular damage Tubular injury

BUN Proteinuria Urinary NGAL

Creatinine Microalbuminuria Cystatin-c
Cystatin-c
SDMA

• May allow an earlier recognition of ischemic or nephrotoxic kidney

injury

23

Use of SDMA for Early Detection of CKD

• Screening elderly sarcopenic cats?
• Screening non azotemic hyperthyroid cats?
• Cardiac cases for early detection?

But it still measures GFR…

24

12
 4/24/24

Reassessment of "Normal Values” in Dogs & Cats

with CKD
Dogs Cats
• 0.5-1% prevalence • 1-3% increases w age => 30-50% cats >
15 years
• Rate of progression is linear and rapid • Progression unpredictable – stable
many months/years (gradual or
precipitous decline)

It is not possible to improve renal dysfunction caused by CKD

Progression => hypertension, (systemic & intraglomerular), soft-
tissue mineralization, proteinuria (dogs >> cats)

Grauer ACVIM 2015

25

Early diagnosis of CKD: Creatinine

• Markers of GFR
Cr Stage 1 Stage 2 Stage 3 Stage 4
mg/dL < 1.6 1.6-2.8 2.9-5.0 > 5.0
μmol/L < 140 140-250 251-440 > 440

– Reference intervals and methodologies differ w each lab

• Creatinine dependent on muscle mass
• Longitudinal assessment is excellent tool
– E.g., 0.7 => 1.4 mg/dl over several y > 50% êGFR
– 80 => 160 μmol/L

26

13
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Early diagnosis of CKD: SDMA

• Two longitudinal studies: one in dogs and one in cats that developed
CKD, SDMA concentrations increased > normal approximately 17
months prior to serum creatinine concentration > normal
– >160 mmol/L in dogs and > 185 mmol/L in cats
– (> 1.8 mg/dl in dogs and > 2.1 mg/dl in cats)

• But…

Grauer ACVIM 2015

27

Early diagnosis of CKD: SDMA

• If a serum creatinine concentration of > 141
mmol/L (1.6 mg/dl) had been considered
abnormal in the feline study, both serum
creatinine and SDMA would have identified
renal azotemia in these cats at nearly the same
time.
• The 21 healthy geriatric control cats in this
study had serum creatinine concentrations
between 62-141 mmol/L (0.7-1.6 mg/dl); mean
106 mmol/L (1.2 mg/dl)

Grauer ACVIM 2015

28

14
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Using SDMA to upgrade stage?

1 2 3 4

29

What can affect SDMA?

• 21 cats and 12 dogs
• No significant difference in increased SDMA
between patients with (13/21, 62%) and
without (5/12, 42%) renal disease
• Only 4/11 (36%) IRIS stage 1 patients had
increased SDMA
• Patients with weight loss had significantly
lower SDMA

Coss BSAVA Abstract 2018

30

15
 4/24/24

What else affects SDMA?

• 262 non-azotemic hyperthyroid cats and 206 aged-matched, clinically normal cats.
• Finding a high serum SDMA concentration in a hyperthyroid cat can help predict
development of azotemia after treatment. The test has high diagnostic test
specificity (few false-positive results) but relatively low sensitivity (fails to predict
azotemia in most hyperthyroid cats).

• Hyperthyroidism may increase a cat’s GFR and thereby decrease serum creatinine
and SDMA concentrations, masking the presence of CKD.

Peterson JVIM 2018 Geddes JFMS 2022

31

• Objectives: To determine the relationship between serum SDMA,

creatinine and total thyroxine (TT4) concentrations in hyperthyroid cats
before (T0) and 3 months after (T1) receiving a PO fixed dose of
radioiodine.
• n=80 hyperthyroid cats

Yu JVIM 2020

32

16
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• Non-renal influences on SDMA (negatively affects specificity)

• There is biological and individual day to day variability for SDMA
• Age may be an influence on SDMA (kittens vs adults)
• In Birmans, SDMA may be a more accurate reflection of renal function than
creatinine concentration although no direct GFR or renal imaging performed
• Large tumour burden could result in elevated SDMA concentration
• SDMA is lower in cats with diabetes
• Some concurrent diseases may influence SDMA concentrations which highlights the
need for further research

Sargent JSAP 2020

33

= 2.18 mg/dL

34

17
 4/24/24

What Stage is Foxy’s renal

disease?

35

IRIS staging of renal disease

Stage I Non- II Mild III Moderate IV Severe
azotemic renal renal renal
renal azotemia azotemia azotemia
disease
Creatinine < 1.6 mg/dl 1.6 – 2.8 2.9 – 5.0 > 5.0 mg/dl
mg/dL (<140 mg/dl mg/dl (> 440
(mmol/L) mmol/L) (140-249 (250-439 mmol/L)
mmol/L) mmol/L)

2.18 mg/dL/ 193 umol/L pethelpful.com

36

18
 4/24/24

Important!
• WE CAN’T STAGE or
PROGNOSTICATE UNTIL CAT
IS REHYDRATED!

37

Specific vs. Supportive Therapy

• Antibiotics • Late stage 3 and 4, clinical
– Duration manifestation of patient need to
• Calcitriol? be addressed
• Chemotherapy – Disease-associated
symptomatic therapy
• Antihypertensive agents
• Alkalinizing agents, correct
• Antiproteinuric agents
electrolyte imbalances
Hydration • Diuresis
Nutrition
Analgesia

38

19
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Staging: Manage Factors to

• Slow progression • Improve well-being and longevity
– Azotemia – Hyperphosphatemia
– Metabolic acidosis – Proteinuria
– Anemia – Hypertension

Predictive
• Weight loss
• Poor body condition
• PU/PD, elevated Cr, low usg

39

Staging: Manage Factors to

• Slow progression • Improve well-being and
– Azotemia* longevity
– Metabolic acidosis* – Hyperphosphatemia*
– Anemia – Proteinuria
– Hypertension

Hydration
Nutrition
Analgesia

40

20
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SUBSTAGING:
PROTEINURIA &
BLOOD PRESSURE

41

The goal is to identify the risk for future target organ damage.

iris-kidney.com
42

21
 4/24/24

iris-kidney.com
43

CLINICAL RELEVANCE:
PROTEINURIA

44

22
 4/24/24

Proteinuria
• Determined by evaluating urine protein:creatinine ratio =
Urine protein (mg/dL) or mmol/L
Urine creatinine (mg/dL) or mmol/L

• Nonproteinuric = UPC < 0.2

• Borderline proteinuria = UPC 0.2-0.4
– Re-evaluate after two months
• Proteinuria = UPC > 0.4

45

Proteinuria: 4 Q
• Is it real?
• Is it persistent?
• Where is it from?
• What kind of protein is it?

• Anti-proteinuric therapy is not

indicated in all patients with
proteinuria

46

23
 4/24/24

Clinical relevance of proteinuria

• UPC has a high specificity but a low sensitivity (i.e., very few false
positives, lots of false negatives) [Lyon]
• Persistent renal proteinuria is associated with
– Progression of chronic kidney disease
– Survival time
• UPC > 0.4ó increased mortality

47

When should I do a UPC?

• Persistent proteinuria with normal inactive (quiet) sediment or hyaline casts
suggests glomerular disease
• Need concurrent complete urinalysis (urolithiasis, trauma, bacterial cystitis)
• Not useful in patients with prerenal/non urinary or postrenal proteinuria
• If inflammation present, treat based on culture and sensitivity (i.e., if bacteriuria
and pyuria present)
• Then repeat urine protein evaluation (dipstick or SSA) before deciding whether
UPC is needed
• UPC doesn’t differentiate between glomerular, lower urinary inflammation or
hemorrhage

48

24
 4/24/24

Treat: ACE Inhibitors /Angiotensin II receptor blocker

• Benazepril (Fortekor) • Telmisartan (Semintra)
– In cats with urine protein:creatinine • Antihypertensive that affects the
ratio > 0.4
• 0.2-0.4?
AT-1 receptor subtype, which
mediates the adverse effects of
Ang II on the cardiovascular and
renal systems.
– In cats with urine protein:creatinine
ratio > 0.4
• 0.2-0.4?
– Synergistic with ACE inhibitors

49

Treat: ACE Inhibitors /Angiotensin II receptor blocker

• Benazepril (Fortekor) • Telmisartan (Semintra)
– In cats with urine protein:creatinine • Antihypertensive that affects the
ratio > 0.4
• 0.2-0.4?
AT-1 receptor subtype, which
mediates the adverse effects of
• Monitor creatinine, after 3-5 days, Ang II on the cardiovascular and
BP and UPC renal systems.
• Continue to monitor serum – In cats with urine protein:creatinine
chemistries at 2 weeks ratio > 0.4
• May reduce GFR • 0.2-0.4?
• Monitor quality of life, appetite, – Synergistic with ACE inhibitors
body weight, coat condition

50

25
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The goal is to identify the risk for future target organ damage.

iris-kidney.com
51

CLINICAL RELEVANCE:
HYPERTENSION

52

26
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Clinical relevance of hypertension

• Cats w progressive CKD had BP >
than those w stable CKD (155 vs.
147 mm Hg)
• In 69 cats with naturally
occurring CKD, high time-
averaged systolic blood pressure
(159 vs. 136 mm Hg) was
correlated with Chakrabarti
glomerulosclerosis and
hyperplastic arteriolosclerosis

53

Hypertension
• 60% of cats with CKD have
hypertension (Kobayashi) (Stiles)
• May promote progression?
(glomerular injury)

• Treat when systolic pressure is

consistently > 160mm Hg
– Earlier if hypertensive
complications are present

Drawing from Semintra HT promo material

54

27
 4/24/24

Risks of sustained hypertension

• ACVIM Panel on Hypertension (2018)
• Believe increases > 160 mm Hg

< 140

140 - 159 Prehypertensive

• Target organs = brain, eye, kidneys, heart

55

56

28
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Taylor JFMS 2017

catvets.com/hypertension-toolkit

57

Blood pressure in healthy cats

• Role of stress/white coat effect/”situational hypertension”

• 780 healthy cats in rehoming centers
• Doppler – systolic BP
• 120.6 (110.4-132.4) mm Hg median (interquartile range)
• Variation explained by increased age, increased nervousness, male sex,
neutering, history as stray

Payne JVIM 2017

58

29
 4/24/24

Treatment of hypertension
• Goal = get BP < 160 initially, then to 140
mmHg
1. Amlodipine (Norvasc)
– Calcium channel blocker that affects
systemic vascular resistance
• 0.625 mg q24h (0.2 mg/kg PO q24h)
• If starting BP > 200, 1.25 mg po q24h
• Titrate to effect
• Minimal cardiac effects

59

Treatment of hypertension
2. Telmisartan (Semintra HT)
– Angiotensin receptor blocker (Affects RAAS)
• Affects the AT-1 receptor subtype, that mediates the adverse effects of Ang II
on the cardiovascular and renal systems
– 2 mg/kg PO q24h

Combine amlodipine and telmisartan if either drug alone does not

lead to adequate control of blood pressure.

60

30
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NOTE: re drugs affecting hypertension

• Don’t use in any cat that is clinically dehydrated or is showing signs of
hypovolemia.
• Correct dehydration before using these drugs otherwise glomerular
filtration rate may drop precipitously.

61

What about?
• ACE inhibitors
• Beta-blockers

• Ineffective on their own in cats

62

31
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Diagnostics

1. Blood pressure should be measured in all cats with kidney disease and
renal function should be assessed in all hypertensive cats.

Paepe JFMS 2013

63

64

32
 4/24/24

• 21 cats stable IRIS stage 2 or 3

• 1 group placebo, 1 group meloxicam 0.02 mg/kg/d X 6 months
• No statistical difference on BP, BUN , Cr, SDMA, GFR, urine transforming
growth factor-ß:creatinine ratio, urine clusterin, urine cystatin B or
serum inosine
• 4 cats adverse GI effects
• And…

KuKanich JFMS 2020

65

• Mean UPC was greater in the

meloxicam group (0.33) than the
placebo group (0.1) at 6 months
(P=0.006)
• Weigh the risk of potential
increased proteinuria against
quality of life benefits when
considering meloxicam for
analgesia in CKD cats

KuKanich JFMS 2020

66

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ETIOLOGY-SPECIFIC Pyelonephritis
Uretero/nephroliths
THERAPY Hypercalcemia
Neoplasia

67

Bacteriuria, I thought?
1. Bacteria were nonviable in the urine at time of collection (e.g.,
antimicrobial therapy, immunological defenses)
2. Urine sample was improperly handled/preserved resulting in death of
bacteria.
3. Organisms were fastidious and did not survive time between collection
and culture outside of the body.
4. Improper culture technique selected (e.g., anaerobic organism
processed as an aerobe).
5. Bacteria misidentified in sediment (look-alikes)

68

34
 4/24/24

Bacteriuria without LUTS/Pyelonephritis

• Perform C&S on cystocentesis sample

– While awaiting results, start treatment
for Enterobacteriaceae based on regional
susceptibility patterns
– Depending on region, fluoroquinolone
initially

Weese, Vet J, 2019

69

Pyelonephritis

• Treat for 10-14 days

• Repeat urinalysis and culture 1 week
after starting treatment
– If same organism still present, add a
second antimicrobial from C&S
• Culture 1 week after finishing
treatment

Weese, Vet J, 2019

70

35
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Ureteroliths/nephroliths
• 10X increased diagnosed frequency
Take radiographs
– N Am, last 20 years, CaOx
– Risk of hydronephrosis and loss of renal function*
• Fluids +/- mannitol
• Opioids
• Ureteral relaxation: (amlodipine, amitriptyline, tamsulosin, or glucagon)
• Glucocorticoid
• ACE-I (reduce fibrosis)

71

• Abdominal radiograph review of 204 cats from

4-year period
• 37/204 (18%) had at least one urolith
• Located in multiple locations in 15/204 cats
– Nephroliths and cystoliths were each present in
19/204 cats
– Ureteroliths and urethral calculi less common
– 11 cats (30% of those with uroliths) presented with
lower urinary tract signs

Galliano BSAVA Congress Proceedings 2018

72

36
 4/24/24

Hydration
Nutrition
ETIOLOGY-NON-SPECIFIC Reassessment
THERAPY Proteinuria
Hypertension
73

Manage Factors to
• Slow progression • Improve well-being and
– Azotemia* longevity
– Metabolic acidosis* – Hyperphosphatemia*
– Anemia – Proteinuria
– Hypertension

Hydration
Nutrition
Analgesia

74

37
 4/24/24

Hydration
• Critically important to perfuse tissues with oxygen,
& nutrients and scavenge waste. [Grauer 1998]
• Aids in acid-base homeostasis and helps improve
renal blood flow and GFR.
• Despite polydypsia, with an impaired ability to
concentrate urine, exogenous fluids (isotonic,
polyionic fluids IV or SQ) are needed if the cat is
unable to maintain hydration.
• Supplement with water-soluble vitamins?

75

Rehydrate
Example: Ideal healthy hydrated weight: 4.8 kg (10.6lb)
Ill, dehydrated inappetent weight: 3.7 kg. (8.2lb)
• Estimated deficit (based on the findings of firm feces, delay in skin
elasticity, slightly dry oral mucous membranes, normal eye position): 8%

76

38
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Maintenance and dehydration fluid volume

requirements
Maintenance (= 60 ml/kg/day) Ml/kg/day
+ % dehydration (factor) 4.8 X 140 =
Maintenance + 1% 70 672 ml/day
Maintenance + 2% 80
Maintenance + 3% 90 These 672 ml can be given IV
Maintenance + 4% 100 at 28 ml/hour over 24 hours
Maintenance + 5% 110 OR as three SQ boluses of
Maintenance + 6% 120 224ml over 24 hour period
Maintenance + 7% 130
Maintenance + 8% 140 After rehydration: 60 X
Maintenance + 9% 150 4.8/day = 288 ml/day
Maintenance + 10% 160 Adapted from DiBartola

77

More small meals => more drinking

• Effects of Feeding Frequency on Water Intake in Healthy Cats

• For a given energy level, the water intake (ml/g dry matter) significantly
increased by increasing meal frequency. [Kirschvink, ACVIM 2005]

Puzzles…

78

39
 4/24/24

Dehydration: painful? + acidosis

• Headache?
• Inappetence?
• Nausea?
• Lethargy?
• Grumpy
• Constipation My cat is lethargic,
eating less, less
interactive, seems
nauseous

79

Metabolic acidosis: common

• Present in half of cats with late stage 3 and stage 4 (Cr >400 mmol/L, 4.5
mg/dL) [Elliott 2003]
• Acidosis causes muscle wasting through catabolism of endogenous
proteins inhibition of protein synthesis.
• Exacerbates azotemia (regardless of diet) and worsens hypokalemia. In
most cats, readily alleviated by subcutaneous fluid therapy.
• Should be aggressively corrected
• Acidosis => K shift into ECF => hypokalemia

80

40
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Managing hydration
• Clean water
• Canned food/adding water to food
• Water fountains
• Wide bowls in quiet locations
• Subcutaneous fluids
– Monitor success with SQ fluids

81

60 ml/kg ideal weight/day!

82

41
 4/24/24

hypurr@aol.com

83

Tips for SC fluids

• Warm fluids
• Treats
• Treats
• Treats
• Pull skin over needle

84

42
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FEEDING CATS WITH

CHRONIC KIDNEY DISEASE
Photos: Bayer AG

87

They have to eat ENOUGH CALORIES

• Identify underlying metabolic • Consider
problems – Appetite stimulants
– Dehydration – Anti-emetics
– Hypokalemia
– Anemia • Consider assisted feeding early
– Hypertension

88

43
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Inappetence, nausea & vomiting

Generic Name Product™ Dose

Mirtazapine Remeron 2 mg/cat PO q48h

Maropitant Cerenia 0.5-1.0 mg/kg SC q24h
Ondansentron Zofran 0.1-0.15 mg/kg slow IV q6-12h

Metoclopramide Reglan 1-2 mg/kg CRI IV over 24 h

• Uremic gastritis Uremic gastritis is different in cats

McLeland 2014
– H2 receptor antagonists
– Proton pump inhibitor

89

Cats with CKD are NOT hyperacidic

• No difference in gastric pH
• No significant difference in serum gastrin

90

44
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Maropitant
• Demonstrated to palliate
vomiting associated with CKD
• May be helpful in the nutritional
management of cats with CKD

Quimby JFMS 2015

91

Conclusion and Clinical Importance: Only twice-daily PO administered

omeprazole significantly suppressed gastric acidity in healthy cats,
whereas once-daily omeprazole and standard dosages of ranitidine were
not effective acid suppressants in cats.

Dose: 1 mg/kg PO BID

Sutalo JVIM 2015

93

45
 4/24/24

rt term
nl y sho
a ndo
us l y
di c i o
U s e ju

94

Ross Vet Clin N Am 2016

95

46
 4/24/24

What should cats

with CKD be fed?
96

Feeding cats with chronic kidney disease

• Dietary therapy cornerstone since 1950’s Clinical studies
• Studies of naturally occurring stable CKD
feeding renal diets
showed benefit, but…

“Individually or in combination similar dietary modifications

in the present study may have minimized the number of
uremic crises and mortality rate.”
Harte 1994, Barber 1999, Elliott 2000, Plantinga 2005, Ross JAVMA 2006, Geddes 2013

97

47
 4/24/24

Should protein always be restricted?

Renal diets: > protein restriction
– Reduced phosphorus
Renal effect
– Alkalinizing
– Higher caloric density
– Increased potassium
– Fatty acids
– Antioxidants

98

Feline chronic kidney disease(s)

• Common, especially in older cats
• > 30-40% of geriatric cats
• Typically SLOW progression
• Cats live a long time compared to dogs

• Primarily tubulointerstitial inflammation and

fibrosis

99

48
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Nutrition is key!
• Cats w CKD are old; cats w CKD live a long time
– Nutritional needs of aged cats need to be met for cats w CKD
• Poor body condition ó poor prognosis
• Reassess
• Perceived QoL by client

100

Manage Factors to
• Slow progression • Improve well-being and
– Azotemia longevity
– Metabolic acidosis – Hyperphosphatemia
– Anemia – Proteinuria
– Hypertension

101

49
 4/24/24

Hyperphosphatemia
• Many cats in Stage 2 will have normal plasma phosphate concentrations but will
have increased plasma PTH concentration. A chronic reduction of phosphate intake
to maintain a plasma phosphate concentration below 1.5 mmol/l (but not less than
0.9 mmol/l; <4.6 mg/dl but >2.7 mg/dl) is beneficial to patients with CKD.

• Cats with serum phosphate within the IRIS target (4.5 mg/dl or 1.5 mmol/l) may be
at increased risk of developing hypercalcemia when on renal diets.

iris-kidney.com
102

Mineral bone disease

• Renal secondary hyperparathyroidism is more prevalent than
hyperphosphatemia!
• Consider measuring PTH to ensure that phosphorus restriction is
adequate even when serum phosphorus within IRIS recommended
range
• FGF-23 (fibroblast growth factor-23)
– A “phosphatonin”

103

50
 4/24/24

FGF23
• Measuring FGF23 may help to identify cats which would benefit from
dietary phosphate restriction where plasma phosphate is in the target
range. FGF23 >400 pg/ml in the absence of hypercalcaemia, anemia or
marked inflammatory disease is an indication to start dietary phosphate
restriction.

• Monitor serum calcium and if total calcium exceeds 12 mg/dl (3 mmol/l)

switch the cat to a less phosphate restricted diet.

iris-kidney.com
104

Alkalinization
• Acidosis contributes to protein catabolism, decreased
protein synthesis, loss of lean body mass, increased
calcium and potassium excretion
• In humans, correcting acid-base imbalance => clinical
improvement
– Nausea, vomiting, anorexia, weight loss, weakness,
lethargy
– Less loss of LBM We lack data for cats
– May slow progression of CKD

Franch J Am Soc Nephrol 1998; Franch Am J Physiol Renal Physiol 2004

105

51
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Hypokalemia
ü Due to: ü Results in:
• Polyuria • Muscle weakness
• Acidosis • Constipation
• Anorexia • Anorexia
• Vomiting and diarrhea • Progression of renal disease

TREAT using oral supplements or in subcutaneous fluids

Start early – keep serum K > 4.0 mEq/L

106

So, what about

protein?

Isn’t low
protein the
holy grail for
CKD?

107

52
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Does protein cause uremia?

• Creatinine and urea a result of: Small water soluble solutes
Asymmetric dimethylarginine
Protein-bound solutes
3-Deoxyglucosone
Middle molecules
Adrenomedullin

– Protein metabolism (ingested Benzylalcohol

-Guanidinopropionic acid
CMPF
Fructoselysine
Atrial natriuretic peptide
2-Microglobulin

and stored) -Lipotropin

Creatinine
Glyoxal
Hippuric acid
-Endorphin
Cholecystokinin
Cytidine Homocysteine Clara cell protein
• > 60 uremic toxins Guanidine
Guanidinoacetic acid
Hydroquinone
Indole-3-acetic acid
Complement factor D
Cystatin C
Guanidinosuccinic acid Indoxyl sulfate Degranulation inhibiting protein I
Hypoxanthine Kinurenine Delta-sleep-inducing peptide
Malondialdehyde Kynurenic acid Endothelin
Methylguanidine Methylglyoxal Hyaluronic acid
Myoinositol N-carboxymethyllysine Interleukin 1
Orotic acid P-cresol Interleukin 6
Orotidine Pentosidine Kappa-Ig light chain
Oxalate Phenol Lambda-Ig light chain
Pseudouridine P-OHhippuric acid Leptin
Symmetric dimethylarginine Quinolinic acid Methionine-enkepahlin
Urea Spermidine Neuropeptide Y
Vanholder Kidney Int 2003; Lisowaska-Myjak Nephron Clin Uric acid Spermine Parathyroid hormone
Xanthine Retinol binding protein
Pract 2014; Stenvinkel Nephrol Dial Transplant 2000; Tumor necrosis factor alpha
Vanholder Semin Dial 2002

108

Does protein cause uremia?

• Creatinine and urea a result of:
– Protein metabolism (ingested
and stored)
• > 60 uremic toxins
• From inflammation, malnutrition, hypoalbuminemia
• Non-nutritional toxins

Vanholder Kidney Int 2003; Lisowaska-Myjak Nephron Clin Pract 2014; Stenvinkel Nephrol Dial Transplant 2000; Vanholder Semin
Dial 2002

109

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Evidence for protein restriction?

• Results from studies have not been consistent or have been

limited by study design or size.
• Unable to perform meta-analysis

We lack clinical studies in cats with naturally

occurring disease that selectively compare
protein levels.

110

The bigger picture

• Obligatory carnivore
• Evolved to manage a high protein
load
• Cope with restricted protein as
long as minimum requirements
are met

Hewson-Hughes J Expl Bio. 2011; Eisert J Comp Physiol B 2011; Hewson-Hughes J Comp Physiol B 2013; Plantinga Br J Nutr. 2011;
Green J. Nutr. 2008

111

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 4/24/24

Should PROTEIN be restricted?

PROS CONS
• Several studies show benefit • Less palatable
• Alleviation of uremic clinical signs – Look for other causes or hyporexia
– > 2 of depression, lethargy, • Lower protein
anorexia, vomiting, ammonia • Muscle loss
breath, uremic stomatitis
– Look for other causes
• Reduced serum phosphorus and
PTH

112

So what should I feed from stage 2 onwards?

• Exclusively renal diet
• Renal diet + supplementary protein
• Renal diet + geriatric diet
• Geriatric diet (if phosphorus restricted)
• Other lower phosphorus diets
• Anything the cat will eat + intestinal phosphate binders
• Anything the cat will eat

113

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 4/24/24

Supplementing protein
Add 28g (1 oz)
cooked chicken/day
~7g protein

Protein 240 g/1000 kcal

Phos 0.6 g/1000 kcal
= 6 g protein/7 g scoop

114

Controlling serum phosphorus

• Diet
– At what stage?
– Assess muscle condition!
• Intestinal phosphate binders

115

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Phosphorus
• Hyperphosphatemia reflects decreased GFR
• Restriction in moderate azotemia (stage 2-4) affects detrimental effects
(soft tissue mineralization)
• Difficult to have diet replete in protein and restricted adequately in
phosphorus
• Hyperphosphatemia IS associated w progression
– Phosphate restriction may modulate severity of renal pathology
– Phosphate restriction is probably responsible for apparent improved longevity

117

Phosphorus targets
• Increase GFR and decrease absorbed phosphorus
• Reducing phosphorus intake to maintain serum phos between
– 1.29-1.61 mmol/L (4.0-5.0 mg/dL) protects functional nephrons,
improves survival

118

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Phosphorus
• Restriction in moderate azotemia (stage 2-4) reduces risk for renal
secondary hyperparathyroidism
• Intestinal phosphate binders
• Within 2 hours of meal
• Amphogel, AlOH,
• Sucralfate
• Ca salts: Ca carbonate, Ca acetate
• Epakitin, Pronefra

119

Dietary prescription

Renal diet to reduce phosphorus

Moderate
Mild protein Severe protein
protein
restriction restriction
restriction

Supplement protein if not regaining muscle

120

58
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Staged protein restriction

121

Diet choice will depend on

• Phosphorus levels
• Potassium levels
• Uremic or not?
• Proteinuric or not?
• Need to individualize and reassess
• Protein restriction? Every meal?

122

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Vet Clin Small Anim 46 (November 2016)

123

How much energy does an aged cat or cat with

CKD need?
• There is no single equation to calculate MER for any individual patient.
• Average energy needs for adult cats in normal to moderate BCS is about
50 to 60Kcal/kg
– 70 Kcal/kg 0.67 for lean cats
– 130 Kcal/kg 0.4 for overweight cats

Average energy needs for older, lean cats is about

70Kcal/kg ideal body weight

Adapted from slide courtesy D. Laflamme

124

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Feeding aged cats and cats w CKD

• Many aged cats lose weight and • Focus on meeting needs of aged
muscle cat rather than just kidneys
– Decreased ability to digest protein
and fat
• Many cats w CKD are aged but
live years
• Maintaining weight and
condition prolongs life www.dreamstime.com

Perez-Camargo Comp Cont Edu Pract 2004; Harper J Nutr 1998; Laflamme VCNAm 2014; Laflamme JFMS in press; Villaverde
VCNAm 2014; Cupp J Appl Res Vet Med 2008; Cupp Proc Nestlé Purina Comp Anim Nutr Summit 2010; King JVIM 2007; Boyd
JVIM 2008

125

They have to eat ENOUGH CALORIES

• Reassess!!!
– Weight
– Body condition score
– Muscle condition score

• Must individualize nutrition

– Response to renal diet is extremely variable
– Variable etiologies resulting in CKD

126

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Monitor response!

127

Manage Factors to
• Slow progression • Improve well-being and
– Azotemia longevity
– Metabolic acidosis – Hyperphosphatemia
– Anemia – Proteinuria
– Hypertension

128

62
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Anemia of CKDs
• ~ 15-30% of geriatric cats will develop CKD
• 30-65% of these will develop anemia
• Non-linear relationship
1. Iron sequestration (“chronic disease”)
2. Protein malnutrition
3. Blood loss ???
4. Erythropoietin deficiency
5. Decreased rbc lifespan due to azotemia
Anemia => weakness

129

Erythropoietin
• When PCV < 20% (25%?) Monitor response!
• 100 U/kg SC 3X/week until PCV ~35%
• Iron
– Iron dextran 50 mg IM q3-4 weeks
• Monitor PCV q 2 weeks (60-90 days)
– anti-epo antibodies
– maintenance: 100 U/kg SC 2X/week or 50 U/kg 3X/week
• Monitor blood pressure

130

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Erythropoietin
• Anti-epo Ab:
– Transfusion dependency 2-4 months
• “Meeting the unmet needs”
• … some patients may experience adverse effects but no patients can
benefit if it isn’t used
• Darbopoeitin: AranespTM: may be less antigenic than epo
– Dose less frequently
– 0.45 mcg/kg/week

131

Transfusions?
• Some cats with renal disease need them
– Regardless of epo therapy
– With diligent and proper preparation and monitoring (type and cross
match)
– Multiple red cell transfusions are well tolerated
• Cross match each time

132

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Antioxidants in chronic kidney disease

• High aerobic metabolic rate
• Require 10% of total body oxygen consumption
• Sensitive to hypoperfusion from hypovolemia or
hypotension => at risk for ischemic injury
• Injuries óacute renal failure (e.g., toxins, anaesthetic
accidents, obstructed outflow) may heal if addressed
quickly
• Ongoing oxidative stress may => progression of chronic
kidney diseases

133

Not enough research yet

Vectorstock.com

134

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Fatty acids in chronic kidney disease

135

Summary
• Determine IRIS Stage
– Evaluate for hypertension
– If increased urinary protein in a “quiet” sediment, consider UPC
• Hydrate and maintain hydration
• Calculate and ensure calories received
– Communicate - medical record and to client
– Consider short-term feeding tube
– Assess body and muscle condition for protein adequacy
• Treat specific etiologies if identified
• Monitor, follow-up, reassess

139

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IRIS Stage Treatment

1 Discontinue nephrotoxic drugs and rule out treatable underlying disease (e.g.,
pyelonephritis);
Correct dehydration, maintain hydration;
Correct other pre- and post-renal causes or azotemia;
Monitor blood pressure and treat hypertension;
UPC 0.4-1.0 treat and monitor;
UPC 1.0-2.0 investigate underlying cause, treat and monitor;
UPC > 2.0 renal biopsy, treat and monitor
2 As Stage 1 plus treat if UPC > 0.4;
Aim to maintain phosphate levels < 1.45 mmol/L;
Consider early renal diet (i.e., phosphate restricted but not protein restricted);
Maintain serum potassium > 4.1 (potassium gluconate)
Consider subcutaneous fluids to correct acidosis, azotemia, hyperphosphatemia
3 As Stage 2 plus aim to maintain phosphate levels < 1.6 mmol/L;
Treat anemia if PCV < 20% (iron and erythropoietin/darbopoeitin);
Ensure consuming adequate calories and protein with early or advanced renal diet (body
condition score, muscle condition score (MCS), calculate and communicate food
quantities);
Manage nausea (proton pump inhibitors, antiemetics);
Stimulate appetite and be proactive with feeding tubes;
Daily subcutaneous fluid therapy
4 As Stage 3 plus aim to maintain phosphate levels < 1.9 mmol/L;
Focus on maintaining nutritional status;
Consider advanced renal diet (greater protein restriction) but ensure that MCS isn’t
declining

140

IRIS Stage Treatment

1 Discontinue nephrotoxic drugs and rule out treatable underlying disease (e.g.,
pyelonephritis);
Correct dehydration, maintain hydration;
Correct other pre- and post-renal causes or azotemia;
Monitor blood pressure and treat hypertension;
UPC 0.4-1.0 treat and monitor;
UPC 1.0-2.0 investigate underlying cause, treat and monitor;
UPC > 2.0 renal biopsy, treat and monitor
2 As Stage 1 plus treat if UPC > 0.4;
Aim to maintain phosphate levels < 1.45 mmol/L;
Consider early renal diet (i.e., phosphate restricted but not protein restricted);
Maintain serum potassium > 4.1 (potassium gluconate)
Consider subcutaneous fluids to correct acidosis, azotemia, hyperphosphatemia
3 As Stage 2 plus aim to maintain phosphate levels < 1.6 mmol/L;
Treat anemia if PCV < 20% (iron and erythropoietin/darbopoeitin);
Ensure consuming adequate calories and protein with early or advanced renal diet (body
condition score, muscle condition score (MCS), calculate and communicate food
quantities);
Manage nausea (proton pump inhibitors, antiemetics);
Stimulate appetite and be proactive with feeding tubes;
Daily subcutaneous fluid therapy
4 As Stage 3 plus aim to maintain phosphate levels < 1.9 mmol/L;
Focus on maintaining nutritional status;
Consider advanced renal diet (greater protein restriction) but ensure that MCS isn’t
declining

141

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IRIS Stage Treatment

1 Discontinue nephrotoxic drugs and rule out treatable underlying disease (e.g.,
pyelonephritis);
Correct dehydration, maintain hydration;
Correct other pre- and post-renal causes or azotemia;
Monitor blood pressure and treat hypertension;
UPC 0.4-1.0 treat and monitor;
UPC 1.0-2.0 investigate underlying cause, treat and monitor;
UPC > 2.0 renal biopsy, treat and monitor
2 As Stage 1 plus treat if UPC > 0.4;
Aim to maintain phosphate levels < 1.45 mmol/L;
Consider early renal diet (i.e., phosphate restricted but not protein restricted);
Maintain serum potassium > 4.1 (potassium gluconate)
Consider subcutaneous fluids to correct acidosis, azotemia, hyperphosphatemia
3 As Stage 2 plus aim to maintain phosphate levels < 1.6 mmol/L;
Treat anemia if PCV < 20% (iron and erythropoietin/darbopoeitin);
Ensure consuming adequate calories and protein with early or advanced renal diet (body
condition score, muscle condition score (MCS), calculate and communicate food
quantities);
Manage nausea (proton pump inhibitors, antiemetics);
Stimulate appetite and be proactive with feeding tubes;
Daily subcutaneous fluid therapy
4 As Stage 3 plus aim to maintain phosphate levels < 1.9 mmol/L;
Focus on maintaining nutritional status;
Consider advanced renal diet (greater protein restriction) but ensure that MCS isn’t
declining

142

IRIS Stage Treatment

1 Discontinue nephrotoxic drugs and rule out treatable underlying disease (e.g.,
pyelonephritis);
Correct dehydration, maintain hydration;
Correct other pre- and post-renal causes or azotemia;
Monitor blood pressure and treat hypertension;
UPC 0.4-1.0 treat and monitor;
UPC 1.0-2.0 investigate underlying cause, treat and monitor;
UPC > 2.0 renal biopsy, treat and monitor
2 As Stage 1 plus treat if UPC > 0.4;
Aim to maintain phosphate levels < 1.45 mmol/L;
Consider early renal diet (i.e., phosphate restricted but not protein restricted);
Maintain serum potassium > 4.1 (potassium gluconate)
Consider subcutaneous fluids to correct acidosis, azotemia, hyperphosphatemia
3 As Stage 2 plus aim to maintain phosphate levels < 1.6 mmol/L;
Treat anemia if PCV < 20% (iron and erythropoietin/darbopoeitin);
Ensure consuming adequate calories and protein with early or advanced renal diet (body
condition score, muscle condition score (MCS), calculate and communicate food
quantities);
Manage nausea (proton pump inhibitors, antiemetics);
Stimulate appetite and be proactive with feeding tubes;
Daily subcutaneous fluid therapy
4 As Stage 3 plus aim to maintain phosphate levels < 1.9 mmol/L;
Focus on maintaining nutritional status;
Consider advanced renal diet (greater protein restriction) but ensure that MCS isn’t
declining

143

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 4/24/24

IRIS Stage Treatment

1 Discontinue nephrotoxic drugs and rule out treatable underlying disease (e.g.,
pyelonephritis;
Correct dehydration, maintain hydration;
Correct other pre- and post-renal causes or azotemia;
Monitor blood pressure and treat hypertension;
UPC 0.4-1.0 treat and monitor;
UPC 1.0-2.0 investigate underlying cause, treat and monitor;
UPC > 2.0 renal biopsy, treat and monitor
2 As Stage 1 plus treat if UPC > 0.4;
Aim to maintain phosphate levels < 1.45 mmol/L;
Consider early renal diet (i.e., phosphate restricted but not protein restricted);
Maintain serum potassium > 4.1 (potassium gluconate)
Consider subcutaneous fluids to correct acidosis, azotemia, hyperphosphatemia
3 As Stage 2 plus aim to maintain phosphate levels < 1.6 mmol/L;
Treat anemia if PCV < 20% (iron and erythropoietin/darbopoeitin);
Ensure consuming adequate calories and protein with early or advanced renal diet (body
condition score, muscle condition score (MCS), calculate and communicate food
quantities);
Manage nausea (proton pump inhibitors, antiemetics);
Stimulate appetite and be proactive with feeding tubes;
Daily subcutaneous fluid therapyQuality of life
4 As Stage 3 plus aim to maintain phosphate levels < 1.9 mmol/L;
Focus on maintaining nutritional status;
Consider advanced renal diet (greater protein restriction) but ensure that MCS isn’t
declining

144

What’s important in management?

• Nutrition: vital to address any causes of inappetence that could result in
diet change failure.
dequate
– Phosphorus Ensure a
early
– Muscle wasting indicates inadequate protein nutrition
• Hydration
• Hypertension
• Hypokalemia
• Anemia
• Relationship!
Quality of life
145

69
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Resources

www.iris-kidney.com
www.acvim.org
• ACVIM Proteinuria consensus statement 2005
• ACVIM Hypertension consensus statement 2018
• ACVIM Gastrointestinal protectants consensus statement 2018

146

Sparkes JFMS 2016

147

70
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hypurr@aol.com

148

Resources

149

71
 4/24/24

Thank you!
Do you have any questions?
hypurr@aol.com
150

72
 4/24/24

Feline Eosinophilic
Granulomas:
Complex or maybe
not?

Margie Scherk
DVM, Dip ABVP (Feline Practice)
Vancouver, Canada

Thank you to

for sponsoring
2

1
 4/24/24

Background
• Three “entities”?
1. Indolent (eosinophilic) ulcer
2. Eosinophilic plaque
3. Eosinophilic granuloma

Background
• Three “entities”?
1. Indolent (eosinophilic) ulcer
2. Eosinophilic plaque
3. Eosinophilic granuloma
• Or are they all allergic?

2
 4/24/24

Feline dermatology at Cornell University: 1407

cases (1988–2003)

Scott JFMS 2012

• 1407 cats with dermatologic diagnoses

– 1887 diagnoses
– all cats seen at the university hospital (22,135)

Scott JFMS 2012

3
 4/24/24

Top 10
(#, % of skin cases; % of cats seen at hospital)

• Allergy (298; 15.8%; 1.35%), • Feline acne (74; 3.9%; 0.33%),

• Atopic dermatitis (194; 10.3%; 0.88%), • Flea-bite allergy (70; 3.7%; 0.32%),
• Bacterial folliculitis/ furunculosis (189; • Cutaneous adverse drug reaction (56;
10.0%; 0.85%), 3.0%; 0.25%),
• Otodectic mange (115; 6.1%; 0.52%), • Idiopathic eosinophilic-granuloma
• Flea infestation (99; 5.2%; 0.45%), complex (55; 2.9%; 0.25%)
• Abscess (51; 2.7%; 0.23%)

Scott JFMS 2012

Overall
• Allergies of all types, combined, accounted for 32.7% of all the
feline dermatoses!
• Himalayans and males were significantly over-represented

Scott JFMS 2012

4
 4/24/24

Scott Japanese J Vet Dermatol 2012

Clinical features: EGC all forms

• Firm, well circumscribed papules
or nodules
• Initially skin and hair is normal
• Alopecia develops if in haired
region
• Colour change (erythematous,
yellow, orange)
• May ulcerate and crust

10

5
 4/24/24

1. Indolent ulcer
• “Rodent” or “eosinophilic ulcer”
• Mucocutaneous junction of lip
• Raised, well-demarcated
• Non-pruritic
• Differentials: focal trauma, SCC,
mast cell tumour

11

Rodent ulcers have nothing to do with

rodents…unlike Feline leprosy
(Mycobacterium lepraemurium or M. visibilis)

12

6
 4/24/24

Feline Leprosy
Mycobacterium lepraemurium
or M. visibilis

Malik JFMS 2002

13

Feline leprosy
• Raised, fleshy, tumorlike lesions of the skin and subcutis
– Initially localized but can enlarge and ulcerate.
– +/- lymphadenopathy
– On head, forelimbs
• +/- signs of systemic illness

14

7
 4/24/24

EOSINOPHILIC GRANULOMAS

23

2. Eosinophilic plaque
• Any haired location
– Ventral abdomen, inguinal region, thighs, paw pads, face, neck
• Raised, well-demarcated, alopecic, flat-topped, erythema,
crust
– May look like coalescing miliary dermatitis
• Intensely pruritic

24

8
 4/24/24

Eosinophilic plaque

25

Eosinophilic plaque
• Differentials: dermatophytosis, lymphoma, SCC, MCT, mammary
adenocarcinoma, cutaneous viral (FHV-1), mycobacterial, fungal
infection

• Plaques and nodules are caused in most cases by infectious, allergic,

metabolic or neoplastic diseases
• Cytology
• Histopathology needed to confirm diagnosis

Colombo, Feline Derm 2020

26

9
 4/24/24

3. Granulomatous variant
• Raised, well-demarcated, non-inflammed, erythematous caudal thigh:
“Linear granuloma”

27

Granulomatous variant: feet

• Firm nodules in interdigital spaces or on pads

Copyright © TheSkinVet.co.uk

28

10
 4/24/24

Granulomatous variant: chin

• Soft swelling chin or lower lip: • Hard, ulcerated lesion +/- gritty
“pouting” yellow-white material

www.vetlive.com

29

Eosinophilic and mast cell allergic reaction

30

11
 4/24/24

Granulomatous variant: oral

31

Granulomatous variant: oral

veterinarydentistry.net www.vetnext.com

32

12
 4/24/24

• 38 cats
• Tongue most common
• Oral discomfort, difficulty eating
• Ulcers common
• 2/3 of cats had more than 1 lesion
• Cats with palatal lesions are more likely to show respiratory signs and
less likely to respond to treatment
• Response to treating with antimicrobial + immunosuppressive average 2
months
• ALSO, other treatments

Soltero-RiveraJAVMA 2023

33

From Soltero-Rivera JAVMA 2023

34

13
 4/24/24

• 297 oral cavity lesions

• Males, 7-10 years, European shorthair

Falcão JFMS 2020

35

Top 2 most common

(a) Chronic gingivostomatitis (b) Eosinophilic granuloma complex

Falcão JFMS 2020

36

14
 4/24/24

Granulomatous variant: pinna

• Uncommon

37

Granulomatous variant
• Differentials: dermatophytosis, lymphoma, SCC, MCT, mammary
adenocarcinoma, cutaneous viral (FHV-1), mycobacterial, fungal
infection, bacterial folliculitis/furunculosis/abscess, foreign body
reaction, sterile granuloma

38

15
 4/24/24

Granulomatous and indolent variants

39

Distribution of EGC lesions

• 55 cases out of 1407 feline dermatology patients (4%)
• 42% on lips (+/- commissure, chin, thigh, paw)
• 22% caudal thigh
• 18% chin

• 82% lesions in > 1 location

Scott, Jpn J Vet Dermatol, 2012

40

16
 4/24/24

Etiology
• Mostly hypersensitivity reaction • Less commonly:
to: – Mites
– Environmental allergens (atopy) – Bacteria (1ry vs 2ndy?)
– Food – Dermatophytes
– Insects (fleas) – FHV-1
– Self? – Foreign body (insect or plant parts,
hair shafts)
– Genetic predisposition (eosinophilic
dysregulation)?

41

Mites + EGC
• Lynxacarus radovskyi are “fur
mites” found on hair shafts

42

17
 4/24/24

• “Salt and pepper” fur

• “EGC is immune response to many insults esp. to allergies, and the
treatment of choice are corticosteroids”
• Treated with:
– Moxidexin + Imidacloprid or Fluralaner
– Treat all in-contact cats
– + Environmental cleaning!
– Cats w EGC lesions also received prednisolone

Da Rocha J Parasit Dis 2019

43

Diagnostics
• Confirm diagnosis
• Cytology: touch impression
skinvet.wordpress.com -

Kimberly S. Coyner‬ www.jpathology.com

44

18
 4/24/24

Wood’s lamp

leicesterskinvet.com veterinarypage.vetmed.ufl.edu

45

Microscopic exam: skin scrapings

loudoun.nvcc.edu

46

19
 4/24/24

Skin biopsies
• Biopsy oral lesions
• Non-ulcerated lesions
www.ed.ac.uk

www.aafp.org myhealth.alberta.ca

47

• Chronic recurrent unilateral

anterior uveitis
• Improved with treatment
• 4 year history allergic/immune
mediated skin disease
• Eventual enucleation (glaucoma)
• Periocular crusting, swelling
• Histologic diagnosis eosinophilic
infiltrate inside anterior chamber

Newbold Vet Ophthal 2022

48

20
 4/24/24

Evaluate for systemic disease

• CBC, serum biochemistries
• FeLV/FIV serology
• Urinalysis
• Toxoplasmosis titre
– If cyclosporine therapy considered
• Ectoparasite elimination trial 6-8 weeks
– All in contact cats and environment
• Dietary trial 6-8 weeks

49

• Eosinophilia uncommon
• Toxoplasmosis titre
– If present, protected
– Negative, at risk if exposed while on cyclosporine
• Serum allergy testing?
• Intradermal allergy testing?

50

21
 4/24/24

Therapy
• Specific
– Itraconazole for dermatophytosis
– Fleas
– Trigger allergen avoidance
• Immunomodulatory therapy
– Prednisolone
– Cyclosporine
– Chlorambucil
– Essential fatty acids

51

Prednisolone
• Oral preferable
• 1-2 mg/kg PO q24h
• Higher dose if needed
• Taper to alternate day when lesions resolve

52

22
 4/24/24

Chlorambucil
• Give concurrently with prednisolone
• 2 mg/cat PO 2-3 X/week
• If corticosteroids contraindicated, use alone
• CBC q 2 weeks for 3 months to monitor for marrow
suppression

53

Cyclosporine
• 5 mg/kg PO q24h
– Equivalent to prednisolone 1 mg/kg
• Higher dose if needed
• Treat for 4 weeks then taper to alternate day and to twice a
week
• Caution for drug interactions (cytochrome P3A)

54

23
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Lappin et al. Am J Vet Res 2015;76:351–357

OBJECTIVE
• To evaluate whether anti-inflammatory doses of cyclosporine
activate Toxoplasma gondii in chronically infected cats or
potentiate infection in cats exposed for the first time.

55

Background

• High doses of cyclosporine are used to reduce the chance for organ
rejection in cats undergoing renal transplantation.
• At lower doses, cyclosporine has been used in the treatment of
inflammatory bowel disease, stomatitis, and dermatitis in cats that are
refractory to other drugs and has been approved at a dose of 7 mg/kg
for the treatment of feline allergic hypersensitivity dermatitis.
• At high doses, the drug has been associated with activation of a variety
of chronic infectious diseases, including toxoplasmosis, or worsening of
disease if primary exposure occurred while the cat was receiving
immunosuppressive dosages.
Lappin et al. Am J Vet Res 2015

56

24
 4/24/24

Study design

• 30 T gondii–negative cats divided into 3 groups of 10 cats

• Group 1 (control) cats received a placebo for 126 days
• Group 2 cats received a placebo for 84 days, followed by cyclosporine at
7.5 mg/kg/d, PO, for 42 days
• Group 3 cats received cyclosporine at 7.5 mg/kg/d, PO, for 126 days
• Cats were orally inoculated with T gondii on day 42. Results for fecal
flotations, PCR assays, and histologic examinations and IgM and IgG
titers were analyzed. Cyclosporine concentrations were measured on
selected days.
Lappin et al. Am J Vet Res 2015

57

Results

• All cats became infected by T gondii and developed signs of self-limiting

gastrointestinal tract infection
• Group 3 had the highest incidence and severity of CNS and pulmonary
histopathologic findings typical of toxoplasmosis. One cat in group 3
died of systemic toxoplasmosis; that cat had a cyclosporine
concentration of 1,690 ng/mL
• Group 2 cats infected with T gondii before cyclosporine administration
did not have repeated oocyst shedding
• Group 3 cats shed fewer oocysts for a shorter time than did control cats

Lappin et al. Am J Vet Res 2015

58

25
 4/24/24

Conclusions and clinical relevance

• Oral administration of cyclosporine in accordance with the
protocol for this study did not potentiate the enteroepithelial
phase of T gondii infection
BUT
• Cats with high cyclosporine blood concentrations at the time of
primary T gondii infection may be at risk of developing
systemic toxoplasmosis

Lappin et al. Am J Vet Res 2015

59

Omega 3:6 fatty acids

• May benefit skin barrier and decrease inflammatory cascade

60

26
 4/24/24

Outcome
• In 55 cases of Idiopathic eosinophilic granuloma, only 22% received
treatment yet all went into remission over 1-9 months
– Spontaneous resolution possible?
• When allergic, need immunomodulatory therapy!

Scott, Jpn J Vet Dermatol, 2012

61

• 9 year old NM DSH

• Multiple deep lesions on all 4 limbs, nodule on R
pinna, pad discolouration

Hopke JFMSOR 2019

62

27
 4/24/24

History and management

• Indoors only, single pet • Histopathology: EGC with
• No trauma ulceration, necrosis
• Lesions appeared abruptly – Prednisolone, hydrolyzed food trial
• No apparent pain or pruritis
• Retrovirus negative, blood, urine,
thoracic Xrays, abdominal
ultrasound normal
– Eosinophilia
• Biopsied
– Pradofloxacin, buprenorphine
• Reassessment: improvement
Hopke JFMSOR 2019

63

Client missed recheck

• Exacerbation after finishing steroids
• Cultured methicillin-resistant Staph
pseudointermedius
– Chose appropriate antibiotics and restarted
corticosteroids
• Recheck improvement

Hopke JFMSOR 2019

64

28
 4/24/24

Antibiotic choice
• Sensitive to amikacin and
chloramphenicol
• Extended sensitivity panel:
vancomycin, rifampicin, linezolid
– Pharmacologist recommended
linezolid
• Linezolid – 3rd tier
– Should be reserved for human use
and only when nothing else works

65

Pinna
• Ear nodule continued to grow
• Ruptured intermittently
– Bleeding, e-collar, miserable
• Start cyclosporine and taper
prednisolone
– No improvement
• Pinnectomy
• Histopathology: hemangiosarcoma

Hopke JFMSOR 2019

66

29
 4/24/24

9 months later – still on prednisolone

• Continuing low-dose pred and cyclosporine, diet, fluralaner

Hopke JFMSOR 2019

67

Moving
along…

68

30
 4/24/24

What about other allergies or acne?

69

Acne?

70

31
 4/24/24

Chin Acne

71

Yumi

72

32
 4/24/24

Yumi

73

74

33
 4/24/24

Feline atopic skin syndrome (FASS)

• Feline atopic skin syndrome refers specifically to allergic skin disease
caused by environmental allergens.
• Presentations:
– Miliary dermatitis
– Symmetrical alopecia
– Facial head and neck pruritis
– Eosinophilic granuloma complex

Vargo TVP 2022

75

Feline atopic skin syndrome (FASS)

• Diagnosis:
– Pruritis and inflammation that is not food associated
– Allergy testing not helpful
• Treatment:
– Glucocorticoids
– Cyclosporine
– Oclacitinib (Apoquel) off-label (1 mg/kg PO BID)
– Allergen-specific immunotherapy

hypurr@aol.com
Vargo TVP 2022

76

34
 4/24/24

Atopic chin and nose

77

Atopic chin and face

78

35
 4/24/24

Skin allergy

79

l ergy
f al
s eso
ca u
her
fo r ot
k
Lo o

80

36
 4/24/24

81

For in-clinic tools visit www.cavd.ca

hypurr@aol.com

82

37
 4/24/24

Thank you. Do you

have questions?

hypurr@aol.com

83

38
 4/24/24

UPDATE IN FELINE
GASTRO-ENTERIC
SYNDROMES

Margie Scherk DVM, DABVP (Feline)

Vancouver, Canada

Thank you to

for sponsoring
2

1
 4/24/24

Diarrhea In The Cat:

Stool’s Too Soft

2
 4/24/24

Clarify ?Diarrhea
What kind of diarrhea is this?
• Acute vs. chronic
• Consistency
• Colour • Volume
• Odour • Frequency
• Small bowel diarrhea?
• Large bowel diarrhea?
• Due to systemic disease?

Ask: “Would you say

his feces are…?”
• Hard pellets?
• Moist logs?
• Cow patties?
• Coloured water?

Please describe what

happens when he defecates?

Image: Iams

3
 4/24/24

ww.infofit.ca/healthy-poop/

4
 4/24/24

Chronic or recurrent diarrhea

Intestinal (luminal or mural)
• Inflammatory
• IBD
• Dietary intolerance or hypersensitivity
• Neoplastic
• Lymphoma, plasma cell tumour, adenocarcinoma
• FIP
• Infectious
• Bacterial, viral, fungal, parasitic

Inflamed reservoir

Image from felineconstipation.org

10

5
 4/24/24

Large vs. Small bowel

• Increased frequency • Normal or increased
• Decreased volume frequency
• Urgency • Normal or increased
volume
• Tenesmus
• Undigested food or fat
• Blood
• Abnormal colour
• Mucus
• Weight loss
• Vomiting
• Polyphagia
• Vomiting
• Rarely blood

11

But is it even intestinal?

• Cholangitis
• Pancreatitis
• Hyperthyroidism
• Systemic infections
• Exocrine pancreatic insufficiency

• Compression
• Obstipation

12

6
 4/24/24

Clinical history
• Age
• Indoors/outdoors
• Travel? Boarding?
Showing?
• Retroviral status
• Changes in diet and
• Multiple cat household supplements
• Health of other cats • Medications
• Concurrent illnesses • Behaviour changes
• Vaccination and
deworming history

13

Physical examination
• Mucous membrane colour - pallor?
• Coat quality – hydration, digestion
• Muscle condition
• Skin turgor - hydration, age
• Effusion or edema – inflammation, neoplasia, protein balance
• Thyroid enlargement/asymmetry
• Intestinal palpation
• Abdominal discomfort
• Lymph node enlargement

14

7
 4/24/24

• Deworm,
Well • Feed bland
Acute intestinal diet
• Deworm
Diarrhea Ill • Correct
Chronic hydration
status;
• If persists, treat
as chronic

15

• Fast 24h, feed

Well bland intestinal
Acute
diet
Diarrhea
Chronic Deworm • Blood work,
urinalysis, fecal
exam
Ill • Therapeutic trial
• Imaging
• Biopsy

16

8
 4/24/24

Causes of recurrent or chronic feline diarrhea

• Infectious: Tritrichomonas foetus, Giardia sp., Cryptosporidium sp., ascarids,
tapeworms, whipworms, hookworms, Strongyloides sp.; FeLV, FIV; Salmonella sp.,
Campylobacter jejuni, Clostridium sp.; Histoplasma capsulatum
• Inflammatory: lymphoplasmacytic, eosinophilic, neutrophilic etc., enterocolitis
(inflammatory bowel diseases)
• Neoplastic: alimentary lymphoma, adenocarcinoma, intestinal mast cell disease
• Metabolic/systemic: hyperthyroidism, cholangiohepatitis, pancreatitis, EPI,
portosystemic shunt, cobalamin deficiency, folate deficiency
• Toxic/drug-induced: house plants, insecticides, NSAIDs, anthelmentics,
antibacterials, lactulose
• Diet-associated: intolerance (milk, spicy foods), indiscretions (garbage, hair,
bones, plants, string, etc), specific protein hypersensitivities

17

Etiology
• Infectious
• Inflammatory
• Neoplastic
• Metabolic/systemic
• Toxic/drug-induced
• Diet-associated

18

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Etiology
• Infectious
• Inflammatory
• Neoplastic
• Metabolic/systemic
• Toxic/drug-induced
• Diet-associated

19

Infectious
SMALL BOWEL LARGE BOWEL
• FeLV/FIV, Panleukopenia • Strongyloides
• Hookworms (Ancylostoma), & • Trichuris
roundworms (Toxocara, Toxascaris) • Tritrichomonas foetus
• Coccidia (Isospora) • Clostridium spp.
• Giardia
• Cryptosporidium
• Salmonella, Campylobacter
• Histoplasma

20

10
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Diarrhea - Initial
diagnostics

• Response to broad spectrum

dewormer
• FeLV/FIV testing
• Fecal flotation-centrifugation
• Direct fecal smears
• Rectal cytology (large bowel)
• Giardia fecal antigen
• Tritrichomonas foetus testing (large
bowel)

21

Chronic diarrhea Advanced diagnostics

• CBC, chemistry panel, total T4 • Imaging (ultrasound, radiography)
• Urinalysis • Partial obstructions, masses
• Dietary trial • Cobalamin, folate, fPLI, fTLI
• Imaging-assisted biopsy
• Intestinal biopsy

22

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Fecal examinations
• Fecal flotation separates parasites and
objects in feces based on their differential
densities.
• Regular flotation: nematode ova, coccidia
oocysts, Giardia cysts
• Organisms that are heavier than the solution will sink to the
bottom. Spinning in a centrifuge, places a much greater force on
the heavier objects, resulting in a more rapid and efficient
separation of parasites and debris, and greater yield

23

Why don’t we do fecal exams

• Disgusting
• Many false negatives
• Save client money
• We have a false sense of security that a “broad spectrum” product
is all that is needed
• All-in-one products create resistance
• All-in-one products seldom actually cover “all”
• All-in-one products discourage risk-based purrsonalized parasite
management

CPEP: Guidelines For The Management Of Parasites In Dogs And Cats 2019
24

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Why (we need to) do fecal examinations?

• Tailor anthelmintic use for individual
• Detect developing anthelmintic resistance
• Reduce unnecessary use of anthelmintics in low risk situation
• Detect parasites not treated/affected by routine anthelmintics
(cestodes, protozoans)
• Giardia
• Detect new parasites in new regions and changing climate

CPEP: Guidelines For The Management Of Parasites In Dogs And Cats 2019
25

Use fecal centrifugation - not flotation

Why fecal centrifugation is

better:
capcvet.org/expert-articles

wcvm.usask.ca/learnaboutparasites/diag
nostics/faecal-sedimentation.php

CPEP: Guidelines For The Management Of Parasites In Dogs And Cats 2019
26

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www.youtube.com/watch?v=mZunPcRr7C4
27

Excellent resource – which test for which organism

• https://todaysveterinarypractice.com/wp-
content/uploads/sites/4/2016/09/T1307C02.pdf

29

14
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Direct fecal smear/wet mount

• To look for protozoal trophozoites
• Giardia and Tritrichomonas
• Rice grain-size feces from surface of fresh, warm feces (mucus)
or from rectum
• Mix with saline
• Examine drop microscopically 40X

30

Diarrhea diagnostics: rectal cytology

• Esp. for large bowel diarrhea ü Inflammatory cells,
• Saline moisten swab neoplastic cells, fungal
four slides hyphae, Cryptosporidium,
• Cytology and gram stain Campylobacter-like
organisms
ü Clostridial spores: fecal
enterotoxin assay
• Interpret results carefully

31

15
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Tritrichimona
Pmns, mixed with
s
trophozoites, few
Cocci
rods and very thin
Rods
spirillaform bacteria

Trophozoites,
mixed
bacteria &
fecal yeast

32

Fecal culture – When?

• Not routinely and not routine culture medium
• For specific pathogens
• Specific media needed: Salmonella, Campylobacter, Clostridia
• Acute/recurrent outbreak in multiple cats in household or after showing

33

16
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Dietary trial
• If still no answers, before biopsies
• Highly digestible, single novel protein
• To minimize antigen –antibody complex formation in intestinal wall
• No other food for 2-3 weeks
• If improvement occurs, then continue for 6-8 weeks total for
healing
• Complete and balanced diet

34

Tritrichomoniasis – What?
• Tritrichomonas foetus (T. blagburni)
• Worldwide
• Foul smelling soft-liquid stool
• Mucus, hematochezia, straining,
incontinence, flatulence
• Generally good condition and energy +/-
stained/inflamed perineum

35

17
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What?
• Occasionally (20%?) severe systemic disease
• Fever, anorexia, vomiting, weight loss
• Look for concurrent cause?
• Subclinical infection exists – carriers shed trophozoites
• Housemates of affected cats should be tested

36

Where? Who?
• Chronic large bowel diarrhea • Young cats (esp < 1 year)
• Organisms in the ileum, cecum, • High density populations (living
colon with > 5 cats),
• Live in crypts and in mucus • Purebred increases risk, but
• Lymphoplasmacytic and neutrophilic singletons can develop disease
colitis years after infection
• Shed trophozoites that are
• Not stable in environment if dry
• In moisture may survive up to 7 days
• Fecal oral transmission if feces still
wet

37

18
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Testing - How?
• Gloved finger
• Saline flush of colon
• Microscopic exam
• Culture
• PCR

Tolbert, Compendium 2009

38

Testing - How?
Test type Sensitivity Specificity Cost Comments
Fecal flotation 0% 0% $ No cyst stage
Direct fecal 14.7% Identify by $ Best if use fecal mucus
smear (wet shape and False negatives common-
mount/rectal motility multiple samples may be
cytology) needed
Difficult to differentiate from
non-pathogenic
Pentatritrichomonas hominis
Fecal culture
MDM/InPouch TF 26.4%/58.8% 100% $$ Up to 10 days

Histopathology 56% high Sensitivity increases with #

biopsies
PCR 90+% high $$$ Indicated when repeated direct
exam and culture are negative

39

19
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T. Foetus vs. Giardia

“forward movement” “falling leaf”

CDC photo

40

41

20
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42

Testing - Culture

43

21
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44

Testing - PCR
• No recent antibiotic therapy
• Freshly voided abnormal feces
• No cat litter
• Don’t refrigerate
• Feces into sterile tube topped up with alcohol
• PCR in diarrheic cats, 10-31% are positive for T. foetus – as high
as 70% of cats on PCR but that includes healthy cats

45

22
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Treatment
• Self-limiting but duration 5-24 months (median 9 months)
• Ronidazole can speed response. Limit dose to 30 mg/kg PO SID
for 14 d due to neurotoxicity (reversible)
• Not tinidazole, metronidazole or other antibiotics
• Controversy exists regarding whether or not to treat subclinically infected,
shedding cats.
• Pregnant or nursing queens and very young cats (under 8 weeks) should
not receive ronidazole.

46

Prognosis
• Good
• Clinical cure with ronidazole
• Relapses common
• Little known re immunity
• In remission, 50% of cats remain PCR positive and may shed
• If it doesn’t resolve, look for other cause/concurrent infection

47

23
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Prevention & Public health

• Trophozoites readily killed by drying, refrigeration, temperatures >
40C (105F)
• Good hygiene, nutrition, low stress, lower population density
• Infection control – remove fresh moist feces. Replace litter,
disinfect boxes. Keep surfaces clean and dry

• Not a public health risk

48

When to suspect T. foetus

Young cat from Chronic large
cattery, shelter, bowel diarrhea,
multi-cat home malodorous

Diarrhea
Normal appetite, responds to
no weight loss antibiotics or diet
but returns

No response to
treatment for
Giardia

49

24
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Two excellent resources: T. foetus

Gruffydd-Jones JFMS 2013, Gookin JFMS 2017

50

s na s
i o n m o
i n fect itricho
u rrent um, Tr
c i
Con osporid
pt
i a, Cry
ia rd
G

51

25
 4/24/24

Gut barrier immunity

• Is increased intestinal permeability a cause or a result of
inflammation?

• Cause ó consequence?

52

Neiger JVIM 2000

53

26
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Helicobacter & gastrointestinal disease

• H. pylori is serious in humans
• Gastritis, peptic ulcers and gastric cancer
• Concern re zoonotic risk from cats, dogs
• Stray cats – Helicobacter spp. in oral secretions but unrelated to
• +/- colonization of gastric mucosa
• Species of Helicobacter

54

Helicobacter & gastrointestinal disease in

cats
• Many cats (and dogs) are
infected and have gastric
pathology, yet unclear what
role bacteria play
• Most infected patients are
healthy
• Some with chronic vomiting ,
inappetence, diarrhea, and
weight loss respond to therapy

55

27
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Hypotheses re Helicobacter heilmannii in

cats
Associated with
• 2008: lymphoblastic lymphoma
• 2016: large intestinal mucinous adenocarcinoma

Suggestive evidence
• Cats with large cell lymphoma more likely to have a variety of
invasive bacteria, (intravascular and serosal) than small cell
lymphoma or lymphocytic-plasmacytic enteritis
• Higher rate of sepsis in large cell lymphoma

56

Diagnosing Helicobacter heilmannii

• Breath urease testing (in humans +/-
cats)
• Histopathology
• Cytology
• Fluorescent in situ hybridization
(FISH)
• Superior to silver staining

Lertpiriyapong J Med Microbiol 2014

57

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Treating Helicobacter heilmannii in cats

Only treat if: Combination:
• Clinical signs • Two antibiotics
• Histopathologic confirmation • Eg. metronidazole + amoxicillin
or clarithromycin + amoxicillin
• Other disease ruled out
• Plus antacid
• For 21 days

Generally will not result in long-term eradication of Helicobacter spp

58

Etiology
• Infectious
• Inflammatory
• Neoplastic
• Metabolic/systemic
• Toxic/drug-induced
• Diet-associated

59

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Stundiene, World J Clin Cases, 2020

60

Chronic diarrhea - Inflammatory

• Inflammatory bowel diseases
• Lymphoplasmacytic, eosinophilic, neutrophilic, etc.,
enterocolitis
• Multiple locations
• Location and extent => clinical signs
• Pathologists’ descriptions differ
• Controversy as to what is “normal”

61

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Idiopathic Inflammatory Bowel Disease

• What is it?
• Hypersensitivity (immunological)
• Dietary intolerance (non-immunological)

Highly digestible
diet
Limited, unique
antigen diet

Hydrolyzed protein
diet

62

IBD diarrhea history & differentials

• Chronic, nonresponsive • Hyperthyroidism
• Weight loss may be dramatic • Lymphoma
• Stool character varies widely • Exocrine pancreatic insufficiency
• +/- voracious appetite • Cholangitis
• +/- not use litter box • Bacterial overgrowth?
• Otherwise unremarkable history • Endoparasitism (giardiasis)
• Adenocarcinoma
• Histoplasmosis
• FIP/FeLV/FIV

63

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Is it IBD or Chronic Enteropathy?

• IBD is a histopathologic diagnosis (biopsy required for
confirmation)
• CE is a broader term for a syndrome of diarrhea, vomiting, and
weight loss of > 3 weeks duration

• More accurate to refer to “CE” pending a diagnosis.

www.catvets.com/public/Powerpoints/Update-on-IBD-CE-Managment-NOTES.pdf

Datz: Update on management of CE (IBD) in cats Nov 2020

64

Summary from Dr. Datz’s presentation: 1.

• Cats with intermittent or continuous GI signs > 3 weeks have
chronic enteropathy (CE)
• Some cats with CE have IBD, others have lymphoma or less
common causes
• CE/IBD can be food-responsive, antibiotic- responsive, steroid-
responsive, or non- responsive (idiopathic)

www.catvets.com/public/Powerpoints/Update-on-IBD-CE-Managment-NOTES.pdf

Datz: Update on management of CE (IBD) in cats Nov 2020

65

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Summary from Dr. Datz’s presentation: 2.

• After diagnostic workup and ruling out causes such as parasites,
start a dietary trial
• Up to 3 weeks of exclusive diet (no treats, human foods, etc.)
• Gastrointestinal
• Novel protein, limited ingredient
• Hydrolyzed protein
• Home-cooked recipe (ACVN diplomate, BalanceIT.com)

www.catvets.com/public/Powerpoints/Update-on-IBD-CE-Managment-NOTES.pdf

Datz: Update on management of CE (IBD) in cats Nov 2020

66

Summary from Dr. Datz’s presentation: 3.

• Don’t give up if first trial doesn’t work. May need 2, 3, or 4 different
diets sequentially.
• If all dietary trials fail, offer biopsies
• If biopsies not available, start a steroid or antibiotic trial
• Steroid trial first
• Wait on antibiotic trial until other treatments have failed
www.catvets.com/public/Powerpoints/Update-on-IBD-CE-Managment-NOTES.pdf

Datz: Update on management of CE (IBD) in cats Nov 2020

67

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Therapeutic trial IBD

• Evaluate for any and all allergens possible
• Dietary hypersensitivities?
• Limited/unique antigen diets 6-8 week trial
• Hypoallergenic diet
• Deworm
• Treat for hairballs
• Metronidazole trial?
• Prebiotic?

68

IBD- Diagnostics -Next step

• Abdominal ultrasound to evaluate all structures
• Cobalamin, folate, fPLI, fTLI
• Biopsy: quality and quantity

69

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Progression of disease: from IBD to lymphoma

• Chronic insult
• Unknown whether severe
lymphoplasmacytic IBD is pre-
cancerous
• Mechanism unknown

71

Lymphoma in cats
• > 30% of all feline tumours
• Risk factor: second-hand
smoke exposure
ts
• Relative risk of lymphoma for
& ca
cats with any household ETS
exposure was 2.4
• > 5 years exposed to smoke →
increased risk by 3.2 X

Bertone Am J Epidemiol 2002

72

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73

Location matters
• Lymphoma: muscularis +/- • Most common sites for IBD or
serosa, more severe infiltration, small cell lymphoma (T):
villus and crypt architectural ileum & jejunum (70-90%)
changes severe • Stomach: IBD (29%) > small cell
lymphoma (7%)
• IBD: 50% mild, 30% moderate, • 41% cases small cell lymphoma
20% marked plasma cell had concurrent IBD
infiltration of mucosa
• Large cell lymphoma (B) stomach

Briscoe 2011

74

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GI Diagnostics
• Can clinical signs, clinicopathological findings and abdominal
ultrasonography predict the site of histopathological abnormalities of
the alimentary tract in cats?
• Clinical signs, and clinicopathological and ultrasonographic
abnormalities lack precision for hepatic and pancreatic
histopathological lesions in cats with alimentary tract signs and cannot
reliably predict from which organs biopsies should be collected.
• Exploratory coeliotomy is necessary to determine the site of
histopathological abnormalities in feline alimentary tract disorders.

Freiche JFMS 2016

75

When is it IBD vs. small cell lymphoma?

Norsworthy, JAVMA 2013

76

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50: 50?
• 100 cats with small bowel
disease signs &
ultrasonographically
thickened small bowel
• 49 had enteritis (l/p >> eos)
• 46 had lymphoma

Norsworthy, JAVMA 2013

77

Question
How do you differentiate between IBD and intestinal lymphoma?
Severity of clinical presentation
1. Serum biochemistries
2. Response to dietary trial
3. Ultrasound findings
4. Endoscopic biopsies
5. Full-thickness biopsies

79

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Answer
How do you differentiate between IBD and intestinal lymphoma?
Severity of clinical presentation
1. Serum biochemistries
2. Response to dietary trial
3. Ultrasound findings
4. Endoscopic biopsies
5. Full-thickness biopsies

80

Distinguishing lymphoma from IBD

1. Flow cytometry is preferred if it is possible to obtain a fresh
sample
• Provides phenotypic information that PARR cannot
2. PARR if only rare suspicious cells are noted or sample can’t be
fresh cells
3. Occasionally need to run both

csu-cvmbs.colostate.edu/academics/mip/ci-lab/Pages/Lymphoid-Neoplasia-Testing.aspx

81

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Treatment low grade alimentary/small cell

lymphoma
Three groups:
• Oral prednisolone and high-dose pulse chlorambucil
• Modified Madison-Wisconsin multi-agent protocol
• Combination of both protocols
• Good to excellent response in 76% (13/17)
• 1999 Fondacaro: Disease free interval = 20.5 months (5.8 - 49 months) -
Chlorambucil 2 mg PO/cat q2 or 3 days
• Stein 2010: overall clinical response rate 96%, with median clinical remission
of 786 days
• Rescue: 100% w cyclophosphamide + glucocorticoid

Lingard J Feline Med Surg 2009

82

Diarrhea

General Therapeutics

83

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Principles of diarrhea therapy

• Restore and maintain fluids and electrolytes
• Modify diet
• Gastrointestinal protectants
• Antibiotics only if bacterial enteritis
• Immunomodulatory agents if IBD

84

Question
• The most appropriate diet to feed cats with diarrhea is a diet
characterized as:
1. Low fat
2. Low residue
3. High digestibility
4. High fiber
5. High protein

85

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Answer
• The most appropriate diet to feed cats with diarrhea is a diet
characterized as:
1. Low fat
2. Low residue
3. High digestibility
4. High fiber
5. High protein

OR sometimes

86

Answer
• The most appropriate diet to feed cats with diarrhea is a diet
characterized as:
1. Low fat
2. Low residue
3. High digestibility
4. High fiber
5. High protein

87

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Therapeutic diets – Small bowel

• Do not withhold food
• Intestinal cells need direct contact with food
• Highly digestible: moderate amount of single source protein,
carbohydrate without gluten or lactose

• Ingredients associated with adverse food reactions in cats:

• In nearly 80% of cases, beef, dairy and fish involved

88

Therapeutic diets – Large bowel

• Intestinal cells need direct contact with food
• Low residue vs. high fiber?
• Varies with case
• Low residue, highly digestible, hypoallergenic (like small bowel)
• Add psyllium fiber if ineffective

89

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Fiber
• Fiber essential for mucosal health
• Bacteria digest soluble fiber (oat bran, pectin, beet
pulp) → short chain fatty acids and bind water (GEL,
slows transit)

• Insoluble fiber bind toxins and may increases transit

time (cellulose, lignin)

90

Therapeutics: non-specific
• Intestinal protectants: local action, adsorb bacteria, toxins and
protect mucosa
• Bismuth subsalicylate (Pepto-bismol 17.5 mg/ml: 0.5-1 ml/kg PO
q12h X 3d)
• Antibacterial, antienterotoxic, antisecretory, anti-inflammatory
• Kaolin (1-2 ml/kg PO q2-6h)

91

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Antimicrobials: specific pathogens only

• Giardia: metronidazole or
fenbendazole

• Tritrichomonas: ronidazole

• Cryptosporidium: tylosin or
azithromycin

92

Immunosuppressive therapy
• Metronidazole (7.5-10 mg/kg PO q12h long-term)?
• Biopsy diagnosed IBD
• Prednisolone (1-2 mg/kg PO q12h)
• Taper, 3 month minimum treatment
• Chlorambucil (2mg PO q3d)

Metronidazole?
• Great against anaerobes, ineffective against aerobes
• May reduce ability to resist colonization w Salmonella spp and E. coli
• May increase intestinal inflammation

93

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Folate & Cobalamin

• Low folate ← severe chronic malabsorption or
exocrine pancreatic insufficiency
• 0.5 - 1.0 mg PO q24 X 1 month

• Low cobalamin (Vit B12) ← malabsorption due

to chronic intestinal disease or EPI, fibrosis
• 125- 250 mcg/kg SC q7d X 6 weeks

95

Cobalamin levels

• One-third of 75 symptomatic cats with hypocobalaminemia or low-normal

cobalamin concentrations may have an ultrasonographically normal small
intestine.
• For the majority of cats in this study, histopathologic abnormalities were
observed in the small intestine, regardless of ultrasound changes.
• These findings suggest gastrointestinal disease should not be excluded
based on low-normal cobalamin concentrations, even with a concurrent
normal ultrasound examination.

Jugan JFMS 2017

96

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Therapeutics: non-specific
• Motility modifiers: avoid if invasive
microorganisms
• Loperimide (0.1-0.2 mg/kg PO q8h)

• Antioxidants: Vit E, Vit C, omega 3 fatty acids?

97

Margie Scherk CONSTIPATION & MEGACOLON:

DVM, DABVP (Feline)
Vancouver, Canada
TOO HARD

98

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hypurr@aol.com

99

Constipation
• The infrequent or difficult
evacuation of hard stool
• Common, acute or chronic
• Tenesmus, vomiting
• +/- blood, mucus
• Not in litter tray
Address concurrent
medical, behavioural &
environmental problems

100

48
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hypurr@aol.com

101

• 25 rehoming centers/shelters in United Kingdom

• Findings:
• Diarrhea associated with being a kitten and being housed in a
multi-cat pen
• Severe diarrhea was associated with being senior

• Constipation associated with increasing age and winter

German JFMS 2015

102

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Q: 1
In the majority of cases, what is the underlying cause for
constipation?
a) Eating dry food
b) Poor digestion
c) Decreased motility
d) Colonic dysfunction
e) Systemic dehydration

103

Q: 1 ANSWER
In the majority of cases, what is the underlying cause for
constipation?
a) Eating dry food
b) Poor digestion
c) Decreased motility
d) Colonic dysfunction
e) Systemic dehydration

104

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What is constipation?
• Indicates progressive dehydration
• Cellular water content
• Treat underlying problem dehydration before focusing
on motility or stool consistency

105

Dehydration

106

51
 4/24/24

= Dehydration

107

Factors contributing to constipation

Musculoskeletal Toileting (behaviour)

108

52
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Toilet: hygiene & desirability

• Encourage frequent use

109

Constipation as a clinical SIGN

• Reflects:
• Dehydration
• Pain
• Mechanical obstruction
• Functional obstruction
• Behaviour

110

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Causes
• Increased H2O loss
• Decreased H2O intake
• Behavioural dislike
• Pain associated with defecation
• Mechanical obstruction

111

Causes
• Increased H2O loss • Functional obstruction
• Decreased H2O intake • Neuromuscular disease
• Spinal cord disease
• Behavioural dislike • Electrolyte imbalance
• Pain associated with defecation • Drugs
• Mechanical obstruction • Metabolic disease

112

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Human vs. feline megacolon

1) Congenital aganglionic • Normal numbers and
“Hirschsprung’s disease” morphology of enteric ganglia

2) Acquired megacolon • Parasympathetic and

sympathetic nerve function
normal as no concurrent lower
urinary tract problems
• Abnormalities in smooth
muscle function

113

Charlie Hi, I’m

Charlie
• Oriental shorthair, NM, 10 years old
• Indoors only
• Concerns
1. Constipation
2. Inappetance
3. Weight loss
4. Decreasing energy
Methimazole for hyperthyroidism

114

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Physical examination
• Weight loss
• Muscle wasting
• Delayed skin elasticity
• Tacky, slightly inflamed mucous membranes
• Dental calculus
• Hard tubular mass
• In region of descending colon

115

Problems
• Inappetence
• Weight loss
• Muscle wasting
• Dental calculus, gingivitis
• Delayed skin elasticity
• “Constipation”
• Difficulty passing hard stool

116

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Problems
• Tubular
abdominal
mass

117

Differentials
• Intestinal obstruction • Dehydration
• Extra-intestinal • Pain
• Mural
• Luminal
• Obstipation
• Megacolon

118

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 4/24/24

Initial treatment & diagnostic plan

• Rehydrate
• CBC, chemistries, electrolytes, urinalysis, T4, blood pressure
• Xray abdomen

119

120

58
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Q: 2
Which clinical description describes the majority of cats with
megacolon?
a) Middle-aged neutered males
b) Manx breed
c) Low body condition score
d) Poorly muscled

121

Q: 2 ANSWER
Which clinical description describes the majority of cats with
megacolon?
a) Middle-aged neutered males
b) Manx breed
c) Low body condition score
d) Poorly muscled

122

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Signalment
• Middle aged (mean 5.8 years)
• Male (70%)
• Domestic short-haired (46%) cats

123

History
• Reduced, absent or painful, elimination of hard stool
• Inappropriate locations
• Tenesmus, posturing

124

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History
• Reduced, absent or painful, elimination of hard stool
• Inappropriate locations
• Tenesmus, posturing
• +/- Irritation mucus, blood
• +/- Intermittent diarrhea
• +/- Vomiting
• Inappetance, weight loss, lethargy, dehydration

125

History

126

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History

127

CONSTIPATION
Constipation History Form [Patient label information here] HISTORY FORM
Date _______________________________________________________
Your name _________________________________________________

dvm360.com
GENERAL BACKGROUND
How old was your cat when you adopted it? ______________________________________________________________________
Does your cat go outside at all? _________________________________________________________________________________
Has your cat’s appetite increased or decreased? __________________________________________________________________
Have you noticed your cat having any difficulties eating, drinking, or swallowing? ______________________________________
What food does your cat eat? ___________________________________________________________________________________
Have you changed your cat’s diet in the last few weeks or months? __________________________________________________
Does your cat get any treats or supplements? _____________________________________________________________________
Are you aware of any weight loss or gain? ________________________________________________________________________

ONSET AND CHRONICITY

How long has your cat been constipated? ________________________________________________________________________
Is this the first time your cat has been constipated? ________________________________________________________________
Do you ever see blood on or in the feces? ____ Mucus on the feces? ____
If not, how often has constipation or straining occurred in the past, and how long has it lasted previously? ________________
______________________________________________________________________________________________________________
What medications or treatments have been given before? __________________________________________________________
______________________________________________________________________________________________________________

INCREASED WATER LOSS

Have you noticed an increase in the amount of urine your cat is producing? __________________________________________
Is your cat vomiting (more than usual)? ___________________________________________________________________________

INADEQUATE WATER INTAKE

How many water stations can your cat access? ____________________________________________________________________
Does your cat appear to drink comfortably? _______________________________________________________________________
Have you noticed a change in the amount of water your cat is drinking? ______________________________________________

PLEASE TURN OVER AND CONTINUE ON REVERSE SIDE.

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Constipation History Form

dvm360.com

hypurr@aol.com

129

Examination
• Palpation
• Radiographs
• With dysautonomia: urinary retention, regurgitation, mydriasis, 3rd
eyelid prolapse, bradycardia

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Constipation

History, Physical Examination

First episode Recurrence

• Rehydrate • Anorectal examination
• Administer enemas • Neurological
• Remove impacted examination
feces • Laboratory evaluation
• Conservative medical • Abdominal/pelvic
therapy imaging
Idiopathic constipation Colonic neoplasia
• Continue medical therapy • Colonic resection

Perineal hernia
Neurologic disease Pelvic stenosis
• Herniorrhaphy
• Manx spinal deformity • Colonic
• Neural injury Congenital hypothyroidism resection or
• Dysautonomia • L-thyroxine therapy pelvic
osteotomy
134

Diagnostics
• Serum biochemistries
• Hypokalemia, hypercalcemia, hypomagnesemia, dehydration
• CBC
• T4
• Hypothyroid kittens

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136

Diagnostics for chronic constipation

• Radiographs
• Neoplasia, pelvic fractures, extra-luminal mass, foreign body, spinal cord
abnormalities
• Barium enemas
• Colonoscopy
• Ultrasound
• CT
• CSF

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138

Q: 3
Which of the following forms of treatment do you reach for first in a
constipated cat?
a) Fluids
b) Enemas
c) Dietary fiber
d) Laxative therapy
e) Prokinetic agents

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Cornerstones of treatment
1. Correct and maintain optimal hydration
2. Remove impacted feces
3. Consider dietary modification
4. Behavioural and environmental management
5. Consider laxative therapy
6. Consider colonic prokinetic agents
7. Surgical correction

140

Rehydrate Enemas Psyllium Laxative Promotility

& &/ manual enhanced s agents
maintain extraction dry diet,
hydration of feces fiber, or low
residue wet
or dry
Pelvic
trauma or Management of
obstipation constipation,
for > 6 Colectom obstipation, &
Consider
months y
surgery megacolon
if: Pelvic Pelvic
trauma < osteotomy
6 months +/-
colectomy

141

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Rehydrate Enemas Psyllium Laxative Promotility

& &/ manual enhanced s agents
maintain extraction dry diet,
hydration of feces fiber, or low
residue wet
or dry
Pelvic
trauma or Management of
obstipation constipation,
for > 6 Colectomy obstipation, &
Consider
months
surgery megacolon
if: Pelvic Pelvic
trauma < osteotomy +/-
6 months colectomy

142

Medical: 1. Hydration
Correct & maintain optimal hydration
• Cellular dehydration
• Renal and gastrointestinal reserves
• Increase fluid intake:
• Canned foods, broths, add water,
water fountains
• Regular SC fluids at home
• No fiber or laxatives until rehydrated

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Rehydration and maintenance

Example: 11 lb (5 kg) dehydrated cat, with ~5% deficit whose
normal, hydrated weight was 12.2 lb (5.5 kg)
Deficit = 5% × 5.5 kg hydrated weight = 275 ml
+ Maintenance = 60 ml/kg/day × 5.5 kg = 330 ml
Total: over first 24 hours = 605 ml

AAHA/AAFP fluid therapy guidelines for dogs and cats. JAAHA 2013

144

Rehydration and maintenance

• After rehydration, for maintenance: This 12.2 lb (5.5 kg) cat needs
330 ml.
• If the cat eats canned food (5.5 oz/156 g with 80% water = 124 ml
water), only an additional 206 ml of fluids are needed.

AAHA/AAFP fluid therapy guidelines for dogs and cats. JAAHA 2013

145

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Maintenance and dehydration fluid volume

requirements
Maintenance (60 ml/kg/day) + Ml/kg/day 5.5 kg X 110 =
% dehydration (factor) 605 ml/day
Maintenance + 1% 70 then
Maintenance + 2% 80 Maintenance =
Maintenance + 3% 90
Maintenance + 4% 100 330 ml/day
Maintenance + 5% 110
Maintenance + 6% 120 Maintenance
Maintenance + 7% 130 is 60 ml/kg/day
Maintenance + 8% 140
Maintenance + 9% 150
Maintenance + 10% 160 Adapted from DiBartola

146

60 ml/kg ideal weight/day!

147

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hypurr@aol.com

148

Tips for SC fluids

• Warm fluids
• Treats
• Treats
• Treats
• Pull skin over needle

hypurr@aol.com

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150

Medical: 2. Clean out

Remove impacted feces
• Reduces toxic and inflammatory stress on
bowel wall
• Pediatric suppositories: DSS, ColaceTM,
Glycerin, bisacodyl, DulcolaxTM

155

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Medical: enemas
• Enemas: warm tap water, DSS, mineral oil, lactulose
• Give slowly
• Vomiting, canʼt soften, may perforate
• Donʼt use DSS and mineral oil concurrently
• Don’t use: sodium phosphate enemas are hyperNa,
hyperPO4, hypoCa
• Avoid hexachlorophene

156

Medical: clean out

• Manual removal:
• Massage, abdominal manipulation

• Cuffed endotracheal tube!!!

157

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Medical: 3. Dietary fiber

• Essential for gut mucosal health

158

Fiber for what?

• GI health?
• Diarrhea vs. constipation?
• Microbiota composition?
• Glycemic control?

159

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Fiber
• Fiber essential for mucosal health
• Bacteria digest soluble fiber (oat bran, pectin, beet
pulp) → short chain fatty acids and bind water (GEL,
slows transit)

• Insoluble fiber bind toxins and speeds up transit time

(wheat bran, cellulose, lignin)

160

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162

% Soluble fiber
Metamucil (psyllium) 79%
Corn gluten meal 51%
Oat bran 50%
Beet pulp 50%
Barley 29%
Brewer’s grains 11% Total dietary fiber
Wheat bran 11%
Wheat middling 11%
Corn 0%
Cooked white rice 0%
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Feline “Fibre Response” diet clinical trial

• 40 cats, 7.99 + 4.3 years (0.75 to 16 years)
• Sex: 2.2 male:1 female
• Weight: 7.2 + 2.2 kg (range of 3.2-10.8 kg)
• Breeds: All domestic except for 3 Manx
• Treatments given:
a) Enemas; lactulose; lactulose and cisapride; lactulose, cisapride,
enemas and SQ fluids
b) Some were facing surgery, some were going to be euthanized

165

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4. Manage behavior & environment

• Consider social stress
• Litterbox cleanliness, size, height, location

Ellis S, J Feline Med Surg, 2013

167

Five pillars for a healthy environment

1. A safe space
2. Multiple and separated resource stations (food, water, toileting
areas, scratching areas, play areas, resting and sleeping areas)
3. Opportunity for play and expression of predatory behaviours
4. Positive, consistent and predictable interactions with humans
5. An environment that respects the importance of a cat’s sense of
smell

168

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Medical: 5. Laxatives
Four types:
1. Emollient
2. Lubricant
3. Hyperosmotic
4. Stimulant

169

Q: 4
Which type of laxative do you use most often in cats?
a) Emollient: Colace or Surfax
b) Lubricant: Mineral oil or petrolatum
c) Hyperosmotic: Lactulose, Mg salts, or PEG
d) Stimulant: Dulcolax

170

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1. Emollient laxatives
• Mechanism: Anionic detergents
• Increase miscibility of water and lipid
• Enhance lipid absorption
• Impair water absorption
• DSS (ColaceTM) 50 mg q24h
• Can cause colitis in other species
• DCS (SurfaxTM) 50 mg q12-24h

171

2. Lubricant laxatives
• Mechanism
• Impede water absorption
• Lubricate for easier passage
• Mineral oil (10-25 ml PO q24h)
• Safer to give by enema
• Petrolatum (1-5 ml PO q24h)
• Chronic use fat soluble vitamin malabsorption

172

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3. Hyperosmotic laxatives
• Mechanism
• Stimulate fluid secretion
• Stimulate propulsive motility
1. Poorly absorbed polysaccharides
– Lactulose 0.5 ml/kg PO q8-12h or kristalose
2. Magnesium salts
– Mg citrate, MgSO4, MgOH- not in renal dz
3. Polyethylene glycols
– GoLYTELYTM, ColyteTM, MiralaxTM - not GI obstruction

173

PEG

• Retrospective, 9 constipated cats

• PEG 3350 (Colyte®) via naso-esophageal tube
• Median total dose given was 80 ml/ kg (range 40-156 ml/kg)
• Median time to significant defecation was 8 hours (range 5 to 24).
• Radiographs or palpation to confirm complete evacuation
• 1 cat vomited

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4. Stimulant laxatives
• Mechanism
• Enhance propulsive motility
• e.g., stimulation of nitric oxide-mediated epithelial cell
secretion
• e.g., stimulation of myenteric neuronal depolarization
• Bisacodyl (DulcolaxTM) 5 mg PO q24h
• Long term use may neuron damage

176

Medical: 6. Prokinetic agents

Stimulate motility
• Older drugs - ineffective in distal GI tract:
• Metaproclomide, domperidone
or - significant side effects:
• Bethanechol
• Benzamide prokinetic drugs newer class:
• Cisapride, Tegaserod, Prucalopride

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Cisapride
• PropulsidTM, PrepulsidTM
• 0.5-1.5 mg/kg PO q8-12h
• Acute toxicosis in dogs: diarrhea, dyspnea, ptosis, tremors,
loss of righting, hypotonia, catalepsy, convulsions
• +/- Ranitidine (ZantacTM, 1-2 mg/kg PO q12h)
• Nizatidine (AxidTM, 2.5-5.0 mg/kg PO q12h)
• Inhibit acetylcholinesterase
• Withdrawn from human market – compounded for veterinarians

178

Other options?
• Newer products:
• Prucalopride: 0.01-0.20 mg/kg PO q12h
• Tegaserod: 0.05-1.0 mg/kg PO q12h?
• Are effective in feline colonic motility
• Erythromycin and motilin ineffective in feline intestinal motility
• (Useful for gastric emptying)

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Gastric motility - healthy

• Metoclopromide and erythromycin shorten gastric emptying time

and improve antral contraction motility index in healthy cats

• Erythromycin and azithromycin shorten gastric emptying time in

healthy cats

Husnik JVIM 2020 Rutherford JVIM 2022 Staywell.mydigitalpublication.com

180

Charlie treatment
• Try to identify cause of constipation
1. Rehydrate (and maintain hydration)
2. Remove feces
3. Discuss environment
4. Fiber: readily digestible diet with psyllium OR low fiber readily
digested diet vs. traditional approach of high fiber
5. Laxatives &/or promotility agents
6. If intractable: surgery

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Rehydrate Enemas Psyllium Laxative Promotility

& &/ manual enhanced s agents
maintain extraction dry diet,
hydration of feces fiber, or low
residue wet
or dry
Pelvic
trauma or Management of
obstipation constipation,
for > 6 Colectomy obstipation, &
Consider
months
surgery if: megacolon
Pelvic Pelvic
trauma < 6 osteotomy +/-
months colectomy

182

Q: 5
How do you feel about performing a colectomy in a cat?
a) Confident
b) Cautious
c) Terrified
d) It depends

183

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7. Surgery - Colectomy
• Recommend early for megacolon or chronic obstipation
–For hypertrophic megacolon, pelvic osteotomy in addition to
colectomy if pelvic fracture more than 6 months ago
• Chronic fecal impaction results in mucosal ulceration and
inflammation, risk of perforation
• Biopsy small intestine at time of colectomy
• Good prognosis

184

• Chronic constipation, nonresponsive to medical management and associated

with idiopathic megacolon, was diagnosed in 38 cats from 1979 to 1985.
• Subtotal colectomy and enterocolostomy (ileum or distal portion of the
jejunum) was joined to a preserved 2- to 4-cm segment of distal portion of the
colon
• Post-op, depressed and anorectic, tenesmus, and liquid tarry feces.
• In 37/38 cats 1 week to 3 months after surgery, feces became soft semiformed
or formed feces.
• One cat had severe diarrhea that was nonresponsive to diet change and
pharmacologic treatment; the diarrhea resolved after 4.5 months.
• All cats regained normal appetite, maintained weight, and were not
incontinent.
Rosin, JAVMA 1988
• 3 cats had sporadic episodes of easily treated constipation.
185 • Histopath (23 cats) inconclusive

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Tips from Dr. Howie Seim (AAFP Oct 2, 2021)

• Don’t elevate colon much
• Pack abdominal cavity w laparotomy sponge
• 1:50 betadine lavage interior of distal incision (at least 30 sec)
• Be CERTAIN none gets into abdomen
• (Flush and suction)

Rosin, JAVMA 1988

186

Screen capture
from
Dr. Seim’s lecture
Oct 2, 2021

187

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Dr. Seim recommends:

• Leave the left colic artery
• Tie off small branches
• Protects rectal blood flow

188

Schallberger and Stanley, Clinician’s Brief, Oct 2010

189

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Dr. Seim says this will disappear

190

Screen capture
from
Dr. Seim’s lecture
Oct 2, 2021

191

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Probiotics in intestinal Current

disease evidence

192

Dysbiosis - imbalance
Caused by: Can result in:
• Bacterial or viral infection, • Maldigestion and
parasites malabsorption
• Diet or diet change • Dietary intolerance or
• Drug therapy hypersensitivity
• Altered gut secretions • Inflammation

193

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Probiotics in human diarrhea

• Help in the prevention of diarrhea, as well as reduce the duration
and frequency of diarrhea in humans
• But variable results
• Specific diarrhea
• Strain of organisms
• # of organisms

194

194

Probiotics, prebiotics and synbiotics

• Probiotics are live organisms of the physiologic bacterial
ecosystem that provide a health benefit to the host when
provided in adequate quantities
• Mechanism: directly inhibit colonization of pathogens &/or enhance
immune effects on gut-associated lymphoid tissue

• Prebiotics are supplements or foods that stimulate the growth or

activity of endogenous intestinal microorganisms
• Products that contains a prebiotic plus a probiotic is a synbiotic

195
Lappin AAFP conference April 18, 2021

195

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Probiotics in cats
• Kittens fed a probiotic had higher CD4+ lymphocyte counts at
week 22 than did placebo fed kittens
• Increased fecal [bifidobacteria] and decreased fecal [C.
perfringens] in weanling kittens fed a probiotic, higher serum IgA
and only 10% developed diarrhea when compared to controls
(60%)
• Cats fed SF68 maintained diverse fecal microbiota when the cats
were subjected to stress than did cats fed placebo

Veir, Vet Ther 2007; Czarnecki-Maulden Comp Cont Ed Vet 2007; Lappin, JFMS 2009

196

In cats with diarrhea

• Shelter cats, 4 weeks • 53 adult cats w chronic diarrhea, daily
• Double-blinded, placebo-controlled administration X 21 days
trial • Fecal flotation, wet mount, IFA:
• Single-species probiotic formulation Giardia & Cryptosporidium;
containing E faecium SF68 (Fortiflora, Tritrichomonas PCR
1× 108 cfu/g) • Synbiotic (multi- species probiotic
• Fewer cats on probiotic had diarrhea plus prebiotics: Proviable–DC)
for >2 days than cats in placebo group • No other therapeutic or dietary
change
• Mean fecal score significantly firmer
• 72% owners perceived an
improvement, 24% no change,
Bybee, J Vet Intern Med 2011, Hart, JFMS 2012

197

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In cats on amoxicillin-clavulanate
• Decreased microbiome diversity whether
given SF68 or not
• Cats on SF68 had fewer clinical signs when
on this antibiotic

Torres-Henderson Topics Comp Anim Med 2017

198

What’s important in a probiotic?

Stable Safe: does not
• Until consumed • Acquire antibiotic
• Manufacturing, shipping, resistance
storage • Transmit antibiotic
• Bacteria numbers must be resistance
ensured until end of shelf life • Produce pathogenic factors
• Survive in GIT • Promotes a normal, balanced
microbiome

199

199

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Weese Can Vet J 2011

200

What to look for

• “Currently, selection of bacterial strains for most commercial
probiotic products is mostly based on their ability to survive the
passage through the stomach and small intestine, their ability to
adhere to mucus, and in vitro immunomodulation.”
• Consistently meet label claim
• Published clinical data for the species

201
Suchodolski Clinical Small Animal Internal Medicine 2020

201

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Resource

202

202

Thank you!
Do you have any questions?

hypurr@aol.com
211

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It hurts: make it stop!

Predict, prevent, recognize,

and treat pain

Margie Scherk,
DVM, Dip ABVP (feline)
Vancouver, Canada

Thank you to

for sponsoring
2

1
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Overview

• Understanding pain
• Consequences of untreated
pain
• Recognizing pain

Pain realities
1. Non-human animals experience pain
2. Anesthetics are not analgesics
3. Pain is harmful
4. No medication is free of risk:
• Use judiciously
Clients relate to pain: expect us to
prevent and alleviate it
We need to look for
More pharmacologic options and & recognize pain
adjunctive therapies available

2
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WSAVA.org

Monteiro JSAP 2022

Catvets.com

3
 4/24/24

Taylor JFMS 2024

Steagall JFMS 2022

Catvets.com

Understanding
pain

4
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Q: Is pain ever beneficial?

a. Yes
b. No

Initially protective, becomes

pathological

Stimulation of nocireceptors
• Crush/tear
• Thermal
• Chemical

10

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NMDA receptors
• Dorsal horn of spinal cord
• Also in brain
• Activated by chronic, painful
stimuli => allodynia,
hyperalgesia, neuropathic pain
• Responsible for opioid tolerance

brainchemist.wordpress.com

11

Stress response to pain

Increases survival (short-term)
Sympathetic tone:
Vasoconstriction
HR and cardiac output
Respiratory drive
Muscular tone
GI tone
Fatigue and end tissue O2 levels

12

6
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Acute vs. chronic pain

• Acute: associated w tissue

damage and serves to change
behaviour in order to minimize
/avoid damage
• Optimizes conditions in which
healing can take place
• Stops once healing is complete
• Self limiting!
www.herald.ie

13

Acute vs. chronic pain

• Acute: associated w tissue • Chronic: persists beyond the

damage and serve to change expected healing process
behaviour in order to minimize • Serves no biological purpose
/avoid damage
• Does not have a clear end-point
• Optimizes conditions in which
healing can take place • Can have significant effect on
physical wellbeing and
• Stops once healing is complete
psychology of the sufferer
• Self limiting!

Radiograph: John Graham

14

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Gruen 2022 AAHA Pain Management Guidelines

15

Pain => Catabolic state

• Chronic pathologic pain

exhaustion and delayed
wound healing
• Hyperglycemia
• Protein catabolism • Especially critical in
• Lipolysis critical patients!
• Retention of water & Na++ • Pain hurts
• Increased K+ excretion • Prevents healing
• Decreased GFR • Pain KILLS
• Sleep deprivation blog.ferplast.com

16

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Chronic pain

• Maladaptive – dysfunctional
• Doesn’t support healing
• Persists
• Reflects nervous system
damage &/or remodeling

Chronic pain may be considered to be a disease state

Honestpaws.com

17

Types of pain

1. Nociceptive (hot plate) 3. Neuropathic (post amputation,

• Initially no inflammation or surgical damage to nerves)
nervous system damage • Nervous system damage
• Adaptive • Maladaptive
2. Inflammatory (surgery) • Dysfunctional
• Active inflammation • Often persistent
• Adaptive 4. Mixed
• Protective during healing • Neoplasia
• Reversible • Sterile idiopathic cystitis

18

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Inflammation: -itis!

19

Pain is different for each individual

Re-evaluate frequently

20

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Pain: more than chemistry

• Pain is influenced by complex
interactions between numerous
internal and external factors;
• These may result in increased or
decreased pain perception

Monteiro Vet Clin N Am 2020

21

4. Brain 3. Spinal pathway

perceives signal transmits signal
and creates
response

2. Peripheral 1. Nociceptors
nerves create signal
transmit signal

22

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Q: How many places can be addressed with

multimodal analgesia?

a. Two
b. Three
c. Four At least!
d. Five

23

Uncontrolled pain => neuropathic pain

• “Wind-up”
• Hyperalgesia
• Allodynia

24

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Neuropathic pain

• Initiated by a primary lesion, injury or dysfunction in the peripheral or

central nervous system
• Changes occur in the peripheral nervous system, spinal cord,
brainstem and brain
• Damaged nerves fire spontaneously becoming hyper-responsive to
both inflammatory and normally innocuous stimuli.
• ANY CHRONIC PAIN condition can develop a neuropathic component

25

Prevent through
adequate and
multimodal analgesia

Pre-emptive and
therapeutic, for a long
enough duration

26

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Consequences of
inadequately
treating pain

27

Emotional & Psychological

28

14
 4/24/24

Recognizing pain
in cats

29

Catvets.com

30

15
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Gruen 2022 AAHA Pain Management Guidelines

31

32

16
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Pain Management Standards (AAHA/AAFP)

• Assess in every patient

• Record in the medical record for every patient evaluation
regardless of the presenting complaint
• Pain: Yes or No
• Grade 1-10/10

33

Behavioural indicators of pain in cats

Hiding at
Willingness back of cage
to interact
Response
to wound
palpation
Grooming
Absence of Presence
normal of abnormal Shaking
behaviours behaviours bandaged
Using litter limb
tray
Licking at
wound or
bandage

Rely on practice staff observing normal behaviours prior to surgery

34

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Q: How do you detect pain?

Choose as many as you want
a. Change in demeanor
b. Less interactive
c. Whisker and muzzle tightness
d. Lowered head to shoulder
e. Vocalizing
f. Sleeping more

35

How do we detect pain?

• Normalization of behaviours after
analgesics given = pain was present
• Re-evaluate often!

36

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Recognizing
ACUTE Pain

37

Behaviours indicating acute pain in cats (1)

• Change in body posture or body position
• Decreased activity and/or playfulness
• Decreased interest in the environment
• Decreased willingness to interact
• Decreased appetite
• Abnormal gait or shifting of weight
• Sitting or lying in abnormal positions (reflecting
discomfort and protection of an injured area)
• Quiet, hiding
• Hissing, growling or fear-related aggressiveness

Monteiro WSAVA JSAP 2022

38

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Behaviours indicating acute pain in cats (2)

• Attention towards a specific area of the
body (usually involving surgical wounds)
• Guarding behaviour
• Stop grooming (or increased grooming in
a specific location)
• Tail flicking
• Hunched position and/or a tense
abdomen
• Difficulties grasping food and increased
head shaking during feeding
• Depression and immobility; appears tense
and distant from the environment
Monteiro WSAVA JSAP 2022

39

In Practice, December 2018; 40: 440-448

• Two validated pain scales

• UNESP-Botucatu Multidimensional Composite Pain Scale (2013)
• 10 categories w 3 subscales (pain expression, psychomotor change,
physiological variables)
• Glasgow Feline Composite Measure Pain Scale (2014, 2017)
• 7 questions

www.animalpain.com.br/en-us/avaliacao- da-dor-em-gatos.php, www.newmetrica.com/acute-pain- measurement

40

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41

42

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Altered facial expression

43

Mouse
facial
pain scale

44

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Q: Do you use the Feline Grimace Scale?

a. Yes, all the time/often

b. No, what is it?
c. I know about it but don’t use it regularly

45

Score 0 for ears and muzzle

Glasgow CMPS-Feline

46

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Before drugs: score of 3: ears 1

and muzzle 2

Glasgow CMPS-Feline
After drugs: score of 1 or 2: ears
Images from Robertson In Practice 2018 0 or 1 and muzzle 1
47

Grimace Scale

48

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49

felinegrimacescale.com

50

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Gruen 2022 AAHA Pain Management Guidelines

52

53

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Date

Time

Colorado State University

Veterinary Medical Center
Feline Acute Pain Scale

Animal is sleeping, but can be aroused - Not evaluated for pain

Rescore when awake
Animal can’t be aroused, check vital signs, assess therapy

Pain Score Example Psychological & Behavioral Response to Palpation Body Tension

0 Content and quiet when unattended Not bothered by palpation of

Comfortable when resting wound or surgery site, or to Minimal
Interested in or curious about surroundings palpation elsewhere

Signs are often subtle and not easily detected in

the hospital setting; more likely to be detected by
the owner(s) at home
1 Earliest signs at home may be withdrawal from
surroundings or change in normal routine
May or may not react to palpation
of wound or surgery site
Mild
In the hospital, may be content or slightly unsettled
Less interested in surroundings but will look
around to see what is going on

Decreased responsiveness, seeks solitude

Quiet, loss of brightness in eyes
Lays curled up or sits tucked up (all four feet Responds aggressively or tries to
under body, shoulders hunched, head held escape if painful area is palpated Mild to Moderate
2 slightly lower than shoulders, tail curled tightly
around body) with eyes partially or mostly closed
Hair coat appears rough or fluffed up
or approached
Tolerates attention, may even perk
up when petted as long as painful
Reassess
analgesic plan
May intensively groom an area that is painful or area is avoided
irritating
Decreased appetite, not interested in food

Growls or hisses at non-painful

palpation (may be experiencing
Constantly yowling, growling, or hissing when Moderate
allodynia, wind-up, or fearful that
unattended
pain could be made worse)
3 May bite or chew at wound, but unlikely to move
if left alone
Reacts aggressively to palpation,
adamantly pulls away to avoid
Reassess
analgesic plan

any contact

Moderate to
Prostrate Severe
Potentially unresponsive to or unaware of May not respond to palpation May be rigid to
surroundings, difficult to distract from pain May be rigid to avoid painful avoid painful
Receptive to care (even mean or wild cats movement movement
will be more tolerant of contact) Reassess
4 analgesic plan

Tender to palpation
Warm
Tense
RIGHT LEFT

Colorado State University Feline Acute Pain Scale

Comments

58
© 2006/PW Hellyer, SR Uhrig, NG Robinson Supported by an Unrestricted Educational Grant from Pfizer Animal Health

Not always straight forward even ACUTE pain

• Factors that can confound pain scores in cats
1. The cat’s personality and demeanour
2. Fear and stress
3. Upper airway disease
4. Anaesthetic drugs
5. The observer
6. A full bladder

59

27
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It’s harder to detect pain in:

• Adults and older cats: more stoic

• Procedural pain
• Severely ill, obtunded patients:
not able to show behavioural
signs of pain

A L K A MILE
W
OES
IN HIS SPHAW
60

Fear and stress

Fear and stress Fear and stress or pain? – post-op

Palpation required

Images from Robertson In Practice 2018

61

28
 4/24/24

Upper respiratory signs challenging

• Half-closed eyes with tight
muzzle and whiskers pulled
back
• Upper respiratory vs. acute
pain

Image from Robertson In Practice 2018

62

Treating acute
pain

63

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 4/24/24

Acute pain
1. If in doubt: assume that
a) procedure will be painful -
prevent pain,
b) pain will be present – treat it
2. Pain is different for each
individual
3. Know medical status to choose
appropriate analgesics • Re-evaluate frequently!

65

General approach to treating pain

• Start early
• Be thorough
• Harder to combat pain once it is established
• Preempt pain where possible
• MULTIMODAL
• Long enough
• Recognize that chronic disease isn’t static

66

30
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Q: What are the top three rules in pain

management?
Choose three
a. Start early
b. Be thorough
c. Harder to combat pain once it is established
d. Preempt pain where possible
e. MULTIMODAL
f. Long enough
g. Recognize that chronic disease isn’t static

67

Treating acute/peri-operative pain

• ALL surgery is painful therefore • Facial, postural and behavioural
should be pre-empted and components
treated with frequent • Reassess frequently
reassessment • Be prepared to change protocol
• Duration of analgesic • Starting point = “predictable”
requirement should be tailored pain
to individual patient
• Pain doesn’t just STOP after 24
• Gold standard is response hours!
to treatment

68

31
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Safe and
effective
analgesia

Multimodal

69

Prioritizing Pain Management Therapies

Gruen 2022 AAHA Pain Management Guidelines

70

32
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Gruen 2022 AAHA Pain Management Guidelines

71

NSAIDs

NSAIDs are indicated for:

• Acute & chronic pain
• Mild to severe pain
• Effective musculo-skeletal pain
control
• Strong anti-inflammatory action

72

33
 4/24/24

Photos Iris Ouellet

73

74

34
 4/24/24

75

Q: Do you use local anaesthesia? (more than

one choice)

a. Dental blocks
b. Other nerve blocks
c. Inside cavities/through drains
d. No

76

35
 4/24/24

Chronic and Neuropathic Pain in Cats:

More than Musculoskeletal

77

Recognizing
CHRONIC Pain

78

36
 4/24/24

CHRONIC

• Feline Musculoskeletal Pain Index

• Client Specific Outcome Measures (CSOM)
• www.cvm.ncsu.edu/research/labs/clinical-sciences/comparative-
pain-research/clinical-metrology-instruments
• Undergoing validation
• Montreal Instrument for Cat Arthritis Testing
• One for client, one for veterinarian
• Undergoing validation
Monteiro JFMS 2019
79

Gradual changes of chronic pain

• Masters of disguise Dehydration

• Feign wellness Metabolic acidosis
Pain
Hypokalemia
• “Just getting older”
Inadequate dietary protein
• “Just slowing down” Muscle wasting
Anemia
• Less energy, sleeping more, less active
• Chronic pain: less predictable than acute pain

80

37
 4/24/24

Dehydration: painful? + acidosis

• Headache?
• Inappetence?
• Nausea?
• Lethargy?
• Grumpy
• Constipation My cat is lethargic,
eating less, less
interactive, seems
nauseous

81

Normal Aging? PAIN

82

38
 4/24/24

Chronic pain: oral disease

83

Pain: common in older cats

• Oral diseases n
i c p ai
o p ath
• Urinary tract stones
• Neoplasia
n eur
nt or
• iDegenerative
e joint disease
a n s
i n tr • Procedural pain
result
ca n
y -itis • Sterile/idiopathic cystitis and IBD
An (not age related)

Image from Facebook

84

39
 4/24/24

Recognizing and assessing pain

• General mobility (e.g. ease of movement,

fluidity of movement)
• Performing activities (e.g. playing, hunting,
jumping, using a litter-box)
• Eating, drinking
• Grooming (& scratching)
• Resting, observing, relaxing
• Social activities involving people and pets
• Temperament

85

Treating chronic
pain

86

40
 4/24/24

Treatment of chronic pain

• Depends on:
• Underlying cause
• Duration
• How well managed in the past
• Cornerstones = NSAIDs + adjunct drug therapies, physical and other
approaches
• Correct dehydration
• Client education observation and reporting
• Regular reassessment

87

Concerns regarding analgesics

• Hydration Balance effects:

• Renal function uncontrolled pain
• Hepatic function vs. risks of drug
• Intestinal health

88

41
 4/24/24

Degenerative Skeletal Disease: -itis

• Lameness may not be present
• Insidious signs
• Inappropriate elimination (near box)
• Decreased grooming
• Dislike being combed
• Reluctance to jump
• Moving less
At what age does osteoarthritis start in cats?
• “Grumpy”
• Seeking seclusion

89

DJD pain started at 1 year of age!!!

Lascelles Vet Surg 2010

90

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All-age incidence of DJD radiographic changes

Axial (55%) Appendicular (91%)

• Thoracic 7-10 • Hip
• Lumbosacral • Stifle
• Lumbar • Hock
• Cervical • Elbow

Lascelles Vet Surg 2010

91

Courtesy of Susan Little

Video courtesy Susan Little

92

43
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Radiographs: John Graham

93

Meloxicam Safety & Efficacy: Evidence

• Mean treatment duration of 5.8 months

• No deleterious effect on renal function was detected in cats studied
• Gastrointestinal upset in 4% of cats was the only adverse effect noted

Gunew JFMS 2008

94

44
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Meloxicam Safety & Efficacy: Evidence

• There was no difference in sequential serum Cr or USG
measurements b/n the ‘non-renal group’ treated with meloxicam vs.
control cats not treated with meloxicam.
• There was less progression of renal disease in the ‘renal group’
treated with meloxicam compared to the age- and IRIS-matched cats
with CKD not given meloxicam. Cats w DJD and CKD + Cats w DJD +
meloxicam meloxicam

Cats w CKD Age-matched cats

Gowan JFMS 2011, 2012

95

• 193 cats, include 40 w CKD (IRIS 1-4)

• SID robenacoxib for osteoarthritis for 1 month
• Blinded, placebo controlled prospective
• Well tolerated
• No renal, hepatic or GIT damage

• Since 2018, licenced in the EU for treatment of pain and inflammation

associated with musculoskeletal disorders for both short and long-term

King JFMS 2015

96

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Meloxicam or robenacoxib use?

• Use lowest effective dose

• Titrate: But not above label dose
• Re-evaluate your patient!
• Use cautiously (or not at all) in cats with moderate-severe (IRIS stages
3, 4) renal disease
• Ensure/optimize hydration
• Avoid in patients with known bleeding disorders or pre-existing GI
bleeding
• Multimodal therapy

97

Do not give NSAIDs with

• Corticosteroids
• Aspirin
• Be careful with ACE-inhibitors, diuretics, warfarin, phenobarb, chemo
agents

98

46
 4/24/24

• 21 cats stable IRIS stage 2 or 3

• 1 group placebo, 1 group meloxicam 0.02
mg/kg/d X 6 months
• No statistical difference on BP, BUN, Cr, SDMA,
GFR, urine transforming growth factor-
ß:creatinine ratio, urine clusterin, urine cystatin B
or serum inosine
• 4 cats adverse GI effects
• And…

KuKanich JFMS 2020

99

• Mean UPC was greater in the

meloxicam group (0.33) than the
placebo group (0.1) at 6 months
(P=0.006)
• Weigh the risk of potential
increased proteinuria against
quality of life benefits when
considering meloxicam for
analgesia in CKD cats
Placebo; Meloxicam
KuKanich JFMS 2020

100

47
 4/24/24

Taylor JFMS 2024

Catvets.com

101

Opioids

• Cornerstone of managing moderate to severe pain

• Highly efficacious and remarkably safe
• Perioperative setting, preemptively and as part of multimodal
protocols
• Useful to reduce inhalant anaesthetic dose
• Not very useful for arthritis (other than possibly breakthrough pain)
• Vary widely in potency , efficacy, receptor specificity and duration

102

48
 4/24/24

Other analgesic agents

• Local anaesthetics
• Numerous delivery modes
• Alpha 2 adenoreceptors agents
• Ketamine
• Amantadine
• Gabapentin
• Imipramine and amitriptyline

103

Alpha 2 adrenoreceptor agonists

• Analgesic adjuvants
• Supplement analgesia and reduce stress
• Reversible (sedation, but analgesia is also reversed)
• Xylazine, romifidine, dexmedetomadine
• Hepatic metabolism, renal excretion
• Only use in HEALTHY animals due to significant hemodynamic
changes
• Contraindications: cardiopulmonary disease, hypo/hypertension,
diabetes, hepatic/renal failure

104

49
 4/24/24

NMDA receptor antagonists: Ketamine

• Modulates central sensitization

• Anti-hyperalgesia effects
• Opioid effects
• Use for major surgery, trauma and to desensitize chronic pain
• For surgery: bolus with 0.5 mg/kg IV, then CRI 0.3-1.2 mg/kg/h
• Discharge, switch to amantadine

105

NMDA receptor antagonist: Amantadine

• NMDA receptor antagonist

• 3-5 mg/kg PO q24h
• High doses can => seizures

106

50
 4/24/24

Cancer pain
• Some but not all
• Oral cavity, bone, genitourinary system, eyes, nose, nerve roots and
gastrointestinal tract cause considerable pain
• Bone
• Neuropathic pain
• Pain is likely to be present and more severe as cancer progresses
• Pain can be associated with the cancer itself, diagnostic procedures, or
treatments, or it can be unrelated to cancer

• We are afraid of cancer pain

Monteiro WSAVA JSAP 2022

107

Treating cancer pain

• Pain can be associated with the cancer itself, diagnostic procedures,
or treatments, or it can be unrelated to cancer
• NSAIDs +
• Opioids, gabapentin
• Bisphosphates, chemotherapy, radiation (as warranted)

108

51
 4/24/24

Gabapentin

• Mode of action not fully understood, many pathways

• Few studies in cats
• Suggested for chronic pain esp. if neuropathic
• Amputation, diabetic neuropathy, pelvic trauma, intervertebral
disc disease
• Start with 5 mg/kg PO q12h, then increase/decrease dose depending
on response
• Treat several weeks
• Gradual withdrawal is recommended
• May be sedating
109

Novel mediators of pain

Nerve growth factor • For CHRONIC pain

• Mediates inflammatory and
neuropathic pain
• Inhibition of NGF alleviates
allodynia

• Monoclonal antibodies
• Felinized anti-NGF Ab NV-01
(Frunevetmab)

111

52
 4/24/24

• 275 cats with OA and pain

• 1.0 mg/kg SQ once a month
or placebo
• Client specific outcome
measures and veterinary
assessment

112

Other modalities for pain management

• Physical rehabilitation • Optimize body condition

• Therapeutic exercise • Dietary supplements
• Physical modalities (heat, • Omega-3 fa (EPA, DHA)
cold, laser, electrical stim, • Glucosamine, chondroitin
etc.) • Green-lipped mussels
• Manual techniques (joint • Caution
mobilization, trigger point,
• Variable quality, potency
massage)
• Conflicting study results

123

53
 4/24/24

Other modalities for pain management

• Nursing
• Acupuncture
• Medical massage
• Surgical salvage procedures

124

Conclusion: Laser acupuncture reduced

postoperative analgesic requirements in
cats undergoing ovariohysterectomy

Marques Evidence-Based Complementary and Alternative Medicine 2015

125

54
 4/24/24

Treating DJD

• Frunevetmab (Solensia) +/- NSAIDs

• Environmental modifications
• Weight management
• Adjunctive analgesics (tramadol, gabapentin, amantadine,
amitriptyline)
• Nutritional supplements, diet change
• Polysulfated glycosaminoglycan s, glucosamine, chondroitin sulfate
• Rehabilitation (including laser)
• Acupuncture

126

Neuropathic pain

127

55
 4/24/24

Exa
Neuropathic pain mpl
es
• May wax and wane or be • Idiopathic cystitis
ongoing • Diabetic neuropathy
• Onychectomy
• Feline orofacial pain syndrome

128

Peripheral and central sensitization

Increased sensitivity around the lesion site

Monteiro WSAVA JSAP 2022

129

56
 4/24/24

Hyperalgesia

• An exaggerated and prolonged response to a normally painful

stimulus
Also may occur when
normal touch applied
to normal tissue
(secondary site)

130

Allodynia

• A pain response to a low-intensity, normally innocuous stimulus such

as light touch to the skin or gentle pressure

131

57
 4/24/24

Treating Neuropathic Pain

• Gabapentin to block acute sensitization peri-operatively or once already

established.
• NMDA receptor antagonists
• Ketamine, then amantadine long-term
d i f i cation
PLUS
ent al m o
m
ironcomponent
d e nv
• NSAID (due to inflammatory of peripheral and central nervous
A
system responses)n
• Opioids (never alone)
• +/- local anaesthetics, alpha-2 agonists, acupuncture, massage, amitriptyline
• Look for aggravating cause (e.g., tooth or bone fragment)

132

Clinical signs suggestive of neuropathic pain

• Repeated chewing, biting, scratching at the same site
• Spontaneous crying
• Adverse reaction to touch without visible pathology
• Poor response to standard therapy (NSAID, opioid)

• Requires treatment of underlying cause as well as the

neuropathic pain

133

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 4/24/24

Neuropathic pain: idiopathic cystitis

• Waxes and wanes

134

Neuropathic pain: diabetic neuropathy

135

59
 4/24/24

Phantom limb pain

136

Neuropathic pain: onychectomy

• 21- day course of:

• Buprenorphine +
• Amantadine +
• Meloxicam

Neuropathic
cliniciansbrief.com

Gaynor, Clinician’s Brief, 2005 Littlebigcat.com

137

60
 4/24/24

Feline Orofacial
Pain Syndrome:
FOPS

138

Clare Rusbridge www.veterinary-neurologist.co.uk/FOPS/

NSAIDS + gabapentin + opioids

139

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 4/24/24

Neuropathic Pain: First Line Treatment in Humans

Dworkin H et al. Arch Neurol. 2003

140

Treating Neuropathic Pain

• Gabapentin to block acute sensitization peri-operatively or once already

established.
• NMDA receptor antagonists
• Ketamine, then amantadine long-term
i f i cat i on
PLUS nt a l m od
i r me
oncomponent
d e nv
• NSAID (due to inflammatory of peripheral and central nervous
A
system responses)n
• Opioids (never alone)
• +/- local anaesthetics, alpha-2 agonists, acupuncture, massage, amitriptyline
• Look for aggravating cause (e.g., tooth or bone fragment)

141

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 4/24/24

• One dose is not enough!

• Follow-up is critical!
• Adopt a rigorous protocol for
assessing pain
• Undertake baseline assessment
• Involve client in ongoing
assessment
• Keep asking!!!
• Perform repeat assessments
• Changes will be subtle -
Assessing response longterm…months
to treatment of pain • Compare to 3-6-12 months ago

142

Predicting &
preventing
pain
If it might hurt
you… assume it will
hurt the patient

143

63
 4/24/24

Anticipate pain (acute or chronic)

• Oral diseases • Tissue trauma

• Inflammation (-itis) • Blood collection, catheter
• Bowel inflammation placement
• Biliary tree disease • Restraint
• Neoplasia (stretch/compression) • Frail, thin, dehydrated
• Idiopathic LUTD • Arthritic

144

Exa
Mild-to-moderate Moderate mpl
es
• Abscesses and their management • Cystitis
• Castration • Dental disease
• Chest drains • Arthroscopy and laparoscopy
• Dental disease • Osteoarthritis (it can be severe if
• Cystitis neuropathic pain is involved; end-life
• Otitis stages)
• Superficial lacerations • Ovariohysterectomy
• Some soft tissue injuries
• Urethral obstruction

Monteiro WSAVA JSAP 2022

145

64
 4/24/24

Moderate-to-severe (varies with degree of illness

or injury)
• Capsular pain due to organomegaly • Mastectomy
• Corneal abrasion/ulceration • Mastitis
• Corrective orthopaedic surgery (osteotomies; • Mesenteric, gastric, testicular or other torsions
cruciate surgery; open arthrotomies) • Mucositis (including radiation therapy associated
• Dystocia mucositis)
• Early or resolving stages of soft tissue • Oral cancer
injuries/inflammation/disease • Panosteitis
• Extensive resection and reconstruction for mass • Peritonitis/Pleuritis
removal
• Stomatitis
• Frostbite
• Trauma (i.e. orthopaedic, extensive soft tissue,
• Glaucoma head)
• Hollow organ distension • Ureteral urethral/biliary obstruction
• Intervertebral disc disease • Uveitis

Monteiro WSAVA JSAP 2022

146

Severe to excruciating pain

• Aortic saddle thrombosis • Inflammation (extensive, e.g. peritonitis,
• Articular or pathological fractures fasciitis)
• Bone cancer • Limb amputation
• Burn injury • Meningitis
• Central nervous system • Necrotizing pancreatitis or cholecystitis
infarction/tumours • Neuropathic pain (nerve
• Ear canal ablation entrapment/inflammation, intervertebral
disc herniation, etc.)
• Fracture repair where extensive soft
tissue injury exists • Spinal surgery
• Hypertrophic osteodystrophy • Thrombosis/ischemia

Monteiro WSAVA JSAP 2022

147

65
 4/24/24

WSAVA Pain management protocols

148

Multimodal for acute pain

• NSAID + opioid +
• NMDA receptor antagonist
• Topical and local anaesthetics
• Short acting corticosteroids?
• Sedation ≠ analgesia

149

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 4/24/24

Multimodal for chronic pain & neuropathic pain

• NSAID plus
• Opioids?
• Better for break-through pain or palliative care
• NMDA receptor antagonist (ketamine or amantadine)
• Sedative
• Tricyclic antidepressant (amitriptyline): idiopathic cystitis
• Gabapentin (anticonvulsant), amantadine (NMDA): neuropathic pain
• Disease modifying agents: polysulfated glycosaminoglycan, glucosamine and
chondroitin sulfate: DJD

150

Q: Have I made my point about multimodal

analgesia?

a. Yes, I get it!

b. No
c. Yawn

164

67
 4/24/24

Multimodal ALWAYS

• ≠ multi-choice
• Tool box
• Menu: opioid + NSAID + local + NMDA receptor antagonist
• Diet
• Physiotherapy
• Laser therapy?
• Stem cell therapy?
• Assess efficacy
• Purrsonalized medicine

165

Keypoints! Be proactive

Treat for longer Reevaluate Use

than you think patients assessment
regularly tools
is needed

Practice Engage the

preemptive, owner as a
multimodal team
management member

Gruen 2022 AAHA Pain Management Guidelines

166

68
 4/24/24

Resources

167

WSAVA.org

Catvets.com

168

69
 4/24/24

WSAVA Pain management protocols

169

felinegrimacescale.com

170

70
 4/24/24

2019: Clinical Reviews

171

Taylor JFMS 2024

Steagall JFMS 2022

Catvets.com

172

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July 2020

September 2020

173

Not
Interested International
in Dinner? Veterinary Academy
It Might of Pain Management:
Be Pain. www.ivapm.org

SEPTEMBER IS ANIMAL PAIN AWARENESS MONTH

Ask your Vet about ways

to treat pain in your pet.

174

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 4/24/24

Goal: Freedom
from pain &
normalize
activity

www.ivapm.org hypurr@aol.com

175

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 4/24/24

LOWER URINARY
TRACT HEALTH:
METABOLISM
AND STRESS

Margie Scherk DVM, DABVP (Feline)

Vancouver, BC, Canada
hypurr@aol.com

THANK YOU TO

for sponsoring
2

1
 4/24/24

Overview
1. Recap:
• Defining the problem
• Main causes of lower urinary tract signs
2. Metabolic
3. Stress and the lower urinary tract
• Pandora syndrome
4. Approach to treatment
• Diet and hydration
• Optimizing quality of life
• Monitoring success

Overview
1. Recap:
• Defining the problem
• Main causes of lower urinary tract signs

2
 4/24/24

“Mommmmm! Stella's
not pooping. She
keeps trying but
nothing's happening.”

“Mommmmm! Stella's
not pooping. She
keeps trying but
nothing's happening.”

3
 4/24/24

INFLAMED RESERVOIR

LOWER URINARY TRACT: CLINICAL SIGNS

• Straining
• Small volumes
• Increased frequency
• Urgency
• Blood
• Inappropriate locations

4
 4/24/24

ETIOLOGIES OF LOWER URINARY TRACT: ANY AGE

Unknown 3

Infection 8

Plugs 10

Uroliths 22

Feline idiopathic cystitis 57

0 10 20 30 40 50 60
Gerber JSAP 2005
9

All ages

Piyarungsri Sci Reports 2020

10

5
 4/24/24

CAUSES OF LUTS Multifactorial within

same patient

1 • Idiopathic cystitis Different etiology

2 • Urolithiasis different episodes
3 • Urinary tract infections

• Other:
• Ureteronephrolithiasis
• Reproductive tract disorders
• Neoplasia
• Anatomic defects

11
SI ina ish
GN r y
S
ct ur
tra wer
Lo

12

6
 4/24/24

Overview
2. Metabolic

13

OBSTRUCTION:
INFLAMMATION OR SPASM: BLADDER OR URETHRA

Anything can cause

obstruction
14

7
 4/24/24

“WHY IS URETHRA OBSTRUCTED?”

Luminal

Mural

Image: Long Beach Animal Hospital External

15

OBSTRUCTIVE NON Obstructive

Urolith + infect

Infection

Uroliths
Be

Obstructive
ha
v io

idiopathic cystitis A na
tom
ura

ic defe
ion

cts

Uroliths Idiopathic cystitis

Plugs

Gunn-Moore JFMS 2003

16

8
 4/24/24

• 53% of obstructed cats had idiopathic disease (IC)

• Not plugs or urolithiasis
• Inflammation => functional obstruction
• Urethal swelling, spasm, reflex dyssynergia
• Inflammation => mechanical obstruction
• Debris, matrix plugs

Gerber JFMS 2008

17

“WHY IS URETHRA OBSTRUCTED?”

• Inflammation
• Iatrogenic
• Inflammation
• Trauma

Image: Long Beach Animal

Images: Hospital
Long Beach Animal Hospital
18

9
 4/24/24

GUARDED PROGNOSIS
• 45 obstructed male cats – 39 followed
• 14 re-obstructed
• 22 w idiopathic - 8 (36%) after 17 days (3-728d)
• 10 w urolithiasis - 3 (30%) after 10, 13, 472d
• 7 w plugs – 3 (43%) after 4, 34, 211d catinfo.org

• Recurrent LUTS including obstruction in 20/39 (51%)

• Frequency independent of etiology
• 8/39 (21%) euthanized due to re-obstruction

Gerber JFMS 2008

19

Catheterization is not without risks

Always be
gentle!

20

10
 4/24/24

• 1293 UO cases
• “Antibiotics were commonly prescribed in cats for treatment of UO
despite minimal evidence in the clinical records of bacterial cystitis.
• Repeat catheterization was common and case fatality rate during a UO
episode was high.
• Repeat catheterization within 48 hours of elective removal of a urethral
catheter was less common in cats that had previously had indwelling
catheters."

Beeston JVIM 2021

21

ETIOLOGY AND AGE

60

< 10 years > 10 years

50

40

30

20

10

Idiopathic Uroliths Urethral plugs Bacterial Urolith + Neoplasia Incontinence

cystitis infection infection

Bartges What's New in Feline LUTD? ECVIM 2002

22

11
 4/24/24

Kaul, JFMS 2019

23

Kaul, JFMS 2019

24

12
 4/24/24

25

26

13
 4/24/24

Aim for < 1.030

Purina UR Technical Report

27

WHAT ABOUT S/O INDEX (ETC)?

• On its own, not a guarantee preventing stones

• Other factors play a role:
• Litter box attractiveness
• Clean, quiet, safe, large, preferred litter type
• Low stress
• Eating small, frequent meals
• Moisture of food

28

14
 4/24/24

Change in mineral
GLOBAL UROLITH COMPOSITION composition of
PLUGS as well
Minnesota Global Urolith Centre Canadian Urolith Centre
feline submissions 2019 feline submissions 16 years
Others 12% Others 6%

CaOx 32%
CaOx 51%
Struvite 56% Struvite 43%

29

CANADIAN UROLITH CENTRE FELINE SUBMISSIONS

Year n Proportion Year n Proportion

CaOx struvite
2015 831 51.7 2015 644 40.0
2016 833 47.6 2016 784 44.8
2017 767 45.5 2017 792 46.9
2018 701 41.6 2018 856 50.8
2019 741 45.2 2019 788 48.0

Proportion among single mineral type stones

Unpublished data from RC Canada

30

15
 4/24/24

EFFECT OF DIET AND FEEDING STRESS

Reduce stress by avoiding numerous diet changes

Kruger NAVC Symposium 2014

31

Overview
3. Stress and the lower urinary tract
• Pandora syndrome

32

16
 4/24/24

BUT THE MAIN CAUSE OF LUTS IS….

1 • Idiopathic cystitis
2 • Urolithiasis
3 • Urinary tract infections
Different etiology
different episodes

Multifactorial within
same patient

33

PREDISPOSING FACTORS FOR IDIOPATHIC CYSTITIS

• 2-7 years
• Neutered male
• Indoor
• Overweight
• Inadequate water consumption
• Dry diets?

• Multiple cat homes

• Susceptible to stress

34

17
 4/24/24

IDIOPATHIC CYSTITIS What causes

the
inflammation?

What causes
the stress?

35

AN ABNORMAL STRESS RESPONSE

Exaggerated
sympathetic nervous
system response and
catecholamine
release

Blunted endocrine
and cortisol
response

Slide courtesy of Liz O’Brien

36

18
 4/24/24

PHYSIOLOGY
Hypothalamus
ACTH RH

Decreased Pituitary
production of ACTH
ACTH RH Stress

Adrenal
Inhibition of
cortex
ACTH RH
cortisol
Negative
feedback

37

PATHOPHYSIOLOGY OF IDIOPATHIC CYSTITIS

Bladder Hypothalamus
(dopamine) ACTH RH

Decreased Pituitary
production of ACTH
ACTH RH Stress

Adrenal
Inhibition of
cortex
ACTH RH
cortisol
Negative
feedback

38

19
 4/24/24

PATHOPHYSIOLOGY

Chronic activation of the sympathetic system

Increased bladder wall permeability

Local inflamation

Pain

39

• Antibiotic?
• Diet?
Let’s get back • Analgesic?
to Stella • NSAID?
• Fluids?
• Glycosaminoglycans?

40

20
 4/24/24

41

42

21
 4/24/24

WHAT DO WE KNOW?

PAINFUL!

43

CAUSES IN PEOPLE?

Chronic disease
Immunological and neurological crosstalk
Frequent comorbidities

44

22
 4/24/24

• Recommended first-line treatments include patient education, self-care

practices, behavior modifications, and stress management.
• Management of IC/BPS may be also improved if both patients and doctors treat
this condition as a chronic disease.

Bosch, Rev Urology 2014 Duh K, Discovery Medicine, 2018

45

WHAT ARE THE CAUSES IN CATS?

46

23
 4/24/24

EPIDEMIOLOGICAL STUDY OF FELINE

IDIOPATHIC CYSTITIS IN SEOUL, SOUTH KOREA

• Objective: to investigate potential risk

factors for the diagnosis FIC in indoor
cats
• n= 58; Questionnaire-based
• Risk factors:
• No vantage point
• Living with other cats
• Using non-clumping litter
• Apartment vs. house
• Male

Kim JFMS 2018

47

CAUSES?
• STRESS

48

24
 4/24/24

I can’t cope!

50

“Although studies of comparative mortality between indoor housed

cats and those permitted access to the outdoors are not available in
the North American veterinary literature, indoor housed cats are
thought by many to be at reduced risk.”

But is it better for them?

Buffington JAVMA 2002

51

25
 4/24/24

PLIGHT OF THE INDOOR CAT

• Monotony
• Overly predictable
environment
• No opportunity to solve
problems, hunt, protect self
• Decreased fitness
• Obesity
• Diabetes
• Problem behaviours
• Behaviour problems

52

WORTH RECONSIDERING?
Increased risk from going outside
• Infectious diseases (FeLV, FIV, rabies, parasites)
• Vehicular trauma
• Altercative trauma (other animals)
• Other trauma (falls)
• Getting lost
“8 out of 10 vets agree – It is a
• Theft
myth that cats need to roam to
• Poison exposure (antifreeze, rodenticide) be happy or that keeping cats
• Eating undesirable food indoors is depriving them of
• Pregnancy their natural lifestyle.”

53

26
 4/24/24

INCREASED RISK FROM LIVING STRICTLY INDOORS

• Lower urinary tract diseases (FIC, • Poison exposure (cleaning chemicals,

urolithiasis) plants, medications)
Hyperthyroidism W! Secondhand smoke
WO
• •

• Boredom • Trauma (falls, blind cords,

• Inactivity, decreased fitness electrocution)
• Obesity • Problem behaviours (spraying,
scratching, aggression)
• Diabetes
• Behaviour problems (obsessive
• Dental resorptive lesions
behaviours)
• Household hazards (swallowing small
• Dermatologic problems (atopic
objects, burns)
dermatitis, acral lick dermatitis)

54

ROLE OF INDOOR HOUSING?

• Asthma
• Idiopathic inflammatory bowel disease
(IBD)
• Pancreatitis
• Cholangitis
• Cholycystitis
• Hyperthyroidism
• Idiopathic cystitis
• Dermatological conditions
Buffington JAVMA 2002
55

27
 4/24/24

CONCEPT: SICKNESS BEHAVIOURS

Even “healthy” cats can develop • Vomiting
sickness behaviors when exposed to • Diarrhea
sufficiently provocative environments. • Anorexia
Meeting their environmental needs is a • Decreased food/water intake
responsibility that falls on all pet
owners. • Fever
• Lethargy
• Somnolence
• Enhanced pain-like behaviours
• Decreased activity, grooming, social
interactions

www.rd.com Buffington JFMS 2014

56

And
b
`1Q phy eyond
s i ca
l
“On the basis of a physiological
understanding of organ-specific
disease and an immunological
understanding of infectious and
inflammatory disorders, we (contest)
that a biomedical understanding is too
limited to embrace complex disease
and breakdown of functions.“

Kirkengen Tidsskr Nor Laegeforen 2007

57

28
 4/24/24

BODY SYSTEMS – NICE FOR TEACHING, BUT…

• “The disparity between physical and psychological stressors in an

illusion. Host defense mechanisms respond in adaptive and meaningful
ways to both.”
• Interconnected

Fleshner Psychoneuroimmonology: then and now. Behav Cogn Neurosci Rev 2004
58

CAUSES?
• STRESS
• Own,
• Maternal?

59

29
 4/24/24

Roseboom, Early Human Development, 2006

Veenendaal, BJOG, 2013

Almond, National Bureau of Economic Research, 2010

60

Yehuda, JAMA, 2007

Malaspina, BMC Psychiatry, 2008

Santavirta, JAMA, 2017

61

30
 4/24/24

DOES THIS APPLY TO CATS?

Birth
Sensitive Period
• ???

Prenatal
maternal
Provocative
stressè
environment
éCRF, SNS,
and adrenal
Genetic cortex size;
Predisposition in fetusê

62

ABNORMALI
TY IS NOT
LOCALIZED
TO BLADDER
• Comorbidities
are common!

63

31
 4/24/24

PATHOPHYSIOLOGY OF IDIOPATHIC CYSTITIS

Bladder and Hypothalamus
other sites ACTH RH

Decreased Pituitary
production of ACTH
ACTH RH Stress

Adrenal
Inhibition of
cortex
ACTH RH
cortisol
Negative
feedback

64

Nickel J Uro 2010

65

32
 4/24/24

PANDORA SYNDROME

• The bladder is not always the perpetrator of LUTS, and suggests that the
bladder can also be one victim of a systemic process associated with a
sensitized central stress response system
• Vulnerability: a susceptible individual in a provocative environment
• May explain impact of stress and waxing-waning nature of signs
• Majority of cats with LUTS have idiopathic disease

Buffington JFMS 2014

66

PANDORA SYNDROME • Idiopathic

cystitis
• Oral/dental
disease
Birth
Sensitive Period • Skin disease
Recover
• GI Tract
disease
Prenatal
maternal • Asthma
Provocative
stressè
éCRF, SNS,
environment • Behavior
and adrenal problems
Genetic cortex size;
Predisposition in fetusê

67

33
 4/24/24

Waxing/waning nature makes it hard to

POSSIBLE OUTCOMES assess effect of treatments

Acute
idiopathic • Clinical signs resolve in 1-7 days
cystitis without treatment in 85% of cats

Signs recur in 40-60% • Frequency decreases with

of cats within 1-2 years increasing age

Chronic • 15% of cats

idiopathic • Is it same etiology
cystitis each time?

68

TREATMENTS
• More than 80 different therapies
(drugs, procedures) have been
tried since 2003
• Few studied*

69

69

34
 4/24/24

Overview
4. Approach to treatment
• Diet and hydration
• Meeting behavioural and environmental needs
• Other therapy – analgesia
• Monitoring success

70

HOW DO WE MANAGE CATS WITH LUTS?

• Urinalysis
• Modify diet

Rule out other causes!

71

35
 4/24/24

URINALYSIS

www.newkidscenter.com

72

73

36
 4/24/24

A REMINDER

Purina UR Technical Report

74

WHICH BRINGS US BACK TO MANAGEMENT

Role of diet Prevent uroliths by increasing urine output

• Diet can help reduce urolith precursor • Increased protein:
concentrations • Benefits lean body mass
• Diet affects urine pH (helpful for struvite) • Drives urinary output (osmotic diuresis
from urea)
• Balance dietary magnesium and calcium
(helpful for CaOx) • Sodium level increases thirst
• Diet can increase frequency and volume • NOT blood pressure or kidney health
of urination Therapy
• Optimize litterbox environment • Struvite uroliths dissolve within 2 weeks
(when fed exclusively)
More on this later…
Torres-Henderson Top Comp Anim Med 2017
75

37
 4/24/24

HOW WE FEED MATTERS

76

EATING BEHAVIOUR

• Small rodents, rabbits, birds, insects, frogs, reptiles

• Adult cats need ~ 50 kcal/kg ideal weight/day
• 70 x (BW kg)0.75
• Thin, old cats need 70 kcal/kg/day
• Average mouse = 30-35 kcal
• Therefore, a 5 kg cat needs ~ 7-8 mice/day

77

38
 4/24/24

EFFECT OF DIET AND FEEDING ON HYDRATION

Cats eating canned food only ingested more water, had larger urine volumes
and lower urine specific gravity (usg) than cats eating dry food only

Greco WSAVA Abstract 2014

78

EFFECT OF DIET AND FEEDING ON HYDRATION

Cats eating multiple snacks (small meals) a day had more neutral urine pH
(smaller pH swings) than cats who were meal fed

Taton JAVMA 1984

79

39
 4/24/24

URINE pH IS AFFECTED BY FEEDING FREQUENCY

7.6"

7.4"

7.2"

7" ad libitum
pH"
6.8" meal feeding
upper neutral
6.6"
lower neutral
6.4"

6.2"

6"
0" 3" 6" 9" 12" 15" 18" 21" 24" Hour
s
Taton, JAVMA 1984
80

EFFECT OF DIET AND FEEDING ON HYDRATION

The more often cats eat, the more water they drink (canned or dry)

For a given energy level, the water intake (ml/g dry matter) significantly
increased by increasing meal frequency.

• Benefits of puzzle feeding

Kirschvink, ACVIM Abstract 2005 Delgado JFMS 2016 Sadek JFMS 2018
81

40
 4/24/24

DESERT
ANCESTOR
Renal concentration
Cope with significant
water loss

Observation.org
82

IN GENERAL, HYDRATION IS MAINTAINED, BUT…

• We don’t know what triggers thirst in cats – not the same as in

other species

• Chronic deficits are problematic…

• Polyuria
• Vomiting
• Diarrhea

83

41
 4/24/24

cbc.ca
84

HOW IS DEHYDRATION LIKE A HANGOVER?

• Hangover = dehydration + acidosis + oxidative stress + inflammation

• Many older cats? Inappetence/anorexia
Nausea/vomiting
Lethargic
Painful
Withdrawn/grumpy
Constipation

85

42
 4/24/24

CONDITIONS ASSOCIATED WITH DEHYDRATION

• Polyuria (despite polydipsia): • Pollakiuria contributes to dehydration

• Chronic kidney disease • Inflammation (anywhere)
• Diabetes mellitus
• Ageing
• Hyperthyroidism
• Constipation…

86

DEHYDRATION – PREVENTION
It’s not just what, but also how and where
What How Where
Water Bowls Away from food
Adding water to food - Bowl material Multiple sites
Ice - Bowl diameter Undisturbed
Nutrient-enriched water* - Bowl height Easy access
Low salt flavoured broth Still vs. circulating

*Healthy cats drinking NW consumed an average of 50% more liquid/day

Zanghi AJVR 2018
87

43
 4/24/24

HYDRATION
• Ensure adequate water intake
• Wide bowls
• Clean (bowls and water)
• Diurese (canned, increase fluids)
• Flavoured water (broths)
• Ice
• Water fountains
• Hydra Care
• Goal specific gravity < 1.030
• Feed multiple small meals

88

Overview
4. Approach to treatment
• Diet and hydration
• Meeting behavioural and environmental needs
• Other therapy – analgesia
• Monitoring success

91

44
 4/24/24

REDUCE
STRESS
Meet environmental needs

92

STRESS AND SICKNESS

• Modify environment to reduce stress

• Changes in the environment, weather, activity,

use of the litter box, food intake, diet, client
work schedule changes, changes in the
population number and individuals of the
household (human and non-human)

93

45
 4/24/24

ALLOW CAT TO MODIFY THEIR STRESS LEVELS

• Give them some control:
• Provide places to hide, provide the
opportunity to play/hunt.
• Consider climbing posts and secure
scratching trees as well as toys to chase
and catch
• Indoor cats may be lacking in stimulation,
especially if they are ”only cats”

94

Journal of Feline Medicine and Surgery (2013) 15, 219–230

SPECIAL ARTICLE

AAFP and ISFM Feline

Environmental Needs Guidelines
1. A safe space
Guidelines rationale: A cat’s level of comfort with its environment is intrinsically linked to
2. Multiple and separated resource stations
its physical health, emotional wellbeing and behavior. Having a basic understanding of the
cat’s species-specific environmental needs and how cats interact with their environment will
provide a foundation for addressing these fundamental requirements.
Providing an opportunity for play and expression of predatory
Sarah L H Ellis
3.
Environmental needs: Addressing environmental needs is essential (not optional) for BSc (Hons) Dip CABC PhD
Guidelines Co-Chair
optimum wellbeing of the cat. Environmental needs include those relating not only to the cat’s
behaviours
physical surroundings (indoors or outdoors; in the home environment or at the veterinary practice)
but also those affecting social interaction, including responses to human contact.
Ilona Rodan
DVM DABVP (Feline)
Guidelines Co-Chair
Five ‘pillars’ framework: The authorship panel has organized the Guidelines around five primary concepts
4. Providing positive, consistent and predictable interactions
(‘pillars’) that provide the framework for a healthy feline environment. Understanding these principles
and the unique environmental needs of the cat will help veterinarians, cat owners and care-givers to reduce
Hazel C Carney
DVM MS DABVP

with humans
stress, the incidence of stress-related disorders, and unwanted behavior in their feline patients and pets.
The recommendations in the Guidelines apply to all pet cats, regardless of lifestyle.
Sarah Heath
BVSc DipECAWBM (BM)
CCAB MRCVS

An environment that respects the importance of a cat’s sense

European Veterinary Specialist
5. in Behavioural Medicine
(Companion Animals)
Why environmental needs?
of smell
Addressing environmental needs –
Irene Rochlitz
how does it help? BVSc MSc PhD MRCVS
Veterinarians have the privilege and responsi- ✜ Fewer unwanted behaviors and less illness
bility to improve the health and wellbeing of ✜ Improved recognition of disease Lorinda D Shearburn
DVM
cats. Along with other health care team mem- ✜ Expansion of services and increased value
bers, veterinarians must advise clients not only of feline care at the veterinary practice Eliza Sundahl
on medical issues and preventive health care, ✜ Easier handling of cats at home and DVM DABVP (Feline)

Ellis JFMS 2013 but also about the importance of meeting the in the practice Jodi L Westropp
environmental needs of the cat. Several dis- ✜ Strengthened bond between owner DVM PhD DACVIM
eases as well as unwanted feline behaviors and cat
95 have been associated with stressful environ- ✜ Reduced stress in multi-cat households
mental situations.1–3 Providing an appropriate ✜ Happier cats!
environment for feline patients in their home
and at the veterinary practice can prevent,
improve or resolve these problems.4,5
The terms environmental enrichment and standing cats and their needs since this is a
environmental modifications have been used relatively new area. Recognizing the importance
extensively in the literature to refer to envi- and benefit also may not be intuitive for some
The AAFP and ISFM welcome
ronmental changes for the benefit of the cat. clinicians.6 Cats often do not express overt signs
These terms are not used in these Guidelines
because it is more accurate to focus on the
of stress and anxiety. Studies have suggested
that even stoic cats can have elevated levels of
endorsement of these guide-
lines by the American Animal
Hospital Association
46
cat’s environmental needs. catecholamines and other stress hormones.1,5 (AAHA).
 4/24/24

A SAFE SPACE
Environmental Need #1
96

MULTIPLE AND SEPARATED RESOURCE STATIONS

Environmental Need #2
97

47
 4/24/24

Bed Water

There is a bed in both the living and There are several water bowls that
bedrooms which are places the cat are in places the cat can readily access.
will want to be with his/her people.

Food
Water Living room and kitchen Hallway

Litter Balcony

Bed Bedroom

Perch
Scratching
Toys Food

Food bowls are placed on a ledge as

Scratching tree/post well as on the floor in three different
locations.
A tall scratching tree is placed near the window for
Litter
observation. Another is in the hall and a shorter
scratching post is in the living room beside the sofa
Three comfortably sized, clean litter boxes
which could otherwise be tempting to scratch.
are placed in quiet, separate locations.

98

OPTIMIZE LITTERBOX ENVIRONMENT

• Encourage frequent, complete
emptying of bladder

99

48
 4/24/24

How many
boxes do I
“see”?

100

• Clean
• Quiet
• Safe
• Right kind of litter
• Right depth
• Large
• Many
• Easy to access

101

49
 4/24/24

102

EASY TO ACCESS

103

50
 4/24/24

Your Cat’s Feline House-Soiling

Environmental Needs Useful Information for Cat Owners
Practical Tips for Pet Owners

Catvets.com
House-soiling is one of the most common reasons why
pet owners abandon or relinquish their cats. Unfortunately,
these cats frequently end up in shelters where they often
are euthanized.

House-soiling can be a complex problem to solve, but there

are ways to prevent, manage, or resolve feline house-soil-
ing behaviors. Your cat does not urinate or defecate outside
the box due to spite or anger towards you, but because its
specific physical, social, or medical needs are not being met.

Sponsored by Sponsored by

104

AN OPPORTUNITY FOR PLAY AND EXPRESSION OF

PREDATORY BEHAVIOURS
Environmental Need #3
105

51
Pillar 5 – Provide an environment
that respects the importance of How cats use pheromones
the cat’s sense of smell Cats investigate different scents and chem- 4/24/24
ical signals produced by themselves Tail
Description and other cats. These chemical
Unlike humans, cats use olfactory and chemi- signals are known as pheromones. Temporal
cal information to evaluate their surroundings Whereas scents are detected by Cheek
and maximize their sense of security and com- the nose, pheromones are detect-
fort. Olfactory information involves many dif- ed by the vomeronasal organ
ferent smells detected by the nose. Chemical located Caudal
Perioral
S P EinC Ithe
A L hard
A R T I Cpalate. Cats guidelines
L E / AAFP/ISFM on feline environmental needs
information is detected by the vomeronasal produce pheromones from vari-
organ. This is an auxiliary olfactory apparatus
Pillar 5 – Provide an environmentous scent glands located on the
that detects pheromones, whichthe
that respects chemicals of body (Figure 12), and useHthem
areimportance ow cats use pheromones
to
the cat’sbetween
that convey information sense ofindividuals
smell Cats investigate different scents and chem-
communicate with other cats and to
of the same species (see box). Cats use olfacto-
Description
ical signals produced by themselves
enhance
and recognition
other cats. These of their own envi-
chemical
Tail
Interdigital
ry and pheromonal Unlikesignals
humans,through the use
cats use olfactory and chemi-
ronment. Cats deposit pheromones by Temporal
signals are known as pheromones.
cal information to evaluate
of scent marking by facial and body rubbing their surroundings Whereas scents are detected by Cheek
and maximize their sense of security and com- facial rubbing and scratching to create a Figure 12 Location of
(Figure 13). This establishes the boundaries
fort. Olfactory information involvesofmany dif-
the nose, pheromones are detect-
senseedofbyenvironmental
the vomeronasalsecurity.
organ the feline scent glands
their core living area
ferentinsmells
which theybyfeel
detected the secure
nose. Chemical located in the hard palate. Cats Caudal
Perioral

and safe. Wherever information

possible, is detected
humans by the vomeronasal
should produce pheromones from vari-
organ. This is an auxiliary olfactory apparatus
be careful not to interfere with a cat’s olfacto-
that detects pheromones, which are chemicals
ous scent glands located on the
body (Figure 12), and use them to
ry and chemical signals and
that convey scent profile.
information between individuals communicate with other cats and to
of the same species (see box). Cats use olfacto- enhance recognition of their own envi- Interdigital
ry and pheromonal signals through the use
Methods of scent marking by facial and body rubbing
ronment. Cats deposit pheromones by
deposit its scent through
facial rubbing and scratching to create a
glands in the
✜ Avoid using products
(Figure 13). orThis
substances
establishes the boundaries of Pillar 5 –ofrationale
sense environmental security. pads of its feet.
Figure 12 Location of
the feline scent glands
their core
(cleaners, detergents, living area
scented litterin which
or theyComparedfeel securewith humans, cats depend much ✜ Avoid cleaning areas that have been
and safe. Wherever possible, humans should
other cat paraphernalia) that may
be careful not to interfere with ato
more upon
cat’s olfacto-
chemical and olfactory information facially marked by the cat (Figure
explore their environment. If cats sense
disrupt the cat’s sensory perception
ry and chemical signals and or scentthreatening
profile.
olfactory or pheromonal informa-
13b), except in the veterinary practice
the scent profile it associates with its tion, or if they cannot express their sensory after patients have been discharged.
Methods deposit its scent through glands in the
customary surroundings.
✜ Avoid using products or substances signals as described above, problematic pads✜of Wash its feet. a cat’s bedding on a rotation
POSITIVE, CONSISTENT AND PREDICTABLE
Pillar 5 – rationale
✜ Place footwear(cleaners,
or shopping bags
detergents, at litter orbehaviors
scented suchwith
Compared as humans,
inappropriate
cats dependelimina-
much ✜ basis so thatareas
Avoid cleaning some thatitems
have beenwill retain the
the home entranceother cat paraphernalia)
to avoid introducing that may tion or scratching and stress-related facially marked(‘olfactory
cat’s scent by the cat (Figure
continuity’).
more upon chemical and olfactory information

INTERACTIONS WITH HUMANS

to explore their environment. If cats sense
disrupt the cat’s sensory perception or illness (eg, urinary tract dis- 13b), except in the veterinary practice
external smells into
the the
scenthome
profile itenvironment.
associates with its
threatening olfactory or pheromonal informa-
ease)
tion, occur.express their sensory after patients have been discharged.
cancannot
or if they
✜ Use synthetic pheromones to reduce
customary surroundings. signals as described above, problematic Other considerations
✜ Wash a cat’s bedding on a rotation
✜ Place
anxiety, and increase footwear orinterest
grooming, shopping in bags at basis so that some items will retain the
tion or scratching and stress-related ✜ Homes with outdoor-access flaps in doors
behaviors such as inappropriate elimina-
the home entrance to avoid introducing
food and appropriate
externaluse of the
smells into litterbox.
26
the home environment. Environmental Need #4
illness (eg, urinary tract dis-
ease) can occur.
cat’s scent (‘olfactory continuity’).
may be at greater risk of other cats or animals
✜ Expose new items ✜ Use tosynthetic
the cat’s scent profile
pheromones to reduce introducing
Other considerations external scents or gaining access
anxiety,aand
by rubbing them with increase
cloth thatgrooming,
has been interest in Homes
✜ into thewith outdoor-access
home. Vigilance flapscombined
in doors with a
food and appropriate use of the litterbox.26 may be at greater risk of other cats or animals
in contact with106
the
✜ cat’s
Exposescent glands
new items to theduring
cat’s scent profile door flap
introducing designed
external scents ortogaining
be operated
access by the cat’s
positive interactions with humans,
by rubbing them with a or spray
cloth that has been implanted
into identification
the home. Vigilance combined microchip
with a are ways
new items with a in synthetic
contact with feline
the cat’spheromone.
scent glands during of avoiding
door flap designedencroachment
to be operated by the of unfamiliar
cat’s
positive interactions with humans, or spray implanted identification microchip are ways
✜ Provide scratching areas
new items withthat allowfeline
a synthetic a catpheromone.
to ofscents.
avoidingAvoid magnet-operated
encroachment of unfamiliar door flaps
✜ Provide scratching areas that allow a cat to sinceAvoid
scents. the magnet-operated
magnets can door attract
flapsforeign
materials.
since the magnets can attract foreign
materials.
✜ Scratching
✜ Scratching areas should areasalso should also be available
be available
outdoors
outdoors for deposition.
for scent scent deposition.
✜✜ Scent
Scent marking
marking as well asasinappropriate
well as inappropriate
elimination should never be punished.34
elimination should never
✜ Ensure that each group of cats within be punished.
the
34

✜ Ensure
home that each
has an opportunity to group
scent mark ofareas
cats within the
home
(by scratchinghasandan facial
opportunity
rubbing) that to scent mark areas
contain their environmental resources.
(by scratching and
✜ A cat returning to a multi-cat facial rubbing)
home from that
b contain
a visit away their
may smellenvironmental
different, disruptingresources.
Figure 13 Facial
the
✜homeA cat returningcommunal
environment’s to a multi-cat
scent home from
profile consisting of scents from all feline
b rubbing (a) allows a
cat to deposit its
a visit away
occupants. maylikely
This is most smell different,
to occur after disrupting
scent throughout its
environment. In order
the to
a visit home environment’s
the veterinarian, where smellscommunal
of scent
Figure 13 Facial
to maintain
rubbing
scent
(a) allows
avoid a
profile consisting
medications, of scents
antiseptics, cleaners and from
even, all feline
continuity,
postoperatively, anesthesia gases can be
Courtesy Sarah Ellis
cat tocleaning
deposit facially
its
marked areas (b).
occupants.
detected by otherThis issuch
cats. In most likely
cases, cats to occur after
a
scentImages
throughout
environment.
courtesy its
of
Sarah Ellis In order
a visit
that to the
previously gotveterinarian,
along well can displaywhere smells of
to maintain scent medications, antiseptics, cleaners and even,
continuity, avoid
cleaning facially
marked areas (b).
postoperatively,
JFMS CLINICALanesthesia227
PRACTICE
detected by other cats. In such cases, cats
gases can be

a Images courtesy of
Sarah Ellis
that previously got along well can display

AN ENVIRONMENT THAT RESPECTS227THE JFMS CLINICAL PRACTICE

IMPORTANCE OF A CAT’S SENSE OF SMELL

Environmental Need #5
107

52
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NEW
catvets.com

Catfriendly.com

108

SECURITY = CHOICE & CONTROL

Meeting unmet needs

to reduce illness,
behaviour problems
and improve quality of
life of cats.

109

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DON’T FORGET ANALGESIA

ANTISPASMODICS
• Phenoxybenzamine - Alpha-adrenergic antagonist
• 2.5-7.5 mg/cat PO q12-24h
• Prazosin - Alpha-adrenergic antagonist
• 0.25-0.5 mg/cat PO q12-24h Choose one P
plus D
• Dantrolene - Skeletal muscle relaxant
• 0.5-2.0 mg/kg PO q8h

110

• 388 cats with urethral obstruction.

• 302 (78%) cats received prazosin, while 86 (22%) did not.
• Within 14 days, a significantly higher proportion of prazosin-treated cats (73/302 [24%])
developed an rUO, compared with the proportion of non–prazosin-treated cats (and 11/86
[13%]).
• The perception of a “gritty feeling urethra” or difficulty of performing the catheterization
was associated with increased risk of rUO.
• Prazosin administration increased the likelihood of rUO by 14 days; ongoing investigation
of other therapies to decrease rUO in cats is warranted. Without specific indications, the
use of prazosin for the prevention of rUO should be discouraged.

Conway JAVMA 2022

111

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FOLLOW-UP CARE

• Analgesia
• Monitor urine output
• Dietary management
• Recheck
• Monitor for hematuria at home
• 10-14 days, then 2 months and 4X/year

112

Overview
4. Approach to treatment
• Diet and hydration
• Meeting behavioural and environmental needs
• Other therapy – analgesia
• Monitoring success

113

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MONITOR
HEMATURIA

Provide analgesia
Reassess
environment

114

MONITORING IDIOPATHIC CYSTITIS AND UROLITHIASIS

38% of cat
parents say
Please! Not a
just thinking
recheck!
about a
veterinary visit
is stressful!

116

56
 4/24/24

Or use granules that detect the presence and degree of hematuria

117

HEMATURIA

118

57
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USEFUL FOR MONITORING

• Resolution or recurrence: • Frequency of use:
• Apparently healthy cats: 1-2X/year
• Stress (idiopathic cystitis)
• At risk cats: 2-4X/year
• Medical (crystalluria, infection)
• History of recent problem: 7-10 days
• Postoperative
• Neoplasia
• Nephrolithiasis
• Trauma
• Others

119

DIAGNOSTIC USE

• House soiling:
• Is spraying or periuria due to stress or medical problem?

• Overgrooming perineum or ventral abdomen:

• Is it stress or medical problem?

• LUT disorder
• Tiny bladder

• Differentiate between iatrogenic and endogenous

120

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 4/24/24

STELLA PLAN – IDIOPATHIC CYSTITIS

• Reduce stressful situations

• Keep diet stable
• Monitor for hematuria
• If cystitis flares up, give analgesic agents
and fluids

121

In summary
1. Prevalence of LUTS
• FIC is most common
• Young and adult cats FIC, seniors bacterial cystitis
2. Role of stress and metabolism
• Pandora - Comorbidities
3. Diet and hydration
4. Meeting behavioural and environmental needs
• Other therapy – analgesia
• Monitoring success

145

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RESOURCES

Catvets.com/guidelines

146

Cliniciansbrief.com

What Cat
Owners Can
Learn About
Captivity

147

60
 4/24/24

NEW
catvets.com

Catfriendly.com

149

Dantas 2016, JFMS

JFMS 2018

Foodpuzzlesforcats.com

150

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 4/24/24

THANK YOU FOR

PARTICIPATING!

Margie Scherk
hypurr@aol.com

151

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Diseases
of the
nasal
planum

Margie Scherk,
DVM, Dip ABVP (Feline)
Vancouver, Canada
1

Thank you to

for sponsoring
2

1
 4/24/24

Nino

• 6 year old NM DSH tabby

• Indoor and out, drinks from fish pond
• Adopted from cat shelter September
• Skin problem started October
• FeLV/FIV negative
• CBC and chemistries unremarkable following March

2
 4/24/24

Medical history
• Had received depo-prednisolone acetate injections by first vet before
biopsies: initially improved
• Lesion got worse, sought second opinion

Second veterinarian
• Skin biopsies: perivascular plasmacytic-
eosinophilic infiltration with secondary
superficial bacterial colonization

• Doxycycline plus dexamethasone

• Flea treatment (imidacloprid)
• Feed turkey breast, Hill’s z/d
• Ceramic bowls
• (on plastic tray on linoleum floor)

3
 4/24/24

Presented to me August 2003

• Inappetance of 2 days
• Wheezing, congested and bleeding
• Weight loss, BCS 4/9
• BAR, timid
• Dehydration
• Submandibular lymphadenopathy
• Dermal ulceration of nose and nasal planum

What is your most likely differential?

What is your most likely differential?

a) Squamous cell carcinoma?

b) Mosquito hypersensitivity?
c) Herpes viral dermatitis?
d) Poxvirus infection?
e) Cryptococcosis?
f) Eosinophilic granuloma?

4
 4/24/24

Biopsy is essential!
• Clinical appearances are similar

• Clinical presentation: q Feline facial dermatitis

• Pruritis, q Dermatophytosis
• Alopecia, q Herpesvirus
• Crusting,
q Atopy
• Ulcerative, or
• Nodular
q Food allergy
• On the: q Mosquito bite hypersensitivity
• Face, q Squamous cell carcinoma
• Non-haired nasal planum, q Bowen’s disease
• Haired skin of the muzzle/face,
• Pinna, and
• Ear canal
Coyner Vet Clin N Am 2020

10

5
 4/24/24

• Facial dermatitis in cats can be caused by a broad range of infectious,

allergic, immune- mediated and neoplastic disorders with very different
treatments and prognoses.
• Baseline dermatologic diagnostics (skin scrapings for mites, cytology for
infection and to characterize inflammatory infiltrate, and dermatophyte
culture) are indicated in all cases; aerobic bacterial skin culture is indicated
if bacteria are found on cytology despite empiric antibiotics.
• Biopsies for dermatohistopathology +/- tissue cultures are indicated in
cases that are not diagnosed on screening tests and that do not respond to
empiric therapy.

Coyner Vet Clin N Am 2020

11

Squamous cell carcinoma

• UV light damage to nose, eyelids, ears
• Actinic keratosis => non-healing ulcer => SCC

Courtesy K Moriello

12

6
 4/24/24

Squamous cell carcinoma

Courtesy L Pierson
13

Squamous cell carcinoma (SCC)

• Therapy: surgery, cryotherapy

4 weeks post op 3 months post op

14

7
 4/24/24

Squamous cell carcinoma

• Photodynamic therapy (PDT):
several sensitizing agents

Flickinger J Feline Med Surg, 2018

15

SCC and PDT (mTHPC)

• FoslipTM = phosphorylated meta-tetrahydroxylphenyl Cl

Flickinger. J Feline Med Surg, 2018

16

8
 4/24/24

17

Actinic keratosis => SCC

• UV light damage to nose, eyelids, ears
• Actinic keratosis => non-healing ulcer => SCC
• TREAT EARLY!
• Actinic dysplasia and
superficial SCC involving
less than 50% of the
nasal planum treated
with 3 cycles curettage
and diathermy
• Excellent response!

18

9
 4/24/24

Actinic keratosis and PDT (mTHPC)

Flickinger. J Feline Med Surg, 2018

19

SCC - Radiation therapies

• Radiation: accelerated proton beam, superficial radiotherapy with
intralesional carboplatin, plesiotherapy (90-Strontium)

www.vettimes.co.uk

20

10
 4/24/24

• Outcome for 58 cats

• High-dose rate brachytherapy
• 30 Gy, one of 2 schedules
• Complete remission in 36 (72%)
• Partial response in 13 (24%)
• Overall survival time 835 days

Lino JFMS 2019

21

Lino JFMS 2019

22

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 4/24/24

Prognostic factors
• Extension from nose to upper lip
• Tumour size < 2 cm
• Male sex
• Response to this high-dose rate brachytherapy
• Previous treatment

23

Effect of previous treatment

24

12
 4/24/24

But there’s more

Berlato JFMS 2019

26

And there’s more

• Retrospective study: 74 cats with nasal planum SCC treated with Sr90
plesiotherapy
• 32 treated with fractionated protocol; 42 with single-dose treatment
• Sr90 plesiotherapy was able to induce complete response in 74% of
cats
• Median DFI was 780 days: fractionated longer
• Overall survival for all cats was 1039 days

Berlato JFMS 2019

27

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 4/24/24

• Other prognostic factors that influenced the overall survival:

• Early-stage disease
• Absence of concurrent problems
• Complete response to the treatment
• Acute and long-term toxicity associated with the treatment were
minimal and the aesthetic outcome was pleasing in almost all cases
• Strontium plesiotherapy is a safe and effective treatment of nasal
planum SCC
Berlato JFMS 2019

28

• 61 cats with SCC of nasal planum and no metastasis (nodes or lungs)

• Treated with electrochemical therapy + bleomycin (cytotoxic, 15,000
UI/m2)
• Tumor size influenced local treatment response (p = 0.008) and
toxicity (p < 0.001)
• ECT is an effective treatment for feline npSCCs and should be
considered as the first-line procedure for low-stage tumors.

Simčič Vet Sci 2021

29

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 4/24/24

Other cancers
• SCC + papillomaviruses
• Fibrosarcoma
• Cryotherapy long term remission
120 months
• Hemangiosarcoma
• Melanoma and melanocytoma
• Basal cell carcinoma

Salmoral JFMS 2024

30

• Retrospective
• 10 cats with histologically confirmed melanocytic tumours of the
nasal planum
• 7 malignant; 3 benign
• Treatment: 6 hypofractionated radiation therapy; 1 surgery; 3 no tx
• 50% of radiated cats complete remission yet all recurred
• All cats euthanized due to tumour progression (median survival time:
265 days)

Reck JSAP 2021

31

15
 4/24/24

Immune-mediated

Image from Anusha Vaddi, MDS

32

Pemphigus foliaceous

Courtesy K Moriello

33

16
 4/24/24

Pemphigus foliaceous

Courtesy D Preziosi

34

Pemphigus foliaceous

Courtesy D Preziosi

35

17
 4/24/24

Cytology: Neutrophils PF

Courtesy K Moriello

36

Histopathology PF

Courtesy D Preziosi

37

18
 4/24/24

Treatment PF
• Lifelong immunosuppressive
doses of corticosteroids +/-
other immunosuppressive
agents, (e.g., chlorambucil or
cyclosporine)

38

Ulcerative Planum Nasal of the Bengal Cat

• Inherited disorder?

Courtesy K Moriello

39

19
 4/24/24

40

Atopy

Courtesy K Moriello

41

20
 4/24/24

Cytology: eosinophils

Courtesy K Moriello

42

Insect bite allergy

Courtesy K Moriello

43

21
 4/24/24

Mosquito-bite hypersensitivity
• Treatment: corticosteroids short-
term
• Indoor confinement long-term

Courtesy H Chisholm

44

Flea Allergy

Courtesy K Moriello

45

22
 4/24/24

Methimazole reaction

Courtesy K Moriello

46

Infectious

47

23
 4/24/24

Herpesvirus dermatitis
• Progressive dermatosis +/- on muzzle
• Diagnosis: histopath immunohistochemistry
• PCR?
• Treatment: Oral famcyclovir fa ce
• Feline omega interferon? s the
l way
t a
t no
Bu

48

FHV-1 upper respiratory & skin

November 1

49

24
 4/24/24

FHV-1 upper respiratory & skin

November 1

50

FHV-1 upper respiratory & skin

November 21

51

25
 4/24/24

FHV-1 upper respiratory & skin

December 1

52

FHV-1 upper respiratory & skin

December 27

53

26
 4/24/24

Herpesvirus + demodex

Courtesy K Moriello

54

Leprosy

55

27
 4/24/24

Cryptococcus

Courtesy K Moriello

56

Other fungal organisms

• Dermatophytes
• Aspergillus
• Penicillium
• Fusarium

Washington State University

57

28
 4/24/24

My differential list for Nino consisted of

q Fly bite or mosquito hypersensitivity
q Flea hypersensitivity
q Food intolerance (what about the fish food in the pond?)
q Plastic hypersensitivity (contact dermatitis to linoleum?)
q Actinic keratosis
q Eosinophilic granuloma complex
q Pemphigus foliaceus
q Mange (notoedric, demodectic, otodectic, trombicular)

58

Less likely due to initial response

q Dermatophytosis (initial response to corticosteroids)
q Deep mycosis (sporotrichosis, cryptococcosis would
expect worse due to corticosteroids)
q Mycobacterial infection (ditto)
q Herpes viral dermatitis
q Poxvirus infection
q Squamous cell carcinoma or other neoplasm (unlikely due to healing of original
lesion)
q Dermatologic manifestation of systemic disease

59

29
 4/24/24

Recommendations
• Repeat blood work and urinalysis
• Soak crusts BID-TID warm saline, apply vaseline
• Nasal decongestant (e.g., Otrivin)
• SC fluids
• Appetite stimulant

60

Recommendations
• Switch corticosteroid type
• Restart doxycycline
• Start clorambucil
• Recheck in one week
• Request review of histopathology slides
• Add on immunoperoxidase stain for Herpes and immunoglobulins

61

30
 4/24/24

Why choose doxycyline?

62

Why choose doxycyline?

• Antibacterial properties?
• Atypical mycobacterial infection?
• Anti-inflammatory properties?
• Anti-viral therapy?
• Anti-histaminic properties?

63

31
 4/24/24

Why choose doxycyline?

• Antibacterial properties?
• Atypical mycobacterial infection?
• Anti-inflammatory properties?
• Anti-viral therapy?
• Anti-histaminic properties?

64

Recommendations
• Switch corticosteroid type
• Restart doxycycline
• Start clorambucil
• Recheck in one week
• Request review of histopathology slides
• Add on immunoperoxidase stain for Herpes and immunoglobulins
• Scraping

65

32
 4/24/24

Courtesy K Moriello

66

Recheck
• No improvement
• Touch impression cytology
• Many neutrophils, degenerate and intact
• Many cocci
• Septic inflammation, likely secondary
• Culture: heavy growth Staph. aureus and scant Pseudomonas. Not
sensitive to doxycycline
• Switch to enrofloxacin
• Start antihistamine, continue triamcinolone

67

33
 4/24/24

Peroxidase staining and IHC

• IgG staining in spaces of epidermis
compelling for pemphigus

• Negative for herpes virus

68

Recheck Oh no! What could I do?

• No improvement
• Noisy breathing
• Good appetite
• Holding left fore paw up for 3 days
• L lateral carpus swollen
• Concern re quality of life, very discouraged

69

34
 4/24/24

Recheck Oh no! What could I do?

• Offer to board and treat pro bono to help and learn

• Debride, cleanse
• Continue treatments and ensure eating well
• Support body function and comfort by attention to:
1) Hydration
2) Nutrition
3) Ability to express normal behaviours
4) Alleviation of pain

70

Get more diagnostics

• Rebiopsy nose and forehead
• Biopsy carpus: hard and eroded
• Collect microbiological samples
• Meloxicam

71

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 4/24/24

Results
• Nasal planum: paraneoplastic
bullous pemphigoid
• Forelimb: round cell tumour
• Undifferentiated mast cell
tumour?
• Probable extension to forehead

Nino 1997-2003

72

• Retrospective
• 10 cats with histologically confirmed melanocytic tumours of the
nasal planum
• 7 malignant; 3 benign
• Treatment: 6 hypofractionated radiation therapy; 1 surgery; 3 no tx
• 50% of radiated cats complete remission yet all recurred
• All cats euthanized due to tumour progression (median survival time:
265 days)

Reck JSAP 2021

73

36
 4/24/24

Do you have any questions about Nino?

hypurr@aol.com

74

37
 4/24/24

SNOTS & SNUFFLES: Margie Scherk

Feline Upper Respiratory DVM, DABVP (feline)
Tract Diseases Vancouver, Canada

Thank you to

for sponsoring
2

1
 4/24/24

Overview
• History
• Presentation
• Etiologies
• Pathology
• Diagnostics
• Therapeutic choices
• Specific and non-specific

2
 4/24/24

Definitions
Upper Respiratory Tract Disease (URTD)
• Syndrome with serous to mucopurulent • ACUTE
ocular and nasal discharges, epistaxis, < 10 days
sneezing and conjunctivitis
• CHRONIC
Upper Respiratory Infection > 10 days
• URTD directly associated with 1 or more
known pathogenic viral, bacterial or fungal
organisms
Lappin JVIM 2017

Feline chronic rhinosinusitis

• Etiology unknown
• Active infection?
• Previous viral damage?
• Secondary bacteria?
• Chronic antigenic stimulation?

• INFLAMMATION

3
 4/24/24

Sneezing…
• Sneezing stimulation of irritant receptors (nose, sinus)
• Chronicity reduction in response accumulation of discharge

• Timing (frequency, time of day/week/year, duration)

• Discharge (serous, mucoid, purulent, sanguinous, mixed)
• Uni-vs. bilateral
• Has it changed?

History and presentation

• Respiratory patterns and sounds may be abnormal
• Hoarse, silent meow
• Inspiratory large vs. expiratory small airways
• Snorting (accumulated discharges)
• Snoring, stertor
• Stridor (inspiratory wheeze)
• Expiratory wheeze, crackles, rales
• Lack of sounds

4
 4/24/24

Examination
• Facial symmetry
• Face-on and from above
• Dentition and alveolar bone
• Mouth, (palates), under tongue, oropharynx
• Neurological assessment:
• Jaw tone (motor V), position, movements and symmetry of the
tongue (XII), gag reflex (IX, X)

Comprehensive physical examination

• Fundic examination
• Lymph node evaluation
• Assess blood pressure
• Symmetry of airflow

10

5
 4/24/24

Differentials for upper respiratory tract disease

• Neoplasia (lymphoma, • Nasopharyngeal stenosis
adenocarcinoma, sarcoma) • Trauma
• Nasopharyngeal polyp • Congenital (cleft palate; extreme
• Foreign body brachycephalic conformation)
• Fungal infection (Cryptococcus, • Dental disease (oronasal fistula; tooth
Aspergillus, Penicillium) root infection or abscess)
• Allergic rhinitis • Inflammatory polyps of the nasal
turbinates

Reed N. Chronic rhinitis in the cat. Vet Clin Small Anim 2014
Henderson SM. Investigation of nasal disease in the cat—a retrospective study of 77 cases. J Feline Med Surg 2004

11

Etiology & Pathogenesis

• Chronic rhinitis
• Usually sequel to acute disease
• Ineffective response to viral infection

• Herpesvirus (FHV-1) as common denominator

• Initiates turbinate resorption
• Secondary bacterial infections (69 - 90% of cases )
• Unchecked inflammation

12

6
 4/24/24

13

• n = 405, 14 breeds
• Rhinitis > neoplasia >
polyps

Ferguson JFMS 2020

14

7
 4/24/24

• Neoplasia: lymphoma >

adenocarcinoma >
undifferentiated carcinoma
• Benign uncommon
• No significant association
between skull conformation
and nasal diseases
• Polyps more likely in younger
male cats
Ferguson JFMS 2020

15

Prevalence of infectious causes???

• Unclear: different
• Regions
• Populations
• Husbandry: pets, shelters, etc.
• Breeds
• Intact vs. altered
• Ages
• Vaccination status
• Duration of disease
• Diagnostic protocols

16

8
 4/24/24

Primary Bacterial Etiologies

• Bordetella bronchiseptica? • Pasteurella multocida
• Mycoplasma spp. po PCR • Streptococcus spp.
pu : p
• Chlamydia felis lat oo
io r
n d hy
g
a s e n s ie n
ick ity, e, h
do liv igh
g in g
wi
th

Helps Vet Record 2005

17

Multiplex quantitative PCR panel

• >3000 samples from cats w • 50% positive
URTD • M. felis alone in 21%
• FCV alone in 16%
• FCV, FHV-1, B bronchiseptica, M • M. felis + FCV in 13%
felis, C felis, and H1N1 influenza • FHV-1 alone in 7%

Nguyen JFMS 2019

18

9
 4/24/24

Multiplex quantitative PCR panel

• 50% positive
• M. felis alone in 21%
• FCV alone in 16%
• M. felis + FCV in 13%
• FHV-1 alone in 7%

Nguyen JFMS 2019

19

Feline Herpesvirus-1 Feline calicivirus

• 80% are lifelong carriers • Persistently shed virus for
• Latent trigeminal nerve weeks-years in ocular, nasal and
• Re-shed under stress oral secretions
• Conjunctivitis, corneal
Vaccination ulcers,severity of illness, not sterilizing
reduces
nasal/ocular discharge, oral • Oral ulcers
ulceration, facial dermatitis
• Prevalence estimated 26-50%
• Prevalence estimated 3-38%

20

10
 4/24/24

Pathogenesis
• Anatomic predisposition

• Irreversible
turbinate damage
inflammatory
mediator-induced
cytolysis

Chronicity ó irreversibility

21

Primary bacteria
Mycoplasma felis Chlamydia felis Bordetella
bronchiseptica
Transmission Commensal to upper Shed in ocular Intermittently
respiratory tract discharge oronasal shed +/-
clinical signs
Clinical signs More typically Mild respiratory signs Wide range: mild
opportunistic but conjunctivitis, URTD to severe
hyperemia, pneumonia;
blepharospasm no cough
Prevalence Possibly in 46% of cats 0-15% 0-30%
with URTD; but also in
20% healthy cats

22

11
 4/24/24

Primary bacteria
Mycoplasma felis Chlamydia felis Bordetella
bronchiseptica
Transmission Commensal to upper Shed in ocular Intermittently
respiratory tract discharge oronasal shed +/-
clinical signs
Clinical signs More typically Mild respiratory signs Wide range: mild
opportunistic but conjunctivitis, URTD to severe
hyperemia, pneumonia;
blepharospasm no cough
Prevalence Possibly in 46% of cats 0-15% 0-30%
with URTD; but also in
20% healthy cats

23

Primary bacteria
Mycoplasma felis Chlamydia felis Bordetella
bronchiseptica
Transmission Commensal to upper Shed in ocular Intermittently
respiratory tract discharge oronasal shed +/-
clinical signs
Clinical signs More typically Mild respiratory signs Wide range: mild
opportunistic but conjunctivitis, URTD to severe
hyperemia, pneumonia;
blepharospasm no cough
Prevalence Possibly in 46% of cats 0-15% 0-30%
with URTD; but also in
20% healthy cats

24

12
 4/24/24

Fungal organisms
• Cryptococcus neoformans var. neoformans & gattii
• Severe inflammation resulting in facial deformity and skin
ulceration
• Unilateral (> bilateral) nasal discharge

• Aspergillosis sp. & Penicillium spp.

• Sino-nasal or sino-orbital presentation

25

Always get a travel history

26

13
 4/24/24

Contributing Factors
• Alteration of form & function:
• Trauma
• Congenital/conformation • Primary inflammation or allergy
• Polyps (lympho-plasmacytic rhinitis)
• Foreign bodies
Chronic inflammation/infection
• Concurrent disease may• predispose
Concurrent to nasal lymphoma?
stressors
• Oral/dental diseases • Social stress
• Neoplasia • Malnutrition
• Nasal discharge secondary to • Environmental
pneumonia/asthma • Retroviral infection
27

Neoplasia
• Most are malignant
• Locally invasive (sinuses)
• Older cats
• Localizing signs:
• Nasal: sneezing, unilateral discharge
• Nasopharyngeal: stertor
• Epistaxis, epiphora, facial deformity

28

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 4/24/24

548_557_Snots and snuffles:FAB 7/6/10 16:16 Page 549

Clinical management R E V I E W / The chronic feline snuffler

Etiologies and pathogenesis signs during periods of physiological or

psychological stress.
Acute disease usually is viral
•Viruses
Chronic rhinitis may be a sequela to Bacteria
Rarely
acute•rhinitis but itneeds antimicrobials
may be a separate
condition altogether. It may represent
Primary bacterial agents include
Bordetella bronchiseptica, which is com-
an ineffective immune response to monly found as a commensal without
persistent viral infection.1 Feline causing morbidity. Mycoplasma species
herpesvirus 1 (FHV-1) may be the may be cultured or amplified by poly-
• Occasionally C. felis, B. bronchiseptica, Strep. canis, Strep. equi
common denominator, initiating merase chain reaction (PCR) from some
zooepidemicus, and Mycoplasma spp. have been identified in PCR
turbinate resorption, with subsequent
secondary bacterial infections and
individuals. They are very common in
acutely affected cats and, thus, likely
virus negative, sick cats
unchecked inflammation exacerbat-
ing the problem.2,3 This is especially severe
FIG 1 The Persian, with
its compressed nasal
play a role in the chronic syndrome. It is
a challenge to identify them in primary care
passages and tiny nostrils,
in anatomically predisposed individuals (con- is anatomically predisposed
practice due to the difficulty of isolating these
formation anomalies, such as the tiny nostrils to unresolving upper airway fastidious organisms.4,5
inflammation. Image,
of the Persian, Fig 1). Irreversible destruction Chlamydophilosis can be a common cause of
• Chronic disease improvement on antibiotics suggests secondary
Wikimedia Commons
of the turbinates may result in viral or conjunctivitis in some catteries but is uncom-
inflammatory mediator-induced cytolysis. mon in client-owned cats with chronic rhinitis.
bacteria
Reactivation of herpesvirus from infected
trigeminal ganglion may result in recurrent
L-forms may also be involved but require spe-
cific targeted culture techniques for verification.
destruction. All of these are potential patho- In one study of cats with and without
genic strategies, but it is not possible to deter- chronic rhinosinusitis, aerobic bacteria were
mine the course/cause in a given individual. cultured from biopsy samples from propor-
Calicivirus infection results in a carrier state tionately more clinically affected cats (4/10,
29 with continuous shedding for variable peri- 40%) than controls (2/7, 29%), while anaerobic
ods of time. FHV-1, like other herpesviruses, bacteria were detected only in the affected cats
results in a state of latency and approximately (2/10).6 Flush samples were collected from the
80% of infected cats are permanent carriers. same cats, with aerobes identified in 5/7 con-
Latency accounts for recurrence of clinical trols and 9/10 affected cats; and anaerobes in

Self-perpetuating cycle of viral-induced inflammation

+/- reactivation
of latent FHV-1 +
virus

turbinates

inflammation
swelling of mucosa
inflammation is +
bacterial self-perpetuating inflammatory mediators
colonisation
and cells

turbinate
destruction

30
JFMS CLINICAL PRACTICE 549

15
 4/24/24

Clinical management if chronic or recurrent

• CBC • Coagulation panel?
• Serum biochemistries • Stop meds affecting hemostasis
• Retroviral serology • Fungal:
• Urinalysis • Cryptococcus cytology, LCAT
• Blood pressure • Aspergillus: IgG ELISA or
AGID
• Lymph node aspirates?

Barrs Vet J 2015

31

Oral examination
• Probe all periodontal pockets
• Palpate soft palate
• Retract soft palate
• +/- dental radiographs

32

16
 4/24/24

Imaging
• Skull radiographs or CT/MRI
• Dentition
• Nasal passages
• Sinuses

33

Radiographs
• Require general anaesthesia

Three standard views:

1. Open mouth ventrodorsal view (nasal cavity, bullae); symmetry is
essential.
2. Lateral view (frontal sinuses); if a change is suspected, follow with
oblique lateral to focus on questionable sinus.
3. Skyline view of frontal sinuses with cat in dorsal recumbency, pulling the
mandible out of the way.

34

17
 4/24/24

Images from www.vetsurgerycentral.com/oral_nasopharyngeal_polyp.html

35

Computerized Tomography (CT)

• Inflammation and neoplasia may overlap
• Neoplasia suspected when:
• Lysis of the ventral aspect of the maxilla or vomer bone;
• Unilateral lysis of the ethmoturbinates or dorsal and lateral
aspects of the maxilla;
• Bilateral lysis of the orbital lamina;
• Unilateral soft tissue opacification of the frontal sinus, sphenoid
sinus, or retrobulbar space

36

18
 4/24/24

Rhinoscopy
• Cuff the endotracheal tube
• Pack oropharynx with known # of swabs
• Irrigate with sterile saline for optimal visualization

• Retroflex flexible scope around soft palate

• For rostral portions: a rigid 1.9 mm arthroscope with a 30 degree
viewing angle or small flexible scope
• Flexible Micro-Endoscope (1.67mm X 20") for dog and cat noses
(e.g., MDS Micro-Endoscope)

37

MDS Micro-Endoscope

Rhinoscopy Flexible Micro-

Endoscope
(1.67mm X 20") for
• Even if mucosa looks normal, dog and cat noses
BIOPSY!
• Evaluate entire cavity (rostral
and caudal) before biopsying to
avoid bleeding
• Keep sedated upon recovery and
hospitalize overnight to prevent
bleeding

38

19
 4/24/24

Rhinoscopy
• Visualize unaffected side first if unilateral disease
• Normal turbinate mucosa is pale pink, smooth
• Hyperemia, irregular turbinate surfaces and
moderate amounts of discharge
• Fungal plaques
• Adenocarcinoma or sarcoma appear as
discrete mass
• Lymphoma may present as
mass or as diffuse infiltrate
Images courtesy of Jeff Mayo
39

Mucus Carpet fiber

Nasopharyngeal stenosis
(“webbing”) Polyp

Images courtesy of
Jeff Mayo
40

20
 4/24/24

Collect samples
• After examination and imaging
• 40 cats underwent rhinoscopy for chronic nasal disease to
compare relative diagnostic yield of cytology and biopsy.
• Only 25% of the cases showed agreement. The conclusion was
that cytology (even brush cytology) does not appear to be a
reliable means for the detection of chronic inflammation and
evaluation of chronic rhinitis in cats.
• Not reliable but better than biopsy for diagnosing bacterial infection
of guiding antibiotic choice

Michiels JFMS 2003

41

Primary Bacterial Etiologies

• Bordetella bronchiseptica? • Pasteurella multocida
• Mycoplasma spp. • Streptococcus spp.
• Chlamydia felis
• Biopsy:
• Aerobic bacteria 2X freq in affected vs. controls (4/10 vs. 2/7)
• Anaerobic only in affected (2/10)

• Flush:
• Aerobic bacteria increased freq in controls (9/10 vs. 5/7)
• Anaerobes only in affected (3/10)
• Mycoplasma only in affected (2/10)
Johnson JAVMA 2005, Johnston JFMS 2009

42

21
 4/24/24

Nasal swabs/lavage
• Pass 6 to 8F sterile catheter into the rostral nasal cavity
• Measure to medial canthus
• Occlude nasopharynx by pressing on the soft palate
• Flush with 2 to 4 mL of sterile saline and aspirate for aerobic and
anaerobic culture
• +/- fungal culture and PCR or Mycoplasma testing where indicated

Johnson L, Proceedings ISCAID 2016

43

Nasal lavage - PCR

• Detects exposure to FHV-1, Chlamydia and Mycoplasma. Holst JFMS 2010

Mycoplasma were found only in sick cats

• Best to sample oropharynx if only sampling 1 site (> nose,
conjunctive, tongue)
• Real-time PCR for FHV-1, FCV and C. felis on 104 cats w URTD.
In 93 of 104 sick cats, organisms were identified with 56%
positive for FHV-1, 50% for FCV and 36% for Chlamydia.
• FCV was found more frequently in the oropharynx and tongue,
whereas FHV-1 and C. felis were found in all locations
regardless of which lesions were present.
Schultz JFMS 2015

44

22
 4/24/24

Burgesser J Vet Diagn Invest 1999

45

FHV-1 PCR
• Relative sensitivity of PCR assays • None of the assays could
for the detection of FHV-1 DNA differentiate between wild-type
assessed in clinical samples and and vaccine virus. Also, test
commercial vaccines. sensitivity (detection limits and
rates) varied greatly between
the tests used.

Maggs AJVR 2005 www.promega.ca/resources/guides/nucleic-acid-analysis/pcr-amplification

46

23
 4/24/24

DIAGNOSTICS in ACUTE disease? Culture or PCR

• Limited usefulness in acute • Consider when outbreak in large
disease population but test multiple cats
• Bacteria and viruses present in
healthy animals
• Recent vaccination limits use of
PCR

Lappin JVIM 2017, Johnson JAVMA 2005, Johnston JFMS 2009

48

Overview
• History
• Presentation
• Etiologies
• Pathology
• Diagnostics
• Therapeutic choices
• Specific and non-specific

49

24
 4/24/24

Therapeutics: SPECIFIC

Lappin JVIM 2017

50

Therapeutics: ACUTE disease

• Observe rather than give antibiotics even when acute bacterial
infection is suspected, (based on a mucopurulent or purulent
discharge), unless fever, lethargy or anorexia are present

• First choice is doxycycline (chase with water/food)

• Amoxicillin if not M.felis or C.felis

Lappin JVIM 2017

51

25
 4/24/24

Therapeutics: ACUTE disease

• ONLY USE
• Amoxicillin-clavulanate if regional antibiograms show beta
lactamase producing organisms

• AVOID
• Cefovecin

Lappin JVIM 2017

52

AVOID Cefovecin
• 48 shelter cats, retrovirus negative
• Conjunctival and nasal swabs
• Oral administration of amoxicillin-clavulanate or doxycycline
appeared to be more effective than a single SC injection of cefovecin
in treating cats with clinical signs of URTD

Lappin JVIM 2017, Litster JAVMA 2012

53

26
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DIAGNOSTICS in CHRONIC disease

• Anaesthesia • Purpose is to ID non-infectious
• Oral examination causes
• Imaging • Nasophayngeal polyps, dental
• Rhinoscopy disease, oropharyngeal
fistula, neoplasia,
• If no treatable cause identified, nasophayngeal stenosis,
perform nasal lavage: allergic disease, trauma
• Cytology, C&S, Mycoplasma PCR, • Cuterebra or fungal infection
fungal culture
548_557_Snots and snuffles:FAB 7/6/10 16:16 Page 549

Lappin JVIM 2017

54
R E V I E W / The chronic feline snuffler

Etiologies and pathogenesis signs during periods of physiological or

psychological stress.
Viruses
Chronic rhinitis may be a sequela to Bacteria
acute rhinitis but it may be a separate Primary bacterial agents include
condition altogether. It may represent Bordetella bronchiseptica, which is com-
an ineffective immune response to monly found as a commensal without
persistent viral infection.1 Feline causing morbidity. Mycoplasma species
herpesvirus 1 (FHV-1) may be the may be cultured or amplified by poly-
common denominator, initiating merase chain reaction (PCR) from some
turbinate resorption, with subsequent individuals. They are very common in
secondary bacterial infections and acutely affected cats and, thus, likely
unchecked inflammation exacerbat- FIG 1 The Persian, with play a role in the chronic syndrome. It is
ing the problem.2,3 This is especially severe its compressed nasal a challenge to identify them in primary care
passages and tiny nostrils,
in anatomically predisposed individuals (con- is anatomically predisposed
practice due to the difficulty of isolating these

Therapeutics: CHRONIC disease

formation anomalies, such as the tiny nostrils to unresolving upper airway fastidious organisms.4,5
inflammation. Image,
of the Persian, Fig 1). Irreversible destruction Wikimedia Commons
Chlamydophilosis can be a common cause of
of the turbinates may result in viral or conjunctivitis in some catteries but is uncom-
inflammatory mediator-induced cytolysis. mon in client-owned cats with chronic rhinitis.
Reactivation of herpesvirus from infected L-forms may also be involved but require spe-
trigeminal ganglion may result in recurrent cific targeted culture techniques for verification.
destruction. All of these are potential patho- In one study of cats with and without
genic strategies, but it is not possible to deter- chronic rhinosinusitis, aerobic bacteria were
mine the course/cause in a given individual. cultured from biopsy samples from propor-
Calicivirus infection results in a carrier state tionately more clinically affected cats (4/10,

• Culture in chronic disease to identify severe secondary bacterial

with continuous shedding for variable peri- 40%) than controls (2/7, 29%), while anaerobic
ods of time. FHV-1, like other herpesviruses, bacteria were detected only in the affected cats
results in a state of latency and approximately (2/10).6 Flush samples were collected from the
80% of infected cats are permanent carriers. same cats, with aerobes identified in 5/7 con-

agents Latency accounts for recurrence of clinical trols and 9/10 affected cats; and anaerobes in

Self-perpetuating cycle of viral-induced inflammation

• Relief from antibiotics likely brief

+
virus

turbinates

inflammation
swelling of mucosa
inflammation is +
bacterial self-perpetuating inflammatory mediators
colonisation
and cells

turbinate
destruction

Lappin JVIM 2017

JFMS CLINICAL PRACTICE 549
55

27
 4/24/24

https://www.youtube.com/watch?v=plVk4NVIUh8&fbclid=IwAR1ZmsK9FqXsREUlVV5CNtr0wSJW71xceUZ4XOMZlUwnUlio2E9jgd
kg91M
https://youtu.be/plVk4NVIUh8

56

57

28
 4/24/24

youtu.be/plVk4NVIUh8

58

Therapeutics: CHRONIC disease

• Recurrent disease: do not change antibiotic
• Increases risk of developing resistance
• Fluoroquinolones and 3rd generation
cephalosporins should not be first choices
and should be used only when C&S shows
possible benefit and when other antibiotics
are not feasible

Lappin JVIM 2017

59

29
 4/24/24

Therapeutics: CHRONIC disease

• Fluoroquinolones and 3rd
generation cephalosporins
should not be first choices and • No evidence that these or
should be used only when C&S azithromycin are superior to
shows possible benefit and doxycycline and amoxicillin for
when other antibiotics are not treating chronic URTD
feasible

Lappin JVIM 2017 Owen JFMS 2003, Rush-Gallie JFMS 2008

60

61

30
 4/24/24

• Objectives The aim of this study was to determine the antimicrobial

susceptibility of Enterobacteriaceae isolated from cats affected by diseases
commonly encountered in practice, and to characterise the third-
generation cephalosporin (3GC)-resistance molecular mechanisms
involved.

• Results Thirty-one percent (n=39) of the isolates were multidrug-resistant

(MDR) and were isolated from 34% (n=31/90) of the cats.

Lo Piccolo JFMS 2019

62

It DOES affect us
• “These results highlight once more the need for bacteriological
examination and susceptibility testing before instituting empirical
antimicrobial therapy if a bacterial infection is suspected, in order to
establish accurate treatment and avoid the antimicrobial selection
pressure on the animal microbiota.”

• Let’s not abuse cefovecin (or anything else!)

Lo Piccolo JFMS 2019

63

31
 4/24/24

Antimicrobial resistance crisis

• Despite the threat of a global
antibiotic-resistance crisis, the
worldwide use of antibiotics in
humans soared 39 percent
between 2000 and 2015, fueled
by dramatic increases in low-
income and middle-income
countries, according to a study in
the Proceedings of the National
Academy of Sciences.
Klein PNAS 2018

64

Antibiotics: CHRONIC disease

• Do not use pulse or intermittent therapy (e.g., one
week/month)
• Repeated short courses of antibacterials may result in
selection for Pseudomonas spp.

• No evidence that topical (intranasal) antibiotics

(ophthalmics) or antiseptics are effective
• IN saline might help

Lappin JVIM 2017

65

32
 4/24/24

Therapeutics: CHRONIC disease

• Pseudomonas aeruginosa:
• Flush to remove loculated secretions
• Fluoroquinolone +/- beta-lactamase inhibitor based on C&S
• Prone to develop resistance

Lappin JVIM 2017

66

Therapeutics duration: CHRONIC disease

• Chronic bacterial with NO evidence
treatable primary disease
• Based on C&S results from nasal lavage
or brushings
• Treat for 1 week after clinical signs have
stopped or stable

• If recurs, try same antibiotic for 48

hours
• If no response, use C&S for new
choice
Lappin JVIM 2017

67

33
 4/24/24

Antibiotics: CHRONIC disease

• Penetrate bone and cartilage, safe for long term use, anaerobic
spectrum:
• Doxycycline
• Clindamycin – also Mycoplasma
• Pradofloxacin – also gram-neg, Mycoplasma
• Other fluoroquinolones
• Amoxicillin clavulanate – also Bordetella

68

Lappin JVIM 2017

69

34
 4/24/24

Minocycline – less costly than doxycycline

• 8.8 mg/kg PO once a day (~ 50 mg/cat)

Tynan JFMS 2015

70

• Compare pradofloxacin to amoxicillin

• FHV-1, Mycoplasma, Bordetella, Staphylococcus, Streptococcus
• No statistical difference
• Both work well

Spindel JFMS 2008

71

35
 4/24/24

• Compare pradofloxacin with doxycycline

• PCR to identify organisms and to assess response
• Mycoplasma eliminated with either drug
• 4/12 (33%) of cats w Chlamydia treated w pradofloxacin remained
PCR +

Hartmann JVIM 2008

72

Consider synbiotics alongside oral antibiotics

• Fortiflora SA for management of amoxicillin-clavulanate-induced
diarrhea
• Proviable-DC with clindamycin reduced GI side-effects (hyporexia,
vomiting)

Lappin ACVIM 2020, Stokes JVIM 2017

73

36
 4/24/24

ANTIVIRALS
Famciclovir, Cidofovir, L-lysine, IN vaccination

74

Antivirals: CHRONIC disease

• Famciclovir:
• Pre-emptive or early use in humans

• In cats:
• Reduces FHV-1 shedding (shelter study)
• 90 mg/kg oral famciclovir q12h
• 3 weeks to long term
• No difference in response to treatment
compared to doxycycline in kittens (low
levels FHV-1 in study)
Cooper JFMS 2019, Kopecny JFMS 2019

75

37
 4/24/24

Antivirals: CHRONIC disease

• Famciclovir 125 mg PO q8-12h, long-term
• 90 mg/kg PO q8h needed to get effective levels in tears
Thomasy et al, AMVJ 2011, Sebbag et al, AMVJ 2016

• Herpetic keratitis: Cidofovir eye drops

• 0.5% solution in 1% methylcellulose, 1 drop BID in affected eye(s)
duration dependent on response.
• Does not burn or cause inflammatory conjunctival reaction.
Fontenelle et al, AJVR 2008

76

FHV-1: L-lysine
• Helps to reduce the frequency of herpesviral recrudescence
• 250 (kittens) – 500 (adults) mg PO q12h long term
• Did not prevent URI in shelter
• Broad use in shelters has not been shown to be of benefit and, given the
costs and stress of handling, other strategies may be better in this setting
• Dietary lysine led to increases in disease severity and the incidence of
detection of FHV-1 DNA in oropharyngeal or conjunctival mucosal swab
specimens
• May still be useful in the home (if administration not stressful)

Rees JFMS 2008, Maggs JFMS 2007, Drazenovich, AJVR 2009

77

38
 4/24/24

Therapeutic vaccination
• Intranasal FHV-1, FCV vaccination appears to induce local innate
immunity
• Less clinical illness
• Provided cross protection against Bordetella bronchiseptica vs.
controls

• MUST use intranasal product, not parenteral product!

Bradley JVIM 2012

78

Therapeutic vaccination
• 1 dose intranasal herpes and calicivirus vaccine was ~ more useful
than 10,000 U/kg alpha 2b interferon SQ q24h X 14 days
• 30% of shelter cats w chronic URTD that failed lysine, doxy and
amoxicillin-clavulanate dropped below study severity when moved to
less crowded housing
• Suggests that fostering chronic respiratory cats may help

• Intranasal vaccination two to three times a year may help to

stimulate local immunity if cat responds to first dose

Fenimore JFMS 2016

79

39
 4/24/24

Other Specific Therapies -

CHRONIC

80

Polyps, foreign bodies, stenosis, etc

• Remove polyps, foreign bodies • Treat dental disease and correct
• Resect nasophayngeal stenosis fistulae
(“webbing”) • Antifungals for Cryptococcus,
Aspergillus
• Neoplasia – surgery, radiation,
chemo

Image courtesy of
Jeff Mayo
81

40
 4/24/24

Sinusitis Therapy
• Drill openings into frontal sinus,
collect histopathologic and
bacterial samples
• Surgical drainage and flushing
• Sinus ablation

82

83

41
 4/24/24

Allergy Therapeutics: Antihistamines

• Amitriptyline (Elavil): 5-10 mg/cat q 12- • Diphenhydramine (Benadryl): 2-4 mg/cat
24 h q 8-12 h
• Chlorpheniramine (Chlor-Trimeton): 2- • Hydroxyzine (Atarax): 5-10 mg/cat or 2.2
4 mg/cat q 12-24 h mg/kg q 8-12 h
• Clemastine (Tavist): 0.68 mg/cat or • Trimeprazine (Temaril): 0.5-1 mg/kg q 8-
12 h
0.05 mg/kg q 12 h
• Cetirizine (Zyrtec): 5 mg/cat q 12 h
• Cyproheptadine (Periactin): 2 mg/cat
• Fexofenadine (Allegra): 10 mg/cat q 12 h
or 1.1 mg/kg q 12 h
• Claritin: 0.5 mg/kg/day

84

Therapeutics: NON-SPECIFIC
Scherk JFMS 2010

85

42
 4/24/24

Maintain hydration
• Humidification
• Steaming/nebulizing
• Saline infusion
• Parenteral fluids

86

Nasal & Sinus Lavage

• Cuffed endotracheal tube
• Count # swabs
• Close one nostril, flush 6 ml aliquots
warmed saline or LRS (60-100 ml)
• Repeat other side
• Remove swabs
• Home care: 2 drops in each nostril on
alternate days

87

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548_557_Snots and snuffles:FAB 7/6/10 16:16 Page 549

Decongestants R E V I E W / The chronic feline snuffler

Etiologies and pathogenesis signs during periods of physiological or

psychological stress.
ORAL
Viruses
Chronic rhinitis may be a sequela to TOPICAL Bacteria
•acute rhinitis but it may be a separate
Diphenhydramine HCl 2-4mg/kg
condition altogether. It may represent PO 1 drop into Primary bacterial agents include
each nostril
Bordetella SID forwhich
bronchiseptica, three is com-
anq8h
ineffective immune response to days only to avoid
monly rebound
found as a congestion
commensal without
persistent viral infection.1 Feline causing morbidity. Mycoplasma species
Dimenhydrinate
•herpesvirus 1 (FHV-1) may 4mg/cat
be the PO q8h • Pediatric otrivin= 0.05%or amplified by poly-
may be cultured
common denominator, initiating merase chain reaction (PCR) from some
Pseudoephedrine
•turbinate 1 mg/kg PO q8h
resorption, with subsequent xylometazoline individuals. They are very common in
secondary bacterial infections and acutely affected cats and, thus, likely
unchecked inflammation exacerbat- • "Little Noses"
FIG 1 The Persian, with play Decongestant Nose It is
a role in the chronic syndrome.
ing the problem.2,3 This is especially severe its compressed nasal
in anatomically predisposed individuals (con- passages
Drops with
and tiny nostrils, phenylephrine
a challenge to identify them in primary care
practice due to the difficulty of isolating these
is anatomically predisposed
formation anomalies, such as the tiny nostrils to unresolving upperhydrochloride
airway fastidious organisms.4,5
of the Persian, Fig 1). Irreversible destruction inflammation. Image,
Wikimedia Commons
Chlamydophilosis can be a common cause of
of the turbinates may result in viral or • Afrin (oxymetazoline)
conjunctivitis in some catteries but is uncom-
inflammatory mediator-induced cytolysis. mon in client-owned cats with chronic rhinitis.
Reactivation of herpesvirus from infected L-forms may also be involved but require spe-
Saline may
trigeminal ganglion Spray/Drops
result in recurrent cific targeted culture techniques for verification.
destruction. All of these are potential patho- In one study of cats with and without
non medicated
genic strategies, but it is not possible to deter- chronic rhinosinusitis, aerobic bacteria were
mine the course/cause in a given individual. cultured from biopsy samples from propor-
Calicivirus infection results in a carrier state tionately more clinically affected cats (4/10,
88 with continuous shedding for variable peri- 40%) than controls (2/7, 29%), while anaerobic
ods of time. FHV-1, like other herpesviruses, bacteria were detected only in the affected cats
results in a state of latency and approximately (2/10).6 Flush samples were collected from the
80% of infected cats are permanent carriers. same cats, with aerobes identified in 5/7 con-
Latency accounts for recurrence of clinical trols and 9/10 affected cats; and anaerobes in

Self-perpetuating cycle of viral-induced inflammation

+
virus

turbinates

inflammation
swelling of mucosa
inflammation is +
bacterial self-perpetuating inflammatory mediators
colonisation
and cells

turbinate
destruction

89
JFMS CLINICAL PRACTICE 549

44
 4/24/24

Anti-inflammatories
• Glucocorticoids?
• Consider use in lymphoplasmacytic rhinitis
• Concern for recrudescence of the virus or virus shedding

90

Anti-inflammatories
• Non-steroidal anti-inflammatories (NSAIDs)
• Piroxicam 0.3 mg/kg PO q48h
• Meloxicam 0.05 mg/kg PO SID
• Robenacoxib 1 mg/kg PO q24h for 3 days (US), q24h (EU)

• Leukotriene blockers to reduce inflammatory cell infiltration

• SingulairTM (Montelukast 0.25mg-0.5mg/kg q24h)
• AccolateTM (Zafirlukast 0.5mg-1mg/kg q12-24h)

91

45
 4/24/24

Other Non-specific
• Maropitant (Cerenia) • Nutrition
• Blocks substance P which may • Balanced
reduce inflammation & mast cell • Quality and quantity
degranulation • Appetite stimulants:
• 2 mg/kg SID X 5 days then three • Cyproheptadine (1 mg/cat PO q12h)
times/week?
• Mirtazapine (2 mg/cat PO q24-48h)

• Acupuncture?
• Laser?

92

Decrease stress!!!

• Findings suggested that the pheromone ↓ stress, and that may have
resulted in decreased sneezing associated with FHV-1.

New data ACVIM 2021: Effect of

Bifidobacterium longum 999
supplementation on stress associated
findings in cats with FHV-1 infection

Contreras JVIM 2018

95

46
 4/24/24

Summary re treating URI in cats

• Acute or first episode: • Recurrent or chronic:
• Supportive care: • Perform diagnostics
• Hydration • Differentials include:
• Nutrition • Polyp
• Humidify airways • Foreign bodies
• Analgesia if stomatitis or • Dental disease
glossitis • Fungal disease
• Neoplasia

Adapted from Lappin Nov 4, 2021

96

Interested in infectious diseases?

SAVE THE DATE Vancouver, October 13-16, 2024
• Come to breathtaking Vancouver, Canada for ISCAID
October 13-16, 2024. There will be excellent
scientific presentations and lots of fun networking.
The venue is the historic Westin Bayshore Hotel on
the harbor adjacent to world-renowned 1001 acre
Stanley Park.

• We’d love to see you here!

• Registration rates are lower for ISCAID members.

Become an ISCAID member today! www.ISCAID.org

97

47
 4/24/24

Prognosis
Client expectation
Improvement in quality of life, not cure
Reduction in sneezing and discharge

Thank you!

Do you have any

questions?
hypurr@aol.com
98

48
 4/24/24

An Update on
Feline Thyroid
Diseases
Margie Scherk
DVM, Dip ABVP (feline)
Vancouver, Canada

Thank you to

for sponsoring
2

1
 4/24/24

Overview
• Up?

• Down?

2
 4/24/24

Hyperthyroidism
• Most common endocrine disorder in cats
• First diagnosed in 1979
• Increasing incidence
• Greater awareness, early screening
• A real increase in incidence

Courtesy of Mark Peterson

Q1
Epidemiologic studies have shown an increased incidence of feline
hyperthyroidism associated with:
a) Access to both outdoors and indoors.
b) Being fed a majority of tinned food in their diet.
c) Repeated exposure to flea control products.
d) Being fed a majority of fish and seafood-based diets.
e) Being exposed to bioavailable TDCIPP and polybrominated diphenyl
ethers
f) Multifactorial in etiology

3
 4/24/24

Q 1 ANSWER
Epidemiologic studies have shown an increased incidence of feline
hyperthyroidism associated with:
a) Access to both outdoors and indoors.
b) Being fed a majority of tinned food in their diet.
c) Repeated exposure to flea control products.
d) Being fed a majority of fish and seafood-based diets.
e) Being exposed to bioavailable TDCIPP and polybrominated diphenyl
ethers
f) Multifactorial in etiology

Etiology
• Epidemiology:
• Majority of tinned food in their diets
• Fish, liver/giblets
• Pop-top lids
• Soy-isoflavins, excess iodine, excess selenium
• Live strictly indoors, use litter
• Not Siamese, Himalayans (Abyssinian?)
• Exposure to flame retardants

4
 4/24/24

Etiology
• North America
• Europe, UK, New Zealand, Australia

• Risk factors implicate environmental, nutritional and

genetic demographics

• Well cared for cats live longer, use litter

De Wet CS. J Feline Med Surg, 2009

10

5
 4/24/24

11

12

6
 4/24/24

Etiology
• Goitrogens:
• Iodine and phyhalates (cat foods)
• Resorcinol, polyphenols, PCBs (fish diets or environment)
• Bisphenol-A-diglycidyl ether (BADGE)
• Metabolized in liver via glucuronidation
• Flame retardants…

13

Ewg.org
14

7
 4/24/24

Hyperthyroidism: one environmental etiology

• PBDE flame retardants are believed to be carcinogens

• Elevated PBDE levels in cats
• Link to hyperthyroidism?
• Flame retardants are endocrine –disrupting compounds
• PBDEs phased out 2004-2010

Dye Environ Sci Technol 2007

15

16

8
 4/24/24

• Silicone passive sampling devices,

or pet tags, quantitatively
assessed the bioavailable flame
retardant exposures of 78 cats (≥7
y) in New York and Oregon using
gas chromatography−mass
spectrometry

Poutasse Environ Sci Technol 2019

17

• Pet tags were analyzed for 36

polybrominated diphenyl ethers, six
organophosphate esters (OPEs), and
two alternative brominated FRs
• Exposure of 39 euthyroid cats • Tris(1,3-dichloro-2-isopropyl)
compared to that of 39 hyperthyroid phosphate levels higher in
cats hyperthyroid pet tags
• Measured total T4, free T4, T3, TSH • Higher TDCIPP associated with higher
fT4 and TT4

Poutasse Environ Sci Technol 2019

18

9
 4/24/24

Higher TDCIPP also found

In homes:
• Using air fresheners
• Built after 2005 compared to
those built earlier
• Where cats preferred to spend
time on upholstered furniture

Indicates that bioavailable TDCIPP exposures are associated w hyperthyroidism

Poutasse Environ Sci Technol 2019 cats.lovetoknow.com

19

Inadequate iodine?
A normal, age-related condition?

20

10
 4/24/24

Effects and
mechanism of action
of iodine deficiency
and thyroid hormone
disruptors

21

Summary pathogenesis
• Numerous nutritional and environmental factors
• Multifactorial
• Continuous, lifelong exposure to environmental thyroid disruptor chemicals or
goitrogens in food or water, acting together in an additive or synergistic manner
to affect multiple sites of thyroid hormone metabolism or action, appears first to
lead to euthyroid goiter and then to autonomous adenomatous hyperplasia and
adenoma, in some cats, eventually progressing to carcinoma

22

11
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Hyperthyroidism
• Benign hyperplastic adenomatous glands
• 97- 99%
• Rare: malignant adenocarcinoma (1-3%)
• 70% cases have bilateral disease

• End result = excess circulating T4 & T3

23

Clinical presentation
• Thin, active, +/-agitated • 5% of cases
• Bounding rapid heart, tachycardia, • Depressed
blub-dub murmur • Weak, lethargic
• Palpably enlarged thyroid • +/- anorectic
• Unkempt coat • +/- obese

Courtesy of Mark Peterson

24

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Diagnosis
• Palpable size of gland and T4 level • Preliminary testing
• Euthyroid vs. hyperthyroid • CBC with differential
• Non- functional vs. functional • Biochemistries
• Cystic thyroid or parathyroid • Urinalysis
• T4
• Blood pressure
• ALT +/- SAP in 90%
• Histopathology, minimal liver
changes

Image Norsworthy, JFMS 2002

25

26

13
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Feeding the Hyperthyroid Cat

• Many metabolic problems • Need high dietary protein
• Age-associated sarcopenia • Modest/low carbohydrates
• Glucose intolerance, insulin
resistance
• Weight loss, muscle wasting Protein Carbohydrate
40% calories; <15% calories;
• May need to increase calories > 55% dry matter < 20% dry matter
by 1.4-2X resting energy < 250 mg phos/100 kcal
requirement (RER) to maintain Peterson, Vet Clin N Am, 2014
weight
Parker Vet Clin N Am 2021
Williams JVIM 2010 Association of iatrogenic hypothyroidism with azotemia and decreased survival time in cats treated for hyperthyroidism

27

Adequate
calories

wsava.org

Adequate
protein

28

14
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Muscle Condition Score

29

How to perform a muscle condition exam

https://www.youtube.com/watch?v=fzEruEe-WRs

30

15
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• ~ 75% hyperthyroid cats lose muscle

mass
• 48 normal cats, 120 hyperthyroid cats
• Ultrasound epaxial muscle height
before and 6 mo after (75 cats) 131I
• Successful treatment restored muscle
mass in 85% of cats
• Muscle condition score 2 (1-3) before
and after 3 (2.5-3)

Xifar JVIM 2022

31

Protein catabolism + muscle wasting

Cachexia

Lean muscle loss

Death

Frailty Sarcopenia

Saker Vet Clin N Am 2021

32

16
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Comorbidities in
underweight
cats

• CKD
• Hyperthyroidism
• Osteoarthritis
• Diabetes

Saito E, Vet Focus 2017

33

Thyroid Storm

Dr Cynthia Ward, University of Georgia

34

17
 4/24/24

What is it? (and does it occur in cats?)

• Rare, life-threatening, multisystemic disorder
• Acute thyrotoxicosis – excessive hormone
• Excess production, secretion
• Leakage from damaged gland
• Exogenous hormone

35

Clinical signs
• Similar to those caused by catecholamines
• Sympathetic overdrive: pyrexia, confusion and tachyarrythmias
leading to hypertension

39

18
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Diagnosis
• At least four clinical signs + precipitating event
1. Thermoregulatory system: fever
2. CNS: agitation through to seizure or coma,
3. GI -hepatic: vomiting, diarrhea, abdominal pain, jaundice
4. Cardiovascular: sinus tachycardia, atrial fibrillation, congestive
heart failure

40

HIGH RISK SUDDEN DEATH!

Video from Mark Peterson

41

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What about CATS?

• Agitation, inappropriate • +/- dehydration, hypovolemia
behaviour • Fever or hypothermia
• Murmur or arrhythmia (gallop) • Hypertension + signs
• Tachypnea, open mouth • Thromboembolic complications
breathing • Cervical ventroflexion, HL
• Pulmonary edema/effusion weakness
• GI signs

42

Thyroid Storm (?)

• Sympathetic overdrive: pyrexia, confusion and tachyarrythmias
leading to hypertension
• Treatment: stabilize heart and treat thyroid
• Esmolol (BreviblocTM) 10 mg/ml in 10 ml vials
• Ultra--short acting beta blocker
• 200-500 mcg/kg IV over 1 min
• Then CRI 25-200 mcg/kg/min
• Monitor BP, ECG, HR

45

20
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Systemic support
• IV fluids
• Vitamin B complex
• Cooling
• Address cardiovascular
abnormalities
• Try to prevent thrombi
• Try to ID and correct
precipitating cause

46

Q2
Have you seen thyroid storm in cats?
a) Yes
b) No
c) I don’t believe it exists in cats

47

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48

Thyroid hormone tests In library

• Basal T4
• Low in hyperthyroidism?
• T4 fluctuations
• Early disease
• “Euthyroid sick syndrome”

• Alternate test OR retest at later

date

49

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Q3
When a healthy cat has a normal total T4 and there is clinical evidence
and suspicion that hyperthyroidism exists, the test that unmasks occult
hyperthyroidism best is:
a) Free T4 (equilibrium dialysis)
b) Thyrotropin releasing hormone (TRH) stimulation test
c) Triiodothyronine (T3) suppression test
d) Use all three tests
e) Retest in 4-8 weeks

50

Q 3 ANSWER
When a healthy cat has a normal total T4 and there is clinical evidence
and suspicion that hyperthyroidism exists, the test that unmasks occult
hyperthyroidism best is:
a) Free T4 (equilibrium dialysis)
b) Thyrotropin releasing hormone (TRH) stimulation test
c) Triiodothyronine (T3) suppression test
d) Use all three tests
e) Retest in 4-8 weeks

51

23
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Diagnostic challenge of occult hyperthyroidism

• Options for confirming diagnosis:
• Repeat the T4 in 4-8 weeks if the patient is stable;
• Perform a free T4 by equilibrium dialysis. On its own, an elevated free T4
may be misleading, however, an elevated free T4 alongside a total T4 of >
30 nmol/L (>2.33 mmol/dL) supports a diagnosis of hyperthyroidism;
• Finding a low thyroid stimulating hormone (TSH);
• Evaluation thyroid function using a thyrotropin-releasing hormone (TRH)
stimulation or T3 suppression tests;
• Performing thyroid scintigraphy

52

Thyroid function tests Dynamic endocrine testing

53

24
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TRH stimulation test

• RelefactTM 0.1 mg/kg IV (maximum 1 vial)
• Serum at time 0 and 4 hours after TRH administration
• ~50% cats become agitated and vomit
• Pretreat with dolasetron or maropitant
• Diagnostic test, rarely “grey zone”
• Hyperthyroid cats wonʼt have T4

54

T3 suppression test
• Baseline T3 and T4, freeze serum
• T3 (Cytomel) 25mcgPO q8h X two days
• Morning of day 3, 7th dose is administered within
2-3 hours of collecting serum for T3 and T4
• Submit both serum samples together to lab
• Hyperthyroid cat, no in T4
• Best done with cat hospitalized

55

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TSH response test

Evaluation of Serum Thyroid Stimulating Hormone Concentration as a
Diagnostic Test for Hyperthyroidism in Cats

• TSH is used for dx of hyperT4 in humans

• Immulite Canine TSH, has been used in cats but not validated for cats
• T4 suppresses TSH secretion, so serum [TSH] should be low in
hyperthyroid cats, possibly even before serum T4 or free T4 are
elevated

Peterson, Animal Endocrine Clinic, Antech, Cornell, ACVIM 2015

56

Euthyroid sick syndrome

• Aka: non thyroidal illness
• Any illness can suppress thyroid
hormones

Fliers J Endo Investig 2021

57

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Serum TSH and Hyperthyroidism

• Goal: Assess whether cTSH is useful for:

• Diagnosing mild to severe hyperthyroidism and in differentiating
hyperthyroid cats (n=786) from healthy cats (n=120) and euthyroid
cats suspected of hyperthyroidism but found not to have the
disease (n=28)

Peterson, Animal Endocrine Clinic, Antech, Cornell, ACVIM 2015

58

Serum TSH and Hyperthyroidism

• In these cats:
• Sensitivity of T4, T3, and FT4 to diagnose hyperthyroidism was 94%, 65%, and
96%, respectively,
• Specificity of each test was 93%, 96%, and 82%, respectively
• Sensitivity of serum TSH as a diagnostic test for hyperthyroidism was 98.2%,
but the test specificity was only 49.3%
• Conclusion: TSH determination represents a highly sensitive but
poorly specific test for diagnosis of feline hyperthyroidism

Peterson, Animal Endocrine Clinic, Antech, Cornell, ACVIM 2015

59

27
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Effect of Non-thyroidal Illness on Serum Concentrations of T4, Free T4

& Thyroid Stimulating Hormone in Cats

• Goals
• To measure TSH in 46 cats w mild-to-severe NTI (and 120 healthy
cats) to determine if the spectrum of [TSH] reported in humans
also occurs in cats
• Conclusions:
• Median serum T4 & FT4 are lower in sick vs. healthy cats, and
these parameters may be inversely correlated w disease severity.
• [TSH] in sick cats were not significantly different from healthy cats.

Davignon, Cornell, Animal Endocrine Clinic, ACVIM 2015

60

Technetium scan
• Safe, easy, reliable
• Extent of involvement
• Treatment planning
• Requires brief sedation

Courtesy of Mark Peterson

61

28
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Therapeutic options:
1. Medical
Management
2. Nutritional
3. Surgical
Curative
4. Radioiodine

62

Medical therapy
1. Methimazole: Inhibits synthesis of thyroid hormones
• Start low (2.5 mg PO q12h) and recheck T4 after 10 days, adjust
dose
• Side effects:
• Facial pruritis (acute)
• GI upset and lethargy (dose dependent)
• Hepatotoxicity
• Marrow suppression
Courtesy of Mark Peterson
Monitor CBC, T4 and usg, BUN, SC q 2-3 months

63

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• Cats evaluated at 4.3 weeks and 5.4 months

• Clinical improvement
• Decreases in T4

• Transdermal advantage: no GI upset

• All other side effects apply

Hoffman, J Feline Med Surg, 2003

64

• Goal: to evaluate the presence of traces of thiamazole in the urine of owners of

hyperthyroid cats treated with oral antithyroid drugs
• Evaluated urine from 24 parents of hyperthyroid cats, five human patients
treated with thiamazole and five healthy humans without any contact with
antithyroid drugs
• Close contact between cats and their people; poor adherence to handling
guidelines
• No thiamazole was detected in the urine of owners of hyperthyroid cats
• “Nevertheless, prudence is still warranted when administering antithyroid drugs.
Whether these results can be extrapolated to the use of transdermal application
requires further investigation."

Schils JFMS 2022

65

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Other medical therapy

2. Carbimazole: precursor to 4. Ipodate (Orograffin):
methimazole • Blocks conversion of T4 to T3
• Fewer side-effects than • monitor effectiveness of therapy by
methimazole? measuring T3
3. Propothiouracil • 15 mg/kg PO q12h
• Higher incidence of side effects than 5. Iopanoic acid (Telepaque)
methimazole
• May still be useful in some cases All medical therapies require life-long
treatment and monitoring

66

• Owners wanted lowest effective dose

• Most were happy to give medication twice a day if it helped their cat

Caney S, J Feline Med Surg,2015

67

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Nutritional therapy
• Hillʼs y/d lower iodine content
• Shown to reduce T4 in hyperthyroid cats
• Risk unknown for unaffected cats
• No other food allowed
• Treats and water must be low iodine

All medical and nutritional therapies require life-long

treatment and monitoring
Van der Kooij M, J Feline Med Surg, 2014

68

Surgery
• Stabilize thyroid pre-op
• Major anaesthetic risk
• Monitor closely intra-op (BP, ECG, auscultation, IV fluids)
• Easy surgery
• Monitor closely post-op (BP, auscultation)
• Monitor serum Ca 48 and 72 hours post-op if bilateral procedure
done

69

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Radioiodine
• Radioiodine (131I)
• Specifically destroys functioning
thyroid cells

• Advantages
• 90% effective
• No parathyroid complications
• No anaesthesia, surgery, pills
• Euthyroid in 7-10 days

70

Gold standard: 131I

• Disadvantages
• Requires referral center
• Cat needs to be hospitalized while radioactive
• Usual stay is 1-3 weeks

• Monitoring post 131I or bilateral surgery

• T4 should be checked after 1 month and then 3 months, then q 6 months

71

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Q4
Select all of the treatment modalities you use in hyperthyroid cats
a) Methimazole oral
b) Methimazole transdermal
c) y/d
d) Surgery
e) Radioiodine

72

73

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74

75

35
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76

Might help reduce risk?

77

36
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COMPLICATED CASES
Hyperthyroidism
plus…
CHRONIC KIDNEY DISEASE
CARDIAC DISEASE
DIABETES MELLITUS
HYPERTENSION AND CKD OR HYPERTHYROIDISM

78

In library

Geddes JFMS 2022

79

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Key points
• Hyperthyroidism and CKD are very common conditions in older cats that
frequently present concurrently.
• Hyperthyroidism > 10% of cats over 9 years
• CKD 80% of cats by 15 years
• Clinical signs and findings of feline hyperthyroidism may mimic those of CKD and
therefore it is important to consider the possibility of the presence of both
diseases.

Weight Polydipsia
Vomiting Sarcopenia Anorexia
loss /polyuria

Geddes JFMS 2022

80

Key points
• The presence of CKD may lead to mild to moderate suppression of thyroid
hormone synthesis, masking the presence of hyperthyroidism.
• Euthyroid sick

• Hyperthyroidism may increase a cat’s GFR and thereby decrease serum creatinine
and SDMA concentrations, masking the presence of CKD.

Geddes JFMS 2022

81

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82

Key points
• It is important to measure systolic blood pressure at diagnosis of CKD and/or
hyperthyroidism. In hyperthyroid cats, if blood pressure is normal, it is
recommended that it is remeasured once euthyroidism is restored.

• Cats with CKD should have their blood pressure monitored every few months.

Geddes JFMS 2022

83

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Renal dysfunction
• Often present in these older cats
• May be masked by hyperthyroid state due to cardiac output
renal blood flow

• Important to monitor renal parameters during thyroid treatment and

treat CKD if becomes evident

84

Renal: thyroid relationship

• Correcting hyperthyroidism by any method results in evidence of
deterioration of renal function
• GFR and urine specific gravity
• BUN and SCr
• Spectrum of renal function

85

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Renal: thyroid relationship

1. By reducing cardiac output by achieving
euthyroidism, GFR is reduced (as much as 50%)
a) Revealing CKD
b) Worsening previously recognized CKD
2. Should see these changes by 4 weeks of
euthyroidism
3. Cannot predict
4. Initial treatment of choice is methimazole
• reassess renal function once euthyroid

86

• Compared cats who developed CKD with those that didn’t after
treatment
• Pre-treatment parameters are not predictive
• E.g., urine specific gravity > 1.035
• Methimazole trial is recommended

Riensche MR. J Feline Med Surg, 2008.

87

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SDMA for Early Detection of CKD

• Screening elderly sarcopenic cats?
• Screening non azotemic hyperthyroid cats?
• Cardiac cases for early detection?

But it still measures GFR…

88

Key points
• Patients diagnosed simultaneously with hyperthyroidism and azotemic CKD
should be treated medically for their hyperthyroidism starting with the lowest
dose initially, while monitoring their kidney function and general wellbeing.

• Iatrogenic hypothyroidism is a recognised complication of all of the treatment

options for hyperthyroidism. Patients should be monitored and treated if they
become azotemic.
Geddes JFMS 2022

92

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Bacterial urinary tract infections

• Prevalence: • Positive urine cultures in:
• Hyperthyroidism 12% • Hyperthyroidism 21.7%
• Diabetes 12% • Diabetes 13.2%
• CKD 22% • CKD 16.9%
• “Recommend culture even if no • Persians, females, older, lower weight
evidence of inflammatory sediment” at greater risk
• “Culture low urine specific gravity
only if pyuria, bacteruria, hematuria
seen”
Bailiff, Vet Clin Path, 2008.
Mayer-Roenne, JFMS, 2007 Litster, Vet Microbiol, 2009

93

94

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Cardiac: thyroid relationship

• Increases systemic metabolic rates
• Thyroid hormones stimulate myocardium mycocardial
hypertrophy + tachycardia increased cardiac output of 2-3X over
baseline
• Chronic increases in preload may congestive heart failure
• Interestingly, HCM is not a consequence of hyperthyroidism

95

Diagnosis and treatment

• Echocardiography
• Hyperthyroid cats with tachycardia: stabilize w beta blocker
• Frequency or dose of propranolol should be reduced
• Altered pharmacodynamics

96

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Q5
Do you diagnose cats with both hyperthyroidism and diabetes mellitus?
a) Yes
b) Not yet

97

Q6
If yes, do you find them more complicated to diagnose or manage?
a) Yes
b) Not yet

98

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Diabetes and the thyroid

• Older cats predisposed to both
• Similar clinical signs
• No epidemiologic data linking the two
• Both catabolic conditions
• Thyroid hormones antagonize insulin insulin resistance

www.allaboutcats.com

99

Diagnosis and treatment

• Because protein turnover is • If hyperthyroid first, treat diabetes
accelerated in hyperthyroidism, as normal
fructosamine levels may be
suppressed • If diabetes first, hyperthyroidism
• Fructosamine concentrations cannot will decline in control of
be used on their own to indicate
diabetes (will need higher doses
glycemic control in the unregulated
hyperthyroid diabetic and reregulation)
• Watch carefully
• Hard to diagnose hyperthyroidism
euthyroid sick syndrome

www.allaboutcats.com

100

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102

Hypertension
• Who is at risk for hypertension?
• Older cats
• Have a disease associated with hypertension (CKD, hyperthyroidism,
adrenal mass)
• Evidence of target organ damage
• Diagnosis requires measurement of blood pressure in conscious cats
using validated methods.

www.petcoach.co

103

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Q7
In whom do you measure blood pressure (select as many as you like)
a) No one
b) Under anaesthesia
c) In sick cats
d) In old cats
e) In all hospitalized cats
f) In all cats over 6 years of age
g) In all cats

104

True prevalence of feline hypertension

105

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Prevalence of feline hypertension

• BP increases with age in healthy • Secondary hypertension
cats • 65% of cats w CKD
• Primary hypertension • 10-23% of hyperthyroid cats
• 13-20% of hypertensive cats • Check during treatment
• 46% of cats with
hyperaldosteronism
• Pheochromocytoma
• Diabetes?

106

Consequences of hypertension

Target organs = brain, eye, kidneys, heart

Drawing from Semintra HT promo material

107

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Hypertensive chorioretinopathy
• Changes begin with BP
persistently > 160 mmHg
• Optical coherence tomography
• Changes occur before
detachment apparent
• Occurs in 50% of hypertensive
cats

108

Hypertensive chorioretinopathy

109

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 4/24/24

Hypertensive chorioretinopathy
• Over 57% of blind cats improve with
treatment
• At least developing a menace response
• Even in some cats blind for 2 months
• May need prolonged period of ophthalmic
treatment (+ BP)
• 20% took > 60 days

110

Encephalopathy and myelopathy

• 15-46% of hypertensive cats • Rapid increase in BP
have neurological signs • Severe hypertension
• Lethargy • Cerebral edema,
• Disorientation arteriosclerosis
• Night-time yowling • MRI
• Vestibular signs • Clinical signs resolve
with treatment
• Seizures
• Hypertension may be
implicated in some cases
of ischemic myelopathy

111

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Cardiovascular injury
• Cardiac murmurs and/or gallop
sounds are common
• Left ventricular hypertrophy is
most common change 2015
• But LVH common in healthy cats as
well (15% of 780 cats) • Rarely, heart failure
• Prevalence increases w age or aortic dissection
have been reported

112

Cardiovascular injury
• Complications may occur if
hypertension superimposed on
pre-existing heart disease or
other risk factors
• Anemia • Effective
• Corticosteroids antihypertensive
• Fluids therapy may result in
cardiac remodeling and
regression of LVH

113

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Kidney damage?
• Increased glomerulosclerosis
and renal arteriosclerosis in
hypertensive cats
• Unclear which came first

114

Kidney damage?
• Increased BP =>
increased proteinuria
• Proteinuria linked to
decreased survival in
cats with CKD or with
hypertension

115

53
 4/24/24

Target organ
damage-
summary

Table from Reusch: Endocrine Hypertension in Small Animals Vet Clin Small Anim 2010

116

117

54
 4/24/24

cat! isfm Blood Pressure Assessment Form

r y
in eve Date Time

re
asu
Cat's name Owner details
Age

M e Sex
Weight
Body Condition Score

Position of the cat

Sitting Sternal recumbency Lateral recumbency Standing

Other (specify):

Position of the cuff:

Right hindlimb
Right forelimb
Tail
Left forelimb
Left hindlimb

Equipment used Size of cuff

Location (room) Others present
Performed by

Subjective assessment of stress:

Relaxed Slightly tense Nervous Very nervous Agitated

Record of all SBP measurements (mmHg):

1. 3. 5. 7. 9.
2. 4. 6. 8. 10.
Mean SBP (mmHg) Strike through readings that are ignored and take mean of the remaining values

118
isfm
International Society of Feline Medicine
(www.icatcare.org/vets) supported by Ceva Animal Health

Harvey

119

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 4/24/24

Harvey presentation
• 8 week old kitten
• One of 4 in litter
• Smaller
• Less weight gain
• Less responsive
• Larger head
• Shorter legs
• Constipated

120

Lab results
• Non-regenerative anemia
• Increased cholesterol
• T4 very low
• cTSH 3.9 (0-0.4)
• Retrovirus negative

121

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 4/24/24

Q8
What’s wrong with Harvey?
a) Pituitary dwarfism
b) Portosystemic shunt
c) Lysosomal storage disease
d) Congenital hypothyroidism

122

Q 8 ANSWER
What’s wrong with Harvey?
a) Pituitary dwarfism
b) Portosystemic shunt
c) Lysosomal storage disease
d) Congenital hypothyroidism Autosomal recessive trait

123

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CONGENITAL IATROGENIC SPONTANEOUS

ADULT-ONSET
Obvious clinical signs + - +/-
Disproportionate + - -
dwarfism
Constipation +++ + +
Mental dullness ++ +/- +/-
Lethargy +++ + ++
Delayed closure of + - -
growth plates and
eruption of adult teeth
Dermatologic signs (scaly + + ++
coat)
Weight gain/obesity + ++ ++
Poor appetite + + ++
Goitre +++/- +/- -

124

Variations in presentation

125

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Treatment of hypothyroidism
• L-thyroxine long-term
• 10–20 mcg/kg PO q 24 hr
• If on methimazole, just decrease methimazole dose

• Goal: mid range normal T4

• 1.5-3.0 mcg/dL [0.8-4.0 mcg/dL]
• 20-40 nmol/L [10-50 nmol/L]

126

• Incompletely erupted permanent

dentition covered by thickened
gingival tissue
• Short stature, a broad, flattened
face, short neck, pendulous
abdomen
• Kitten-like hair coat
• Goiter

Jacobson J Vet Dentistry 2018

127

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Progress
• Treated with L-thyroxine
• Reassessed at 6 weeks
• T4 normal
• Gained weight and size
• By 22 months
• Dentition normal
• Significant growth
• Normal facial morphology
• Growth plates closed

128

Lim J S African Vet Assoc 2014

129

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You can call me

Sir Damien

Damien

130

Damien signalment and history

• 17 year old DLH NM • BP elevated (150 mm Hg)
• 131I for hyperthyroidism • T4 1.4 ug/dL = 18 nmol/L (very low
• 1 month recheck looks good, lab normal)
work normal • USG 1.025
• 14 weeks after procedure, • Creatinine 2.5 mg/dL = 221 umol/L
decreased appetite, lethargy
• Weight loss and muscle wasting
• PU/PD
• Dehydration

131

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CONGENITAL IATROGENIC SPONTANEOUS

ADULT-ONSET
Obvious clinical signs + - +/-
Disproportionate + - -
dwarfism
Constipation +++ + +
Mental dullness ++ +/- +/-
Lethargy +++ + ++
Delayed closure of + - -
growth plates and
eruption of adult teeth
Dermatologic signs (scaly + + ++
coat)
Weight gain/obesity + ++ ++
Poor appetite + + ++
Goitre +++/- +/- -

132

Q9
Iatrogenic hypothyroidism is most likely after which form of treatment?
a) Methimazole
b) 131I radioiodine therapy
c) Thyroidectomy
d) Any of the above

133

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Q 9 ANSWER
Iatrogenic hypothyroidism is most likely after which form of treatment?
a) Methimazole
b) 131I radioiodine therapy
c) Thyroidectomy
d) Any of the above

134

Iatrogenic hypothyroidism
• Possible regardless of form of treatment for hyperthyroidism
• Monitor 1 and 3 months after achieving euthyroidism
• Exam, CBC, biochemistries, urinalysis, T4

• If T4 is subnormal after 3 months, confirm hypothyroidism via T4, free

T4 and cTSH
• All three tests are required Damien’s T4 was low normal,
free T4 was normal and cTSH
was slightly increased

135

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Iatrogenic hypothyroidism
• Important to identify
• Clinical/subclinical is detrimental to renal function
All three tests are required
• Can be challenging to diagnose in:
• Non-thyroidal illness
• Obesity
• Poorly controlled diabetics
• Can have false positive/high cTSH

136

Damien
• After 1 month on L-thyroxine, USG 1.025, Cr 2.1 mg/dL = 186 umol/L
• After 3 months on L-thyroxine, USG 1.030, Cr 1.8 mg/dL = 160 umol/L
• Better appetite, less PU/PD

• T4 4.2 ug/dL – 54 nmol/L

A little high, but I’d like to stay

on L-thyroxine, please

www.somalicatclub.com

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Iatrogenic hypothyroidism
• Occurs in up to 75% of cats treated with radioiodine.
• Up to 49% of cats develop renal azotemia (CKD) within 3-6 months
following any form of treatment resulting in euthyroidism.
• Developing azotemia shortens survival, so it is important to identify
iatrogenic hypothyroidism in order to start thyroid hormone
supplementation.

Peterson, ACVIM 2017

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Iatrogenic hypothyroidism
• Findings using canine TSH assay to monitor cats following treatment
for hyperthyroidism:
1. TSH identifies iatrogenic hypothyroidism earlier and is more
sensitive and specific than T4 or free T4.
2. TSH differentiates between low T4 in cats with CKD that is a result of
iatrogenic hypothyroidism (low T4 with high TSH) and cats with CKD
and low T4 that is due to euthyroid sick syndrome (low T4 with
normal TSH).

Peterson, ACVIM 2017

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Iatrogenic hypothyroidism
3. TSH measurement can be used in cats receiving levothyroxine to
monitor correction of iatrogenic hypothyroidism.
4. TSH and creatinine measurement in cats receiving levothyroxine has
shown improvement in renal function in cats with iatrogenic
hypothyroidism.

Peterson, ACVIM 2017

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Thank you for

participating!
hypurr@aol.com

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