Page 178 - WSAVA2018
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 25-28 September, 2018 | Singapore
Clinical signs
The clinical signs of pancreatitis obviously vary with the severity of the disease. It is only the severe, acute cases
in dogs which show the classical signs of acute vomiting, cranial abdominal pain ± “praying” stance. Concurrent colitis with the passage of small amounts of faeces with fresh blood is common due to local peritonitis affecting the transverse colon as it courses close to the left limb of the pancreas. Severe cases may present collapsed and dehydrated with signs of shock and, in very severe cases, there may be renal shutdown, respiratory distress and DIC.
At the other end of the spectrum, low grade acute
or chronic cases may show few clinical signs: most commonly, anorexia with or without mild bouts of colitis and occasional vomiting, increased borborygmi and no or mild abdominal pain. Dogs with CP, regardless of the cause, most commonly present with mild intermittent gastrointestinal signs. Typically they have bouts of anorexia, occasional vomiting, mild hematochezia, and obvious postprandial pain, which often goes on for months to years without presentation to a veterinarian. The trigger for finally seeking veterinary attention is often an acute-on-chronic bout or the development of DM or EPI. Dogs may become more playful and less picky with their food when they are switched to a low- fat diet, suggesting they previously had postprandial pain. Chronic epigastric pain is a hallmark of the
human disease and is sometimes severe enough to lead to opiate addiction or surgery, so it should not be overlooked or underestimated in small animal patients. In more severe, acute-on-chronic cases, the dogs are clinically indistinguishable from those with classical acute pancreatitis (see above) with severe vomiting, dehydration, shock, and potential multi-organ failure. There is a tendency for the first clinically severe bout
to come at the end of a long (often years) subclinical phase of quietly progressive and extensive pancreatic destruction in dogs. It is very important for clinicians to be aware of this, as these dogs are at much higher risk of developing exocrine and/or endocrine dysfunction than those with truly acute pancreatitis; in addition,
they usually already have protein-calorie malnutrition
at presentation, which makes their management even more challenging. In some dogs, there are no obvious clinical signs until the development of EPI, DM, or both. The development of EPI in a middle-aged to older dog of a breed not typical for pancreatic acinar atrophy
has to increase the index of suspicion for underlying
CP. The development of EPI or DM in a dog of cat with CP requires the loss of approximately 90% of exocrine or endocrine tissue function respectively, implying considerable tissue destruction and ‘end-stage’ disease.
C. Mooney1
1University College Dublin, Small Animal Clincical Studies, Dublin 4, Ireland
Carmel T Mooney MVB MPhil PhD DipECVIM-CA MRCVS
Small Animal Clinical Studies, School of Veterinary Medicine, UCD, Belfield, Dublin 4, Ireland
Hyperthyroidism remains the most common endocrine disease in cats with a prevalence of 10 % or more in older cats presenting to first-opinion veterinary practices. The aetiology remains unclear and although several risk factors have been associated with the disease, none
are definitive and therefore prevention is not possible. Benign adenomatous hyperplasia or adenoma of one or more commonly both thyroid lobes is the most common lesion within affected thyroid tissue and at least initially, the prognosis is good with effective therapy. Palliative treatment options consist of control of thyroid hormone production through administration of the antithyroid drugs or alternatively through feeding an iodine restricted food. Curative options include removal of affected thyroid tissue surgically or destruction through the use of radioactive iodine.Most endocrinologists consider radioactive iodine as being the gold standard treatment method. However, it is not always available and may not be suitable for all hyperthyroid cats. Most commonly, a treatment choice is individualised for
each cat taking into consideration the advantages and disadvantages of each, severity of the illness, facilities and expertise available, cost and owner choice.
Hyperthyroidism is a disease of older cats and it is
not unexpected that a proportion of cats present with concurrent non-thyroidal illness. Hyperthyroid cats with pre-existing azotaemia have a reduced survival time. However, many cats do not have azotaemia prior to treatment but develop it after induction of euthyroidism1. All treatment options can result in unmasking of
kidney disease. Predicting those cats that will develop post-treatment azotaemia is difficult but there is
some evidence that measurement of serum SDMA concentrations and urine specific gravity may be useful in predicting its occurrence2. Development of azotaemia post treatment does not apparently affected survival3. However, there is some evidence that development of hypothyroidism can be detrimental to kidney function and may adversely affect survival4.

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