Page 640 - Clinical Small Animal Internal Medicine

608 Section 6 Gastrointestinal Disease

concentrations are also low. Supplementation of cats chronic pancreatitis, they are usually chronically unwell,
VetBooks.ir with low folate has not been investigated as thoroughly and they do not develop compensatory polyphagia. Cats
also are less likely to produce voluminous stools and
as cobalamin supplementation, but is also readily
achieved with oral supplement products. Often, initial
longed course of the disease in this species, which allows
supplementation by injection followed by oral supple­ frank steatorrhea; this is probably due to the very pro­
mentation in the home environment provides a good other compensatory mechanisms (such as intestinal brush
balance between costs, convenience, and ease of owner border enzyme upregulation) to be more effective.
compliance. Exocrine pancreatic insufficiency should be suspected in
any cat with a history of diagnosed chronic pancreatitis
that then goes on to show worsening clinical signs, particu­
Complications of Pancreatitis in Cats larly weight loss. In some cases weight loss will be the only
additional clinical sign that suggests the onset of EPI.
Given the apparent frequency of chronic pancreatic dis­ Diagnosis of EPI in the cat is based on the measure­
ease in the feline population, the occurrence of severe ment of serum concentrations of TLI, not Spec‐fPL.
complications is actually remarkably low. While objec­ While Spec‐fPL values are almost invariably very low in
tively severe disease in cats presenting with hemody­ cats with EPI, this is also seen in some normal cats,
namic shock, systemic inflammatory response syndrome resulting in an unacceptably low specificity of the Spec‐
and abdominal pain is life‐threatening and associated fPL assay for the diagnosis of EPI in cats. DGGR‐lipase
with a substantial risk for mortality if not addressed activity assays have no diagnostic utility for EPI in cats,
appropriately, most cats with chronic pancreatitis require as most cats with EPI show DGGR‐lipase activities that
life‐long management for their disease, but other than are indistinguishable from normal cat values.
waxing and waning clinical signs, most do not develop Diabetes mellitus can develop in cats with chronic pan­
additional complicating diagnoses. creatitis due to progressive loss of islet tissue with inflam­
The two most common and important complications mation and fibrotic change. These cats may spend extended
of pancreatic disease in the cat are exocrine pancreatic periods as “prediabetic” patients, with reduced glucose tol­
insufficiency (EPI) and diabetes mellitus. erance. The actual frequency of chronic pancreatitis as a
Chronic pancreatitis is most likely the most common cause of diabetes mellitus in the cat is unknown, and likely
cause of EPI in cats. Loss of exocrine tissue due to ongo­ underestimated, due to the low frequency of pancreatic
ing inflammation and fibrosis can eventually lead to the biopsy in these cats. The occurrence of diabetes mellitus in
development of clinical signs related to insufficient feline patients can significantly complicate their manage­
digestive enzyme synthesis. In comparison to dogs, and a ment for chronic pancreatitis, particularly if the cat is being
recurring theme in feline medicine, the way in which EPI managed with glucocorticoid medications to mitigate
manifests in cats is different in terms of both history and inflammation. Equally, the presence of chronic pancreatitis
clinical signs reported. While in the dog the most com­ in a diabetic cat is a common cause of difficulty in achieving
mon cause of EPI is an early‐onset pancreatic acinar adequate glycemic regulation, and chronic pancreatitis is
atrophy (PAA), in the cat the disease is an end‐result of a one of the most important diseases to screen for in cats with
chronic, typically years‐long inflammatory disease. Dogs diabetes that is hard to regulate. The difficulty of managing
with EPI secondary to PAA are usually young and usually diabetic cats with chronic pancreatitis, and the confound­
are otherwise healthy, with good to ravenous appetites. ing influence of glucocorticoid therapy on glycemic regula­
In the cat, there is typically a long history of poor appe­ tion, makes one of the strongest arguments for early
tite and possible weight loss resulting from the underly­ intervention using predominantly dietary changes in the
ing pancreatitis. By the time cats reach an end‐stage of management of chronic pancreatitis in the cat.

Further Reading

Bazelle J, Watson P. Pancreatitis in cats: is it acute, is it in cats with suspicion of pancreatitis: 161 cases (2008–
chronic, is it significant? J Feline Med Surg 2014; 16(5): 2012). J Am Vet Med Assoc 2014; 244(9): 1060–5.
395–406. Pratschke KM, Ryan J, McAlinden A, McLauchlan G.
Caney SMA. Pancreatitis and diabetes in cats. Vet Clin Pancreatic surgical biopsy in 24 dogs and 19 cats:
North Am Small Anim Pract 2013; 43(2): 303–17. postoperative complications and clinical relevance of
Oppliger S, Hartnack S, Reusch CE, Kook PH. Agreement histological findings. J Small Anim Pract 2015; 56: 60–6
of serum feline pancreas‐specific lipase and colorimetric Simpson KW. Pancreatitis and triaditis in cats: causes and
lipase assays with pancreatic ultrasonographic findings treatment. J Small Anim Pract 2015; 56(1): 40–9.