An ultrasound by a specialist is probably the most important test you could
have done.  If may show what is wrong - if anything.  In addition a
specialist will be in a good position to recommend any further testing if
needed.

Update on the Diagnosis and Management of Feline Pancreatic Disease
Waltham Feline Medicine Symposium 2003
Stanley L. Marks, BVSc, PhD, Diplomate ACVIM (Internal Medicine, Oncology),
Diplomate ACVN
University of California, Davis, School of Veterinary Medicine
Davis, CA, USA

PANCREATITIS

Pancreatitis is the most common condition of the feline exocrine pancreas.
Although diseases of the exocrine pancreas have been thought to occur much
less commonly in cats than in humans or dogs, a retrospective study revealed
significant pancreatic pathologic lesions in 1.3% of 6504 feline necropsy
cases and in 1.7% of canine necropsy examinations. In addition, a recent
report of 47 cats with pancreatitis documented a high incidence (59%) of
concurrent fatty change in the cats' livers. The lack of sensitive and
specific markers for feline pancreatitis, as well as the low index of
suspicion for pancreatic disorders in cats have contributed to the
relatively infrequent antemortem diagnosis of pancreatitis in this species.
Chronic pancreatitis (CP) is more commonly seen in the cat and is a
continuing inflammatory disease characterized by irreversible morphological
change, possibly leading to permanent impairment of function.

The cause(s) for feline pancreatitis are poorly understood. Acute
hypercalcemia has been shown to experimentally induce acute pancreatitis.
Other risk factors include infections with Herpesvirus, Toxoplasma gondii,
FIP, and liver flukes. Bile duct obstruction secondary to biliary calculi,
sphincter spasm, tumors, or parasites can also predispose to acute
pancreatitis in cats. Trauma from excessive surgical manipulation,
automobile accidents, or falling from high buildings has also been
associated with acute pancreatitis. Other predisposing factors include
uremia and administration of cholinesterase-inhibitor insecticides.

The association of feline hepatic lipidosis and pancreatitis has been well
documented. Pancreatitis is present in approximately 40% of cats with
hepatic lipidosis and usually warrants a poorer prognosis when present. It
is difficult to predict which disease occurs initially. Speculation is also
increasing about the association between feline inflammatory bowel disease
and pancreatitis. In cats with hepatic lipidosis, the signalment, history,
physical examination, and clinicopathologic findings are generally
indistinguishable in cats with and without pancreatitis; however, cats with
pancreatitis are more likely to be underweight and have coagulation
abnormalities and peritoneal effusion.

Diagnosis

The clinical presentation of cats with pancreatitis is vague and
nonspecific. In a retrospective study of 40 cats with necropsy-confirmed
pancreatitis, reported clinical signs were lethargy in 100% of the cases,
anorexia in 97%, dehydration in 92%, hypothermia in 68%, vomiting in 35%,
abdominal pain in 25%, palpable abdominal mass in 23%, dyspnea in 20%,
ataxia, and diarrhea in 15%. In contrast, vomiting and abdominal pain are
the most consistent clinical signs in dogs and in humans suffering from
pancreatitis. Hematologic abnormalities are uncommon and nonspecific.
Leukocytosis is a relatively common finding in acute pancreatitis. The
patient may have a left shift or have toxic white cells if the disease is
severe. Other hematologic changes reflect fluid loss and hemoconcentration.
Biochemical abnormalities include mild to moderate elevations in ALT, ALP,
and bilirubin and usually reflect concurrent hepatic disease (hepatic
lipidosis or cholangiohepatitis). Azotemia is frequently observed secondary
to dehydration in most cases. Hyperglycemia is far more commonly seen in
cats due to concurrent stress or diabetes mellitus. Hypocalcemia is
occasionally seen due to saponification of peripancreatic fat. Abdominal
radiographs are often subtle and subjective. Decreased contrast in the
anterior abdomen, dilated and gas filled small intestines, transposition of
the duodenum, stomach and colon are commonly reported. Abdominal ultrasound
may reveal a hypoechoic pancreas surrounded by hyperechoic mesentery, with
or without dilated bile ducts. Ascites is occasionally observed.

The measurement of serum lipase and amylase activities is of low value in
the diagnosis of pancreatitis in cats, with serum concentrations appearing
quite variable. Determination of serum trypsin-like immunoreactivity (TLI)
measures antibodies against circulating trypsin and trypsinogen. TLI is
cleared by the kidney; therefore, elevations can occur with renal
dysfunction. TLI values in the normal reference range do not rule out
pancreatitis, and abnormally elevated TLI concentrations are not diagnostic
for pancreatitis. A serum feline pancreatic lipase immunoreactivity (fPLI)
test was recently developed and validated and preliminary findings suggest
that this test is more sensitive than any other diagnostic tool for the
diagnosis of feline pancreatitis. The current "gold standard" for diagnosing
pancreatitis is pancreatic biopsy for histologic evaluation. Peripancreatic
fat necrosis is a typical finding in cats with pancreatitis, with variable
amounts of acinar cell necrosis and inflammation. Chronic pancreatitis is
characterized by interstitial fibrosis with acinar atrophy and lymphocyte
infiltrates. The disease can have a "patchy" or multifocal distribution, and
pancreatic biopsies should always be procured during laparotomy even if the
gross appearance of the organ appears normal.

Therapy

The clinical picture of pancreatitis in cats differs markedly from that in
dogs. Most cats diagnosed with pancreatitis have a more chronic and indolent
form of the disease, with vomiting or diarrhea being relatively uncommon
presenting complaints. Because of these dissimilarities, therapeutic
recommendations for the cat are quite different to those in the dog with
pancreatitis. Many cats are anorectic, and fasting the cat for an additional
3-5 days to "rest" the pancreas will be of little to no clinical benefit. In
addition, there is little clinical evidence to support excessive dietary fat
restriction in cats with pancreatitis. At the University of California,
Davis VMTH, cats with pancreatitis that are anorectic or have lost
significant body weight undergo gastrostomy or esophagostomy tube placement
for enteral feeding. Despite the dogma recommending complete "pancreatic
rest" in patients with pancreatitis, we have not appreciated any clinical
deterioration in these patients associated with enteral feeding. Enteral
tube placement is avoided if the cat is vomiting intractably or has moderate
ascites present. Jejunostomy tube feeding or total parenteral nutrition can
be used in cats that are vomiting despite the administration of antiemetic
therapy. Surgical placement of jejunostomy tubes is preferred over
percutaneous endoscopic placement. Most cats with chronic pancreatitis can
be fed a commercially obtained complete and balanced canned diet formulated
for maintenance of the animal. It is unnecessary to feed human liquid
formulas and liquid veterinary products that frequently contain large
amounts of fat. In addition, most human liquid enteral formulas are too low
in protein, are free of taurine, and deficient in arginine for the
maintenance of feline patients.

The foundation of treatment for cats with severe acute necrotizing
pancreatitis is similar to that in the dog with AP. These cats present with
a more acute history of anorexia, vomiting, and weight loss, and many cats
will be icteric due to extrahepatic bile duct obstruction. Maintenance of
fluid and electrolyte balance is of paramount importance. Most of these cats
will not tolerate intragastric feeding, and jejunostomy tube feeding or TPN
should be administered.Although controversial, antibioticadministration is
best avoided unless the cat is febrile or exhibits toxic changes on the
hemogram. Most pancreatitis cats have a sterile pancreas and inappropriate
antibiotic administration in cats could result in anorexia, salivation, and
vomiting. If indicated, one can administer enrofloxacin (5 mg/kg IV q 12 hr)
and cefotaxime (25-50 mg/kg IV q 8 hr), as these drugs penetrate well into
the pancreas. Antiemetic therapy is indicated if the vomiting is persistent
or severe. Phenothiazine derived antiemetics such as chlorpromazine work
well, although prokinetic drugs such as metoclopramide as a continuous
infusion (1-2 mg/kg/24 hr) may also be helpful. Analgesic therapy (fentanyl,
buprenorphine, or butorphanol) should be given to provide relief if
abdominal pain is severe. Diabetes mellitus is relatively commonly seen in
cats with pancreatitis, and animals should be treated with insulin.
Respiratory distress, neurological problems, cardiac abnormalities, bleeding
disorders, and acute renal failure are all poor prognostic signs, but
attempts should be made to manage these complications by appropriate
supportive measures. Gastric mucosal protection with an H2 blocker is
recommended in patients with acute pancreatitis where gastric mucosal
viability is compromised. Severe pancreatitis is also associated with a
marked consumption of plasma protease inhibitors as activated pancreatic
proteases are cleared from the circulation. Saturation of available alpha
macroglobulins is rapidly followed by acute DIC, shock, and death. Although
controversial, transfusion of plasma or whole blood to replace alpha
macroglobulin may be life saving under these circumstances. Colloid support
to enhance pancreatic perfusion can be supplied with hydroxyl starch or high
molecular weight dextran. Corticosteroids should be given on a short-term
basis to animals in shock associated with fulminating pancreatitis, or on a
long-term basis in patients with concurrent IBD or lymphocytic/plasmacytic
cholangiohepatitis. We have not observed any deleterious effects of
prednisone administration in cats with pancreatitis and concurrent IBD or
cholangiohepatitis when prednisone was administered at a dosage of 10 mg
daily. In those patients in which acute pancreatitis is confirmed at
exploratory laparotomy, removal of any free peritoneal fluid by abdominal
lavage is advisable. In some cases, pancreatitis may be localized to one
lobe of the gland, and surgical resection of the affected area may be
followed by complete recovery.

The use of dopamine by constant rate infusion at 5 ?g/kg/min has been shown
to be beneficial in preventing exacerbation to severe hemorrhagic
pancreatitis in a feline model of pancreatitis. This effect is probably
mediated by ameliorating increases in microvascular permeability that could
promote pancreatic edema. Unfortunately, this effect was only shown when
dopamine was administered within 12 hours of initiating pancreatitis in
these cats. Clinical trials evaluating dopamine in cats with spontaneous
pancreatitis are warranted before this drug can be uniformly endorsed.
Pancreatic enzyme supplementsmay decrease abdominal pain probably by
feedback inhibition of endogenous pancreatic enzyme secretion. Similarly,
somatostatin and its analogues inhibit pancreatic secretions, although
clinical studies have failed to show any ameliorating effects of spontaneous
pancreatitis in human beings.