Opinions on fatty liver/possible pancreatitis problem

I suggest you have both cats tested for Bartonella -- turned out to be the
underlying problem with my 14 year-old who had always been a "barfer." She
developoed cardiomyopathy as a result of the long-term infection, but
Bartonella can now be treated, and the test is not expensive. -- Lotte

"Underwood" wrote in message
...
We have a 6 yr old tabby who was recently introduced (February) to a new
member of the house, a maine coon mix from the local shelter. He
brought what appeared to be a cold home with him, which he transmitted
to Pnut. During most of February, she was dealing with the effects of
the cold or upper respiratory infection. The new cat completely
recovered and is fine now, and never had a problem to begin with.

In early March, we noticed Pnut was looking rather grim. We started
trying to take stock of when she was eating, and couldn't determine if
she was in fact eating sufficiently. After a week of moping around and
looking rotten, we took her to the vet on March 19. The vet diagnosed
jaundice and fatty liver, and sent us home with a feeding tube and a
bunch of Hill's A/D to feed her. It has been extremely difficult to
keep any food down her for the past two weeks. She will vomit at least
once per day on average, and went a few days when we were unable to get
her to keep anything down. I will elaborate on our feeding strategy
further down.

Apparently we had not paid enough attention to her when she was ill with
the cold to realize she had stopped eating to the point where she was
losing weight and developing hepatic lipidosis. The house is full of
busy people though, so when she is depressed and hiding due to an
illness, keeping tabs on her isn't exactly the first thing on our minds.


From the testing at the vet, the blood work looked normal except for
elevated liver values and slightly elevated pancreas values (though I am
told the latter is rather meaningless in general). An x-ray turned up
no gall stones or obstructions. The vet has been reluctant to give any
more information or suggestions besides to have an ultrasound done at a
cost of $250. I am reluctant to do this because I feel very strongly
that the cat is suffering a pancreatitis and/or I.B.S. inflammation
episode brought on by the previous month's cold and/or the stress of
being exposed to a new cat. It seems that the ultrasound will only
serve to rule out terminal illness, and not provide a conclusive
diagnosis in any case.

Before you dismiss the self-diagnosis I just tossed out there as a
logical leap, let me give you a bit of background. In late 2002, after
a previous cat died of unrelated problems (NRG anemia), Pnut underwent a
similar episode to what is happening now, though much less severe. She
simply stopped eating, developed jaundice, was diagnosed with fatty
liver, and a feeding tube was installed. We fed her A/D until she
started eating on her own again. She has always had periodic random
vomiting during her adult life, maybe once per few weeks on average.
Most of the time it is a clear liquid similar to bile. We could never
tell what would bring this on. She also loves to raid the trash despite
our best attempts to keep her out of it, which seems to be a risk factor
for chronic pancreatitis.

Right now, we are trying to keep her nourished with Hill's A/D and
recently I/D which I tried to see if it would have any effect.
Anti-vomit pills (Metaclopramine) and painkiller (Butorphanol) have
little to no effect on the vomiting. The only thing that seems to help
her keep food down is giving antacid, 1/4 of a 10mg pepcid pill 1 hr
before eating for the first time that day. If she misses that dose, she
will vomit all feedings until it is given. If she gets that dose, she
usually will not vomit until an evening feeding. I tried I/D as an
attempt to "go easier" on her digestive system than A/D. An initial
feeding was kept down OK, but an evening feeding (10 hrs after antacid
was administered) was vomited 2.5 hrs after feeding.

In a nutshell, we give antacid in the morning, then try to feed at least
20cc and at most 40cc of a mixture of one can A/D or I/D with 32cc warm
water, three times a day. If she vomits, we cease feeding for at least
six hours and try again later. We flush the feeding tube with 5cc warm
water. If she vomits, she will vomit anywhere from immediately to 3
hours after a feeding. She is passing vaguely normal-looking fecal
matter (occasionally diarrhea) and appears to be urinating regularly, so
at least something is working properly. She is very likely to vomit
when agitated or disturbed, so we leave her in a closed but ventilated
bathroom most of the day. Only the bathroom's visitors disturb her, and
she occasionally vomits when a visitor has just used the facility. (The
smell?)

The vet suspects triad syndrome, and so do I, though I more highly
suspect a simpler combination of pancreatitis and fatty liver that are
working in cahoots with each other (similar to how cholangiohepatitis
and pancreatitis provide a feedback loop for each other in a triad
syndrome situation).

It seems I am in a textbook catch-22 situation.

To address the fatty liver/jaundice, I need to feed her enough to
prevent body mass from being re-appropriated as an energy source. But
if I feed her, it would aggravate any pancreatitis that is present. The
possibility of a I.B.S. episode instead of pancreatitis also exists, but
the vet will not prescribe corticosteroids without ruling out a
pancreatitis episode (since they may make an already difficult
pancreatitis situation even worse). Ruling out the pancreatitis is done
through the ultrasound, and I am told that even if the pancreas is not
visible on the ultrasound, that is not a conclusive diagnosis one way or
the other, just a best guess. Also, to avoid aggravating pancreatitis,
I should be feeding high-carb foods. But it is questionable as to
whether they will provide sustainable nutrition to a critter whose body
is designed to run primarily on proteins and fat.

I (and Pnut) am up a creek. I can't afford the ultrasound or any more
conclusive diagnosis involving tissue biopsies. I can't afford
inpatient treatment. I _can_ afford the diet/Rx foods and the time to
spend with her concocting her food mix, feeding through the tube and
cleaning up messes (as I have throughout the last week). However, I
will not be the primary caretaker in the coming weeks, so I need to come
up with some kind of protocol that "covers all the bases" so to speak.

I have 3 scenarios I wish the group to consider:
1) Triad syndrome. I.B.S. causes pancreatitis and cholangiohepatitis,
followed by hepatic lipidosis.
2) Hepatic lipidosis caused by not eating due to acute pancreatitis or a
chronic flare-up.
3) Hepatic lipidosis caused by not eating due to I.B.S. flare-up. Liver
disturbance triggers pancreatic reaction. Sort of an "acute" triad
syndrome.

I have looked at other possibilities, such as parasites, FIP, distemper,
etc. None seem to fit the circumstances and none were even suggested by
the vet. The vet has generally agreed that we are probably looking at
triad syndrome or something approximating it. But she has offered very
few suggestions for treatment. She suggested cancer at one point, but I
can't help but think cancer would be an _extreme_ coincidence
considering the circumstances (new cat in the house, new cat brought a
cold, and anorexia was undetected for a period of time). Why would a
cancer wait until exactly now to start generating symptoms? How do I
explain the previous episode and chronic random vomiting?

It seems (from reading) that the only avenue of success with
pancreatitis is to withhold food and water for at least 24 hours,
preferably 48; but more than 24 hours requires hospitalization with IV
fluids. I am curious how successful these approaches typically are. I
have a feeling I would be laughed out of the state if I suggested an
approach that included withholding food to my vet, with the cat already
suffering from fatty liver. Is 24 hrs typically safe, assuming the cat
is given under-the-skin fluids to support her that day? Is this to be
considered a reasonable tradeoff between trying to solve the highly
suspected pancreatitis, and not aggravating the fatty liver/wasting
problem too much in the meantime?

What I need is options. I would like any of the following:
- Suggestions for treatment _in the case of_ one of the aforementioned
disease scenarios, to give me an idea of the scope of the problem I'm
likely to be dealing with. This will help me decide whether or not
euthanization is the best option for us in the long run, as much as it
would pain me to make that choice.

- Suggestions to pass along to the vet. She may not have all the bases
covered in diagnosis, nor have relayed all the options to me. If I can
"jog her memory" or get her to do some research on possible angles, it
may help us all out.

- Suggestions to stabilize the current scenario or how to improve on my
current methods of feeding/nursing, to pass on to the primary caretaker
for the next week. Anecdotal suggestions are ok, i.e. "This worked for
Fizban when he showed the symptoms you have described". I am looking
for dietary suggestions (_what_ is good to feed her) as well as
procedural suggestions (_when_ and _how much_ is good to feed her).

Remember that I have been nursing her for two weeks. She is stable and
not in a state of shock, but her stable state is not exactly that great,
and may be invisibly deteriorating. I would like to try to target the
most likely underlying problems, since I don't have the resources for a
proper diagnosis (and such diagnosis seems to be nebulous at best).

As of today, she was given antacid in the morning, given 20cc I/D
mixture at 2:00pm, which she kept down, given 20cc I/D at 7:00pm, which
was vomited at 9:30pm (perhaps due to a disturbance), and I gave 10cc
water at 11pm. Tomorrow is Sunday, so I won't be able to see a vet for
about 36 hours at this point.

Help me formulate a plan of action! I'd like to go in to her office
Monday armed with information instead of frustration.

Thanks for any insight your experiences can provide.

The ideal approach would be to get an exploratory surgery done so that the
liver, intestines, stomach and pancreas can be biopsied and a jejunostomy
tube can be placed. Ultrasound examinations can easily miss pancreatitis in
cats and U/S guided biopsies are not a reliable way to diagnose liver
disease in cats (will seldom diagnose cholangiohepatitis). If you can't
afford this then you may have to discuss altering therapy.

antiemetics: odansetron and dolasetron are very good medications to add to
metoclopramide to control vomiting but are very expensive.
SAM-E: Denosyl increases levels of antioxidants in the liver..most
internists I'm aware of treat feline liver disease with denosyl nowadays
Vitamin E: another important antioxidant for treating liver disease
Milk Thistle: a useful adjunct to other medications for liver disease
URS: I've found this to be the most useful medication for treating fatty
liver disease in cats.
Antibiotics: suppurative cholangiohepatitis needs to be treated with 4-8
weeks of antibiotics. Unless I'm sure this disease is not present I treat
liver cats with antibiotics.
Prednisone: if all else fails I resort to prednisone even if owners can't
afford a full diagnostic work up. Prednisone doesn't aggravate pancreatitis
in cats to the same extent it does in dogs and humans.

"Underwood" wrote in message
...
We have a 6 yr old tabby who was recently introduced (February) to a new
member of the house, a maine coon mix from the local shelter. He
brought what appeared to be a cold home with him, which he transmitted
to Pnut. During most of February, she was dealing with the effects of
the cold or upper respiratory infection. The new cat completely
recovered and is fine now, and never had a problem to begin with.

In early March, we noticed Pnut was looking rather grim. We started
trying to take stock of when she was eating, and couldn't determine if
she was in fact eating sufficiently. After a week of moping around and
looking rotten, we took her to the vet on March 19. The vet diagnosed
jaundice and fatty liver, and sent us home with a feeding tube and a
bunch of Hill's A/D to feed her. It has been extremely difficult to
keep any food down her for the past two weeks. She will vomit at least
once per day on average, and went a few days when we were unable to get
her to keep anything down. I will elaborate on our feeding strategy
further down.

Apparently we had not paid enough attention to her when she was ill with
the cold to realize she had stopped eating to the point where she was
losing weight and developing hepatic lipidosis. The house is full of
busy people though, so when she is depressed and hiding due to an
illness, keeping tabs on her isn't exactly the first thing on our minds.


From the testing at the vet, the blood work looked normal except for
elevated liver values and slightly elevated pancreas values (though I am
told the latter is rather meaningless in general). An x-ray turned up
no gall stones or obstructions. The vet has been reluctant to give any
more information or suggestions besides to have an ultrasound done at a
cost of $250. I am reluctant to do this because I feel very strongly
that the cat is suffering a pancreatitis and/or I.B.S. inflammation
episode brought on by the previous month's cold and/or the stress of
being exposed to a new cat. It seems that the ultrasound will only
serve to rule out terminal illness, and not provide a conclusive
diagnosis in any case.

Before you dismiss the self-diagnosis I just tossed out there as a
logical leap, let me give you a bit of background. In late 2002, after
a previous cat died of unrelated problems (NRG anemia), Pnut underwent a
similar episode to what is happening now, though much less severe. She
simply stopped eating, developed jaundice, was diagnosed with fatty
liver, and a feeding tube was installed. We fed her A/D until she
started eating on her own again. She has always had periodic random
vomiting during her adult life, maybe once per few weeks on average.
Most of the time it is a clear liquid similar to bile. We could never
tell what would bring this on. She also loves to raid the trash despite
our best attempts to keep her out of it, which seems to be a risk factor
for chronic pancreatitis.

Right now, we are trying to keep her nourished with Hill's A/D and
recently I/D which I tried to see if it would have any effect.
Anti-vomit pills (Metaclopramine) and painkiller (Butorphanol) have
little to no effect on the vomiting. The only thing that seems to help
her keep food down is giving antacid, 1/4 of a 10mg pepcid pill 1 hr
before eating for the first time that day. If she misses that dose, she
will vomit all feedings until it is given. If she gets that dose, she
usually will not vomit until an evening feeding. I tried I/D as an
attempt to "go easier" on her digestive system than A/D. An initial
feeding was kept down OK, but an evening feeding (10 hrs after antacid
was administered) was vomited 2.5 hrs after feeding.

In a nutshell, we give antacid in the morning, then try to feed at least
20cc and at most 40cc of a mixture of one can A/D or I/D with 32cc warm
water, three times a day. If she vomits, we cease feeding for at least
six hours and try again later. We flush the feeding tube with 5cc warm
water. If she vomits, she will vomit anywhere from immediately to 3
hours after a feeding. She is passing vaguely normal-looking fecal
matter (occasionally diarrhea) and appears to be urinating regularly, so
at least something is working properly. She is very likely to vomit
when agitated or disturbed, so we leave her in a closed but ventilated
bathroom most of the day. Only the bathroom's visitors disturb her, and
she occasionally vomits when a visitor has just used the facility. (The
smell?)

The vet suspects triad syndrome, and so do I, though I more highly
suspect a simpler combination of pancreatitis and fatty liver that are
working in cahoots with each other (similar to how cholangiohepatitis
and pancreatitis provide a feedback loop for each other in a triad
syndrome situation).

It seems I am in a textbook catch-22 situation.

To address the fatty liver/jaundice, I need to feed her enough to
prevent body mass from being re-appropriated as an energy source. But
if I feed her, it would aggravate any pancreatitis that is present. The
possibility of a I.B.S. episode instead of pancreatitis also exists, but
the vet will not prescribe corticosteroids without ruling out a
pancreatitis episode (since they may make an already difficult
pancreatitis situation even worse). Ruling out the pancreatitis is done
through the ultrasound, and I am told that even if the pancreas is not
visible on the ultrasound, that is not a conclusive diagnosis one way or
the other, just a best guess. Also, to avoid aggravating pancreatitis,
I should be feeding high-carb foods. But it is questionable as to
whether they will provide sustainable nutrition to a critter whose body
is designed to run primarily on proteins and fat.

I (and Pnut) am up a creek. I can't afford the ultrasound or any more
conclusive diagnosis involving tissue biopsies. I can't afford
inpatient treatment. I _can_ afford the diet/Rx foods and the time to
spend with her concocting her food mix, feeding through the tube and
cleaning up messes (as I have throughout the last week). However, I
will not be the primary caretaker in the coming weeks, so I need to come
up with some kind of protocol that "covers all the bases" so to speak.

I have 3 scenarios I wish the group to consider:
1) Triad syndrome. I.B.S. causes pancreatitis and cholangiohepatitis,
followed by hepatic lipidosis.
2) Hepatic lipidosis caused by not eating due to acute pancreatitis or a
chronic flare-up.
3) Hepatic lipidosis caused by not eating due to I.B.S. flare-up. Liver
disturbance triggers pancreatic reaction. Sort of an "acute" triad
syndrome.

I have looked at other possibilities, such as parasites, FIP, distemper,
etc. None seem to fit the circumstances and none were even suggested by
the vet. The vet has generally agreed that we are probably looking at
triad syndrome or something approximating it. But she has offered very
few suggestions for treatment. She suggested cancer at one point, but I
can't help but think cancer would be an _extreme_ coincidence
considering the circumstances (new cat in the house, new cat brought a
cold, and anorexia was undetected for a period of time). Why would a
cancer wait until exactly now to start generating symptoms? How do I
explain the previous episode and chronic random vomiting?

It seems (from reading) that the only avenue of success with
pancreatitis is to withhold food and water for at least 24 hours,
preferably 48; but more than 24 hours requires hospitalization with IV
fluids. I am curious how successful these approaches typically are. I
have a feeling I would be laughed out of the state if I suggested an
approach that included withholding food to my vet, with the cat already
suffering from fatty liver. Is 24 hrs typically safe, assuming the cat
is given under-the-skin fluids to support her that day? Is this to be
considered a reasonable tradeoff between trying to solve the highly
suspected pancreatitis, and not aggravating the fatty liver/wasting
problem too much in the meantime?

What I need is options. I would like any of the following:
- Suggestions for treatment _in the case of_ one of the aforementioned
disease scenarios, to give me an idea of the scope of the problem I'm
likely to be dealing with. This will help me decide whether or not
euthanization is the best option for us in the long run, as much as it
would pain me to make that choice.

- Suggestions to pass along to the vet. She may not have all the bases
covered in diagnosis, nor have relayed all the options to me. If I can
"jog her memory" or get her to do some research on possible angles, it
may help us all out.

- Suggestions to stabilize the current scenario or how to improve on my
current methods of feeding/nursing, to pass on to the primary caretaker
for the next week. Anecdotal suggestions are ok, i.e. "This worked for
Fizban when he showed the symptoms you have described". I am looking
for dietary suggestions (_what_ is good to feed her) as well as
procedural suggestions (_when_ and _how much_ is good to feed her).

Remember that I have been nursing her for two weeks. She is stable and
not in a state of shock, but her stable state is not exactly that great,
and may be invisibly deteriorating. I would like to try to target the
most likely underlying problems, since I don't have the resources for a
proper diagnosis (and such diagnosis seems to be nebulous at best).

As of today, she was given antacid in the morning, given 20cc I/D
mixture at 2:00pm, which she kept down, given 20cc I/D at 7:00pm, which
was vomited at 9:30pm (perhaps due to a disturbance), and I gave 10cc
water at 11pm. Tomorrow is Sunday, so I won't be able to see a vet for
about 36 hours at this point.

Help me formulate a plan of action! I'd like to go in to her office
Monday armed with information instead of frustration.

Thanks for any insight your experiences can provide.

The ideal approach would be to get an exploratory surgery done so that the
liver, intestines, stomach and pancreas can be biopsied and a jejunostomy
tube can be placed. Ultrasound examinations can easily miss pancreatitis in
cats and U/S guided biopsies are not a reliable way to diagnose liver
disease in cats (will seldom diagnose cholangiohepatitis). If you can't
afford this then you may have to discuss altering therapy.

antiemetics: odansetron and dolasetron are very good medications to add to
metoclopramide to control vomiting but are very expensive.
SAM-E: Denosyl increases levels of antioxidants in the liver..most
internists I'm aware of treat feline liver disease with denosyl nowadays
Vitamin E: another important antioxidant for treating liver disease
Milk Thistle: a useful adjunct to other medications for liver disease
URS: I've found this to be the most useful medication for treating fatty
liver disease in cats.
Antibiotics: suppurative cholangiohepatitis needs to be treated with 4-8
weeks of antibiotics. Unless I'm sure this disease is not present I treat
liver cats with antibiotics.
Prednisone: if all else fails I resort to prednisone even if owners can't
afford a full diagnostic work up. Prednisone doesn't aggravate pancreatitis
in cats to the same extent it does in dogs and humans.

"Underwood" wrote in message
...
We have a 6 yr old tabby who was recently introduced (February) to a new
member of the house, a maine coon mix from the local shelter. He
brought what appeared to be a cold home with him, which he transmitted
to Pnut. During most of February, she was dealing with the effects of
the cold or upper respiratory infection. The new cat completely
recovered and is fine now, and never had a problem to begin with.

In early March, we noticed Pnut was looking rather grim. We started
trying to take stock of when she was eating, and couldn't determine if
she was in fact eating sufficiently. After a week of moping around and
looking rotten, we took her to the vet on March 19. The vet diagnosed
jaundice and fatty liver, and sent us home with a feeding tube and a
bunch of Hill's A/D to feed her. It has been extremely difficult to
keep any food down her for the past two weeks. She will vomit at least
once per day on average, and went a few days when we were unable to get
her to keep anything down. I will elaborate on our feeding strategy
further down.

Apparently we had not paid enough attention to her when she was ill with
the cold to realize she had stopped eating to the point where she was
losing weight and developing hepatic lipidosis. The house is full of
busy people though, so when she is depressed and hiding due to an
illness, keeping tabs on her isn't exactly the first thing on our minds.


From the testing at the vet, the blood work looked normal except for
elevated liver values and slightly elevated pancreas values (though I am
told the latter is rather meaningless in general). An x-ray turned up
no gall stones or obstructions. The vet has been reluctant to give any
more information or suggestions besides to have an ultrasound done at a
cost of $250. I am reluctant to do this because I feel very strongly
that the cat is suffering a pancreatitis and/or I.B.S. inflammation
episode brought on by the previous month's cold and/or the stress of
being exposed to a new cat. It seems that the ultrasound will only
serve to rule out terminal illness, and not provide a conclusive
diagnosis in any case.

Before you dismiss the self-diagnosis I just tossed out there as a
logical leap, let me give you a bit of background. In late 2002, after
a previous cat died of unrelated problems (NRG anemia), Pnut underwent a
similar episode to what is happening now, though much less severe. She
simply stopped eating, developed jaundice, was diagnosed with fatty
liver, and a feeding tube was installed. We fed her A/D until she
started eating on her own again. She has always had periodic random
vomiting during her adult life, maybe once per few weeks on average.
Most of the time it is a clear liquid similar to bile. We could never
tell what would bring this on. She also loves to raid the trash despite
our best attempts to keep her out of it, which seems to be a risk factor
for chronic pancreatitis.

Right now, we are trying to keep her nourished with Hill's A/D and
recently I/D which I tried to see if it would have any effect.
Anti-vomit pills (Metaclopramine) and painkiller (Butorphanol) have
little to no effect on the vomiting. The only thing that seems to help
her keep food down is giving antacid, 1/4 of a 10mg pepcid pill 1 hr
before eating for the first time that day. If she misses that dose, she
will vomit all feedings until it is given. If she gets that dose, she
usually will not vomit until an evening feeding. I tried I/D as an
attempt to "go easier" on her digestive system than A/D. An initial
feeding was kept down OK, but an evening feeding (10 hrs after antacid
was administered) was vomited 2.5 hrs after feeding.

In a nutshell, we give antacid in the morning, then try to feed at least
20cc and at most 40cc of a mixture of one can A/D or I/D with 32cc warm
water, three times a day. If she vomits, we cease feeding for at least
six hours and try again later. We flush the feeding tube with 5cc warm
water. If she vomits, she will vomit anywhere from immediately to 3
hours after a feeding. She is passing vaguely normal-looking fecal
matter (occasionally diarrhea) and appears to be urinating regularly, so
at least something is working properly. She is very likely to vomit
when agitated or disturbed, so we leave her in a closed but ventilated
bathroom most of the day. Only the bathroom's visitors disturb her, and
she occasionally vomits when a visitor has just used the facility. (The
smell?)

The vet suspects triad syndrome, and so do I, though I more highly
suspect a simpler combination of pancreatitis and fatty liver that are
working in cahoots with each other (similar to how cholangiohepatitis
and pancreatitis provide a feedback loop for each other in a triad
syndrome situation).

It seems I am in a textbook catch-22 situation.

To address the fatty liver/jaundice, I need to feed her enough to
prevent body mass from being re-appropriated as an energy source. But
if I feed her, it would aggravate any pancreatitis that is present. The
possibility of a I.B.S. episode instead of pancreatitis also exists, but
the vet will not prescribe corticosteroids without ruling out a
pancreatitis episode (since they may make an already difficult
pancreatitis situation even worse). Ruling out the pancreatitis is done
through the ultrasound, and I am told that even if the pancreas is not
visible on the ultrasound, that is not a conclusive diagnosis one way or
the other, just a best guess. Also, to avoid aggravating pancreatitis,
I should be feeding high-carb foods. But it is questionable as to
whether they will provide sustainable nutrition to a critter whose body
is designed to run primarily on proteins and fat.

I (and Pnut) am up a creek. I can't afford the ultrasound or any more
conclusive diagnosis involving tissue biopsies. I can't afford
inpatient treatment. I _can_ afford the diet/Rx foods and the time to
spend with her concocting her food mix, feeding through the tube and
cleaning up messes (as I have throughout the last week). However, I
will not be the primary caretaker in the coming weeks, so I need to come
up with some kind of protocol that "covers all the bases" so to speak.

I have 3 scenarios I wish the group to consider:
1) Triad syndrome. I.B.S. causes pancreatitis and cholangiohepatitis,
followed by hepatic lipidosis.
2) Hepatic lipidosis caused by not eating due to acute pancreatitis or a
chronic flare-up.
3) Hepatic lipidosis caused by not eating due to I.B.S. flare-up. Liver
disturbance triggers pancreatic reaction. Sort of an "acute" triad
syndrome.

I have looked at other possibilities, such as parasites, FIP, distemper,
etc. None seem to fit the circumstances and none were even suggested by
the vet. The vet has generally agreed that we are probably looking at
triad syndrome or something approximating it. But she has offered very
few suggestions for treatment. She suggested cancer at one point, but I
can't help but think cancer would be an _extreme_ coincidence
considering the circumstances (new cat in the house, new cat brought a
cold, and anorexia was undetected for a period of time). Why would a
cancer wait until exactly now to start generating symptoms? How do I
explain the previous episode and chronic random vomiting?

It seems (from reading) that the only avenue of success with
pancreatitis is to withhold food and water for at least 24 hours,
preferably 48; but more than 24 hours requires hospitalization with IV
fluids. I am curious how successful these approaches typically are. I
have a feeling I would be laughed out of the state if I suggested an
approach that included withholding food to my vet, with the cat already
suffering from fatty liver. Is 24 hrs typically safe, assuming the cat
is given under-the-skin fluids to support her that day? Is this to be
considered a reasonable tradeoff between trying to solve the highly
suspected pancreatitis, and not aggravating the fatty liver/wasting
problem too much in the meantime?

What I need is options. I would like any of the following:
- Suggestions for treatment _in the case of_ one of the aforementioned
disease scenarios, to give me an idea of the scope of the problem I'm
likely to be dealing with. This will help me decide whether or not
euthanization is the best option for us in the long run, as much as it
would pain me to make that choice.

- Suggestions to pass along to the vet. She may not have all the bases
covered in diagnosis, nor have relayed all the options to me. If I can
"jog her memory" or get her to do some research on possible angles, it
may help us all out.

- Suggestions to stabilize the current scenario or how to improve on my
current methods of feeding/nursing, to pass on to the primary caretaker
for the next week. Anecdotal suggestions are ok, i.e. "This worked for
Fizban when he showed the symptoms you have described". I am looking
for dietary suggestions (_what_ is good to feed her) as well as
procedural suggestions (_when_ and _how much_ is good to feed her).

Remember that I have been nursing her for two weeks. She is stable and
not in a state of shock, but her stable state is not exactly that great,
and may be invisibly deteriorating. I would like to try to target the
most likely underlying problems, since I don't have the resources for a
proper diagnosis (and such diagnosis seems to be nebulous at best).

As of today, she was given antacid in the morning, given 20cc I/D
mixture at 2:00pm, which she kept down, given 20cc I/D at 7:00pm, which
was vomited at 9:30pm (perhaps due to a disturbance), and I gave 10cc
water at 11pm. Tomorrow is Sunday, so I won't be able to see a vet for
about 36 hours at this point.

Help me formulate a plan of action! I'd like to go in to her office
Monday armed with information instead of frustration.

Thanks for any insight your experiences can provide.

On Mon, 05 Apr 2004 00:51:29 +0000, J. Martin wrote:

The ideal approach would be to get an exploratory surgery done so that the
liver, intestines, stomach and pancreas can be biopsied and a jejunostomy
tube can be placed. Ultrasound examinations can easily miss pancreatitis in
cats and U/S guided biopsies are not a reliable way to diagnose liver
disease in cats (will seldom diagnose cholangiohepatitis). If you can't
afford this then you may have to discuss altering therapy.

Is anyone familiar with a "fine needle aspiration" test? Does this
typically cost significantly less than the ultrasound, and does it
normally provide a conclusive rule-out or diagnosis of cholangiohepatitis?
It seems that it would be beneficial to know whether the liver is the
source of the problem or simply an innocent victim, and the only way I
am currently seeing the liver as being a possible source of the underlying
problem is in the case of cholangiohepatitis. That isn't an entirely
unlikely scenario due to the new cat in the house, though he hasn't shown
any problems himself.

Prednisone: if all else fails I resort to prednisone even if owners
can't afford a full diagnostic work up. Prednisone doesn't aggravate
pancreatitis in cats to the same extent it does in dogs and humans.

Can you provide more information about this? I suggested using steroids
in a previous conversation with the vet, and I got a response like I was
off my rocker for making such a suggestion, due to the possibility of the
cat having pancreatitis. Is there a threshold dosage under which the
pancreatitis interaction normally isn't a big problem? If it _does_
aggravate the problem, are the complications immediately noticeable and
reversible? It's possible that my vet doesn't have much experience using
prednisone (or some other corticosteroid) in a liver case, so this
information would be helpful to us in making a decision.

On Mon, 05 Apr 2004 00:51:29 +0000, J. Martin wrote:

The ideal approach would be to get an exploratory surgery done so that the
liver, intestines, stomach and pancreas can be biopsied and a jejunostomy
tube can be placed. Ultrasound examinations can easily miss pancreatitis in
cats and U/S guided biopsies are not a reliable way to diagnose liver
disease in cats (will seldom diagnose cholangiohepatitis). If you can't
afford this then you may have to discuss altering therapy.

Is anyone familiar with a "fine needle aspiration" test? Does this
typically cost significantly less than the ultrasound, and does it
normally provide a conclusive rule-out or diagnosis of cholangiohepatitis?
It seems that it would be beneficial to know whether the liver is the
source of the problem or simply an innocent victim, and the only way I
am currently seeing the liver as being a possible source of the underlying
problem is in the case of cholangiohepatitis. That isn't an entirely
unlikely scenario due to the new cat in the house, though he hasn't shown
any problems himself.

Prednisone: if all else fails I resort to prednisone even if owners
can't afford a full diagnostic work up. Prednisone doesn't aggravate
pancreatitis in cats to the same extent it does in dogs and humans.

Can you provide more information about this? I suggested using steroids
in a previous conversation with the vet, and I got a response like I was
off my rocker for making such a suggestion, due to the possibility of the
cat having pancreatitis. Is there a threshold dosage under which the
pancreatitis interaction normally isn't a big problem? If it _does_
aggravate the problem, are the complications immediately noticeable and
reversible? It's possible that my vet doesn't have much experience using
prednisone (or some other corticosteroid) in a liver case, so this
information would be helpful to us in making a decision.

Is anyone familiar with a "fine needle aspiration" test? Does this
typically cost significantly less than the ultrasound, and does it
normally provide a conclusive rule-out or diagnosis of cholangiohepatitis?

NO. FNA will not diagnose cholangiohepatitis. FNA's will frequently yield
a diagnosis of fatty liver but this is often secondary to cholangiohepatitis
which will not be picked up by FNA. Ultrasound guided trucut biopsies are
also likely to miss it. The only ways to properly diagnose feline liver
disease is via large biopsy samples taken by laparoscopy or exploratory
surgery. There has to be enough tissue for the pathologist to see bile duct
architecture in order to diagnose cholangiohepatitis.



Prednisone: if all else fails I resort to prednisone even if owners
can't afford a full diagnostic work up. Prednisone doesn't aggravate
pancreatitis in cats to the same extent it does in dogs and humans.

Can you provide more information about this? I suggested using steroids
in a previous conversation with the vet, and I got a response like I was
off my rocker for making such a suggestion, due to the possibility of the
cat having pancreatitis. Is there a threshold dosage under which the
pancreatitis interaction normally isn't a big problem? If it _does_
aggravate the problem, are the complications immediately noticeable and
reversible? It's possible that my vet doesn't have much experience using
prednisone (or some other corticosteroid) in a liver case, so this
information would be helpful to us in making a decision.


Read the excerpt below. The section on therapy discussed using prednisone
in cases of concurrent IBD or cholangiohepatitis.

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 µg/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.

"Ryan Underwood" wrote in message

Is anyone familiar with a "fine needle aspiration" test? Does this
typically cost significantly less than the ultrasound, and does it
normally provide a conclusive rule-out or diagnosis of cholangiohepatitis?

NO. FNA will not diagnose cholangiohepatitis. FNA's will frequently yield
a diagnosis of fatty liver but this is often secondary to cholangiohepatitis
which will not be picked up by FNA. Ultrasound guided trucut biopsies are
also likely to miss it. The only ways to properly diagnose feline liver
disease is via large biopsy samples taken by laparoscopy or exploratory
surgery. There has to be enough tissue for the pathologist to see bile duct
architecture in order to diagnose cholangiohepatitis.



Prednisone: if all else fails I resort to prednisone even if owners
can't afford a full diagnostic work up. Prednisone doesn't aggravate
pancreatitis in cats to the same extent it does in dogs and humans.

Can you provide more information about this? I suggested using steroids
in a previous conversation with the vet, and I got a response like I was
off my rocker for making such a suggestion, due to the possibility of the
cat having pancreatitis. Is there a threshold dosage under which the
pancreatitis interaction normally isn't a big problem? If it _does_
aggravate the problem, are the complications immediately noticeable and
reversible? It's possible that my vet doesn't have much experience using
prednisone (or some other corticosteroid) in a liver case, so this
information would be helpful to us in making a decision.


Read the excerpt below. The section on therapy discussed using prednisone
in cases of concurrent IBD or cholangiohepatitis.

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 µg/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.

"Ryan Underwood" wrote in message

On Mon, 05 Apr 2004 11:15:38 +0000, J. Martin wrote:

Read the excerpt below. The section on therapy discussed using prednisone
in cases of concurrent IBD or cholangiohepatitis.

THANKS! Wow, what a great resource. I will definitely be showing that to
the vet.

On Mon, 05 Apr 2004 11:15:38 +0000, J. Martin wrote:

Read the excerpt below. The section on therapy discussed using prednisone
in cases of concurrent IBD or cholangiohepatitis.

THANKS! Wow, what a great resource. I will definitely be showing that to
the vet.

I had your article faxed to the vet along with a plea to try 5mg
prednisone (or prenisolone) as well as SAM-e and Actigall if they are
available. I also asked about a few other things such as the possibility
of treating for cholangioheptatis without a diagnosis, and anti-vomiting
agents. She didn't call us back today. That frustrates me immensely,
considering we may be running on limited time here.

To the group:

I am thinking about getting a second opinion tomorrow, but I don't know
what the costs will be like. Will they charge to do bloodwork/x-rays all
over again? Will the original vet resent the fact that we went to someone
else, or be cooperative? Any anecdotes you have are fine.

If food is being vomited, what is a decent amount of water to give to
ensure she is not getting dehydrated? We are giving 6cc water in place of
food when she has vomited.

I am getting pressured to euthanize her, but I am firmly against it until
we have exhausted the options. We have spent so much money on diagnosis
and treatment ($500-800 so far, most of it was not on my watch) that it
hardly seems wise to give up at this point, especially considering no
treatment has even been attempted aside from dietary, and she has been
stable for the past week if not slightly improved from the rotten state
she was previously in. Why put her to sleep when you've barely tried and
she is not in any obvious pain?

I don't know if the vet is just plain stonewalling me, or if she is really
concerned about the complications of treating undiagnosed afflictions.
But what harm could it do to try Actigall, SAMe, or a low dose of
prednisone? Trying out the various Rx that would be prescribed anyway
seems to be cheaper than trying to obtain a conclusive diagnosis in cases
like this.

The current situation is that she is in a catatonic state most of the
time, has occasional diarrhea (but produced a solid turd today), seems to
be urinating normally, occasionally gets up and walks around when she has
something on her mind (like escaping the bathroom), and vomits
approximately 1 of 3 feedings, while not interested at all in eating on
her own. The only thing that seems to have been even mildly successful in
controlling the vomiting is Pepcid. Metaclopramide and Butorphonal (for
pain) had no observable effect on the vomiting or her general state. She
grinds her teeth occasionally, and seems to do it more frequently when she
is about to vomit. She does not seem overtly jaundiced anymore, so we may
have the fatty liver under control, but will need a blood panel to verify
that.