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medsurg3
11/4/98
Holt: management of peritonitis

slide: 
inflamed abdominal contents

etiology: the only primary peritonitis we 
deal with in small animals is the coronavirus, FIP, in cats. most others 
are secondary. 

can be septic or aseptic
aseptic: foreign body reaction 
(surgical sponge, suture reaction, glove powder [always rinse gloves off 
with saline before sticking them in the abdomen], pancreatic enzymes, 
bile, urine, stomach contents) 

septic: penetrating wounds, perforation 
of intestines, surgical contamination, extension of urogenital infection


radiographic findings: loss of abdominal detail. this rad shows leakage 
of contrast from the level of prostatic urethra into abdomen - so he has 
chemical peritonitis

pathogenesis of urinary tract peritonitis: when 
urine is concentrated in kidneys, if the urine is then leaked into 
peritoneal cavity, urine is hyperosmolar so it draws fluid in from 
capillaries, like with dialysis.

slide on left is clear - from the 
collection "Wonderful Stomachs I have Known" by david holt. this is a 
necrotic stomach. 

slide on right - dog was hit by car, came in, they 
were not sure if it had diaphragmatic hernia. it didn't. did ok, went 
home. back two weeks later with ascites. they tapped it...he had bile 
peritonitis. often initially aseptic, then septic later. classicly this 
takes 7-10 days to show up after initial injury. he had a ruptured common 
bile duct.

here we see left limb of pancreas - very inflamed, red. 
pancreatitis too causes chemical peritonitis. well, it can.

septic 
peritonitis cases: this is an animal with a foreign body which caused 
jejunal necrosis. jejunum was stapled with an anastomosis instrument, 
anastomosis was not oversewn, contents leaked, got septic peritonitis. 


on the right we see case of septic peritonitis - there is a large, 
purple, neoplastic looking mass on the left, and we see a large area of 
black bowel. this dog thrombosed the mesenteric veins. blue/black stuff 
often associated with severe venous congestion. bacteria migrated across 
bowel wall, into peritoneal cavity.

prostatic/paraprostatic cysts can 
rupture and cause aseptic or septic peritonitis. can have death from 
septic peritonitis when these rupture, very rapidly.

foreign body repair 
gone bad - jejunal leakage caused septic peritonitis.

clinical signs: 
depression, abdominal pain often present, vomiting often present, fever 
variably present. you will hear about dogs adopting the praying position 
- this can occur. if you see this head down, butt up posture, it 
indicates abdominal pain. 

diagnosis:

clinical signs are not diagnostic 
- abd pain, depression, sometimes shock. 
cbc/chem/electrolytes - these 
are useful tests - if creat/K+ is rising, maybe leaking urine into 
peritoneal cavity. if WBC is very high or very low, may be a sign...

rads: decreased detail, free gas. free gas acts as contrast. plain rads 
would be of absolutely no use whatsoever right after surgery - then, you 
will find free gas and fluid in the abdomen which is slowly reabsorbed. 
if you do an enterotomy and you want to know if it is leaking, rads will 
not help - gas and fluid will be there 7-10 days. so, you can do other 
stuff...
four quadrant tap
peritoneal lavage

slides:
GDV - lots of 
detail in abdomen - free gas in there, we see one large black gas pocket 
and a lot of nice outlines of diaphragm and intestines. 

this slide 
shows us we can't really see crus of diaphragm clearly. some areas 
ventrally and caudally have gas pockets, not sure if free or in bowel. 
need to do tap or lavage to tell.

this slide shows decreased abdominal 
detail - think fluid. but really, this dog has carcinomatosis, not fluid 
in there, so you have to tap to be sure.

four quadrant tap: requires 
scrub, gloves, etc. if you tap cranially to umbilicus, worry a bit about 
hitting the spleen. now, if you do a tap, chances of getting diagnostic 
fluid out is about 50-50 due to a couple of studies. if you get nothing, 
you can't say "he has no peritonitis" based on negative tap.  so you do 
lavage.

peritoneal lavage: clip an area caudal to umbilicus, put in 18 
ga cath - make a few fenestrations near it - feed in cath, instill 10-20 
ml/kg body weight of warm balanced electrolyte solution. massage it 
around. then suck some back out. 1-2 cc is all you need, hard to get more 
b/c omentum covers cath. smear the stuff on a slide, spin it, smear, do 
cytology. 

slide: peritoneal fluid cytology - many neutrophils, a few 
mphages. cells look normal.

slide: many degenerative neutrophils, a 
couple of peritoneal macrophages, some bacteria - chains of cocci, etc. a 
few of them are intracellular. if you see bacteria like this, think that 
you have to check your stain to see if bacteria are in there, or if it 
isn't an artifact, do immediate exploratory surgery.

pathophysiology:

pretty easy to understand.
if you go back to 8001 and look at notes on 
wound healing, when you make a wound you get inflammation, and 
vasodilation/capillary leakage. how does this apply to entire peritoneal 
cavity? you can have massive fluid/protein losses.

think of peritoneal 
capillary bed...starts leaking fluid and albumin across peritoneum. 
neutrophil migration into peritoneal cavity. fibronectin, fibrin, and 
fluid also go into peritoneal cavity. if you inject contrast into 
peritoneum, contrast is reabsorbed by lymphatics...but the lymphatics are 
plugged with fibrin in peritonitis situation. there is decreased 
circulating blood volume, decrease cardiac output, decreased perfusion.


bacteria are opsonized by WBC
Hb and mucus enhance bacterial virulence

bacterial synergism: more than one spp of bacteria in the abdomen will 
have greater pathogenicity than sum of individual virulences of the 
bacterial spp.
release of endotoxin, exotoxin, proteses
activation of 
arachadonic acid cascade generating prostaglandins, leukotrienes, all 
leading to cardiovascular insufficiency.

bacteria interact with mphages 
which release endogenous mediators like IL1 and other cytokines like TNF. 
also we get activation of kinins, endorphins, histamine, serotonin, 
myocardial depressant factor from pancreas. Platelet activating factor, 
etc. we end up with CV insufficiency, poor tissue perfusion, multiple 
organ failure, death. not good.

every 5-10 years, a magic bullet theory 
surfaces. it used to be steroids - if you give them early enough to 
animal in septic shock, maybe you can help? well, steroids block 
arachidonic acid cascade, block TNF...but not the other stuff. so 
steroids alone are not enough. 
then, when people started finding all 
these mediators, they thought lets make mAB against TNF and IL1 - and 
they did - but they didn't work. why? well, you blocked those but not the 
arachadonic acid cascade or other stuff. 

the point is, magic bullets 
won't work. by the time you see the animal, these cascades have already 
been activated.

inital treatment: 
fluid replacements - IV crystalloids 
at shock doses - NormR,  saline
90 ml/kg in first hr in dogs, 60 in cats.

protein also being lost into abdomen, so you need to replace that too. if 
you give 2 units of plasma to a yorkie, ok, but if you give it to a 
labrador, that's not that useful. so you need colloids but for big dogs 
with septic shock, probably hetastarch or dextran 70 is best - this has 
really big molecules in it.
monitor response. fluid choice for ongoing 
therapy will depend on response to therapy.

antibiotics: you don't know 
right away what the bugs are, though you can tell a bit from your tap - 
if you see gram + and gram -, you need something to get both kinds of 
bugs. 

basically - broad spectrum bactericidal agents, effective against 
gram pos and neg. you need aerobic and anaerobic coverage. for the 
anaerobes, the cheapest most effective drug is penicillin G. we tend to 
cheat here, b/c we have nasty, resistant enterococcus, so we use 
ampicillin. also an aminoglycoside IF no renal compromise. so, 
gentamicin, amikacin. those are used ONCE a day. it used to be three 
times a day. now, 6 mg/kg once daily IV for gent, 15 mg/kg SID IV for 
amikacin. this is b/c they are concentration dependent. important thing 
is peak concentration, not the whole area under the curve. also, it is 
less nephrotoxic used once daily than used tid. sometimes we also use 
metronidazole for extra gram neg coverage. these all reach 
intraperitoneal levels equivalent to serum levels. so you do not want to 
throw stuff directly into abdomen.
regarding cephalosporins - people are 
starting to use these instead of PCN. the first generations - two types - 
cefazolin/ancef and cephalothin/keflin - in dogs, when you give 
cephalothin at recommended dose 20 mg/kg it does not ever reach 
bactericidal concentrations. even at double dose, rarely. so use 
cefazolin.

corticosteroids: ICU people used to say no animal dies w/o 
benefit of steroids. now, no animal dies w/o benefit of surgery which dr 
holt prefers :)
theoretical benefits of steroids: increased myocardial 
function, blocking formation of pro-inflammatory mediators, stabilizing 
lysosomal membranes (based on some lamely done study from 1950s...), 
prevention of complement activation.

one thing we don't get here is a 
course on critical literature evaluation. people tend to just read 
abstracts. but you have to look at experimental design. it isn't always 
that great. steroid studies usually involved giving steroids prior to 
peritonitis, or within 10 minutes of inducing peritonitis. but we do not 
see animals coming in saying "hi, i'm going to get peritonitis in 10 
minutes, please give me steroids now." also, a dog is not a person, and a 
mouse is not a dog. extrapolating from people to dogs is not the best 
idea, and from mice to dog also not the best. big study in people found 
that two groups of peritonitis people - one got steroids, one got 
placebo. in this study they had to break the code and stop giving the 
steroids b/c the people getting steroids were dying more frequently. so 
experimentally it is good to give steroids, but clinically, it isn't good 
to give them (we think). most people do not give steroids now. bottom 
line: don't tx peritonitis with steroids. (question: did they look at 
people w/septic or nonseptic peritonitis?)

nonsteroidal 
antiinflammatories:
several years ago, a lady called us who did a PhD on 
peritonitis and nonsteroidals. theoretical benefits: improved cardiac 
index and BP, decreased microvascular permeability - really important, 
improved survival time. 

look for Textbook of Critical Care by Shumaker 
- a human medical text. he spoke at the ACVS meeting a few years ago. 
he's done many studies on people with shock and septic shock. he said 
"forget the papers. the only relevant thing in sepsis and shock is 
improving survival. it's not important if CO is raised for 6 hrs. if at 
the end of the day the patient dies, who cares?" 

bottom line is 
survival. so, NSAIDS - improved survival. HOWEVER - in these experimental 
trials, again, NSAIDs were given before or immediately after peritoneal 
bacterial challenge. we do not know if this applies clinically. 

there 
are NSAID side effects - GI hemorrhage, nephrotoxicosis, blood 
dyscrasias. here, in ES and ICU, we don't use these for septic shock 
anymore. 

surgical therapy for peritonitis:
prompt removal of inciting 
cause. you can pray over the dog in ICU a long time...until you remove 
the source the animal will not recover. if there are free bacteria in 
there, go in and treat it. so you have to try to stabilize the animal - 
give fluids 2-4 hrs, then go to surgery.

slide: severely inflamed 
intestines. you need to get into the abdomen and do a complete 
exploratory laparotomy. treat the source, remove it, consider enteral 
nutrition pathway. resect and anastomose damaged bowel. for this dog with 
bile peritonitis - tied of leaky duct, did cholecystojejunostomy to 
divert flow.

slide: dog with urine peritonitis - drain off urine, resect 
necrotic bladder, repair.

slide: dark red intestines

you really need to 
consider enteral nutrition. TPN can be used, but if the gut works at all 
you should really use enteral nutrition. 

you need to put in gastrostomy 
or jejunostomy tube. enteral nutrition improves enterocyte function, and 
may decrease bacterial translocation from gut. people in ICU on TPN often 
experience bacterial translocation due to unhappy enterocytes not getting 
food.

we already learned about treating contaminated wounds - 
debridement and lavage. consider peritoneal cavity like contaminated 
wound.

peritoneal lavage: while you are in there use a lot of warm 
electrolyte fluid to wash it all, then aspirate back out. do not leave 
fluid in there, then you make it harder on animal. you will spread 
bacteria, and suspend it in fluid, separating it from phagocytes.

one 
guy said the modern concept of peritoneal lavage views the contaminated 
peritoneum as a contaminated dermal wound. copious irrigation is major 
component of therapy - large volumes, 10+ liters of saline. 

some other 
guy said that irrigation is never justified, even in presence of gross 
fecal contamination - he said this in 1986. so there are conflicting 
views.

so there are conflicting views. but dr holt prefers to irrigate. 
he would want to be irrigated if he had peritonitis.

adding antiseptics? 
hmm. people are funny. if there is something that works that is simple, 
surely something complex works better? he just told us to use balanced 
electrolyte solution. if that's good, why not add stuff to it? they used 
to do this in vietnam and korea - the MASH units added povidone iodine to 
lavage fluid for patients with shrapnel wounds. should we do that? no. 2 
ml/kg of 10% solu'n in dogs with peritonitis is LETHAL. people keep doing 
studies, how they get funding we do not know...but povidone always either 
kills more animals or at least decreases neutrophil percent and function 
and increases bacterial numbers in rats (which are not dogs so be careful 
but still). chlorhexidine data is more equivocal but we still see no data 
to suggest that it helps. so do not add antiseptics at this time.

adding 
antibiotics? most studies - experimental and clinical - show no benefit 
to adding abx to lavage fluid if you are giving appropriate doses IV. the 
peritoneum is leaky and will permit abx to reach abdominal cavity. some 
studies are looking at residual bacteria. since you can't possibly 
aspirate all the fluid out, one study says, adding tetracycline to lavage 
fluid reduced bacterial numbers in remaining fluid to about zero. not 
sure if this is applicable clincally.

peritoneal drainage - you know 
that for contaminated wounds, after debridement and lavage, you have to 
decide to close or leave open. you look at peritoneal cavity and judge it 
as if it were a wound. is it clean enough to close? regarding drains: 
despite the Davis school of though, all data shows that drains put into 
peritoneal cavity are rapidly obstructed by omentum or mesentery. so we 
do open peritoneal drainage. if it is too dirty to close, sew linea with 
single interrupted leaving gaps of about an inch. cover with sterile lap 
sponges and hand towels; cover with elasticon over the top. 

slide: 
postop dog in ICU, recovering, somewhat painful. needs a lot of fluids, 
colloids, abx, nursing care, change bandages q 6 hrs, then q 12, q 24, 
etc. 
number of fluid pumps and monitoring equipment is inversely 
proportional to prognosis. these are labor intensive cases. assess amount 
of drainage by weighing bandages. when it looks ready to close, you open 
back up, relavage, and close with delayed primary closure.

new 
directions - not really germane to our discussion so we won't discuss 
them. 
---break---

brockman: surgerical diseases of liver and biliary 
tract

indications for sx of liver/biliary tract are few, and when they 
do occur they require a lot of skill. so, we'll talk about the conditions 
and get an idea of what you can achieve, but you are urged to, unless you 
are totally desparate, not attempt this stuff in your first year of 
practice.

hepatic anatomy that is relevant to surgical intervention:

lobes - left division, right, and central divisions
ligaments - 
triangular ligs to diaphragm, hepatorenal, lesser omentum to stom.

hepatic artery: 20-30% of blood flow, 80% of O2
portal vein: 70-80% of 
blood flow; limited O2
hepatic vein: form a small spiral from the 
different hepatic divisions, joins caudal vena cava which runs through 
liver. 

so lobes go left lateral, quadrate, right medial, right lateral, 
caudate, caudate papillary process. caudal vc goes through caudate and 
right lateral. portal vein enters hepatic parenchyma and then divides. 


in most animals the ribcage protects the liver from trauma

the liver 
blood flow is divided into two parts - vasa publica and vasa privita. 
privita is portal vasculature, publica is arterial supply. an angiogram 
here shows us portal circulation in normal liver - cath in jejunal vein. 


hepatic physiology:
metabolism of nutrients
detoxification of exogenous 
and endogenous wastes
blood clotting factors production

phagocytosis/immune reactions

slide: jaundiced sclera in this small 
brachycephalic dog
he's hyperbilirubinemic

Neoplasia of the liver:
most 
important point here is that primary hepatic neoplasia is rare whereas 
metastatic liver neoplasia is relatively common.
slide: metastatic 
disease in liver, diffuse nodular distribution. intestinal, pancreatic 
neoplasms commonly met to liver, LSA commonly diffusely affects liver. 


clinical features of metastatic liver disease are generally few, animal 
usually presents with primary condition signs. 

primary liver neoplasia 
- most common are hepatocellular adenoma, adenocarcinoma, and 
cholangiocellular adenoma and adenocarcinoma. those are most common. 
these generally present very late in the disease due to liver failure, 
hepatic congestion, portal hypertension, and ascites. but more commonly 
we dx this as incidental finding or at PE for more vague illness with 
vague signs of inappetance, hyperbilirubinemai and icterus sometimes also 
present. but usually more like occasional vomiting, general signs of ill 
thrift. you typically palpate these on PE, provoking imaging study.

so, 
metastatic or diffuse liver disease probably one of the more common 
indications for hepatic surgery. this is a good indication for hepatic 
surgery. with diffuse involvement, you can't excise the liver so you are 
trying to just get a biopsy to find out what it is. Dr Littman probably 
explained various methods of biopsy for diffuse disease. techniques like 
FNA, tru-cut are valuable techniques for animals with nonvascular hepatic 
enlargement or diffuse hepatic dz. surgeons are often invited to perform 
surgical biopsy when there is no hepatomegaly or there is abnormal 
clotting profile. 

convenient technique for surgical biopsy:

best way 
to bx liver lobe is to find a convenient lobe such as the easily accessed 
left lateral lobe, and if no clotting disorder simply draw caudal edge 
out of peritoneal cavity, place two kellys on that caudal edge, making 
sort of a triangle with tips near each other, bases away from each other, 
leave those in place, excise wedge of tissue from b/w hemostats. leave 
clamps in place five minutes, then release - should be no hemorrhage. 
this is the simplest method to get a useful biopsy sample surgically. if 
you do experience hemorrhage, there are some things to try: gelfoam or 
other topical hemostatic agent placed directly onto the bleeding site. 
also, the omentum makes a good hemostatic agent, you can put it on there. 
if hemorrhage is more profuse, you can place two or three crushing 
mattress sutures through the parenchyma for hemostasis. most dogs do not 
have hemorrhage, though. 
again, you do this for diffuse liver disease 
that you need to characterize better, as a first biopsy or after failed 
tru-cut/FNA samples. pathologists prefer to have a nice big piece to look 
at, but sometimes tru-cut is best for the patient. 

techniques for 
primary hepatic neoplasia: these are rare tumors. the dogs with these 
tumors generally have vague clinical signs - lethargy, inappetance, frank 
anorexia, weight loss. some of these tumors make insulin-like substance 
and we may see hypoglycemia. so you evaluate whole abdomen 
radiographically or with u/s to see if there is one mass, or multiple 
masses. surgically, you would prefer there to be one solitary hepatic 
mass involving just one liver lobe. you can remove more than one lobe, 
though. liver is very regenerative. you can take out 70% of hepatic mass 
in healthy dog, 6 wks later dog will have normal or larger than normal 
hepatic mass. that's hella cool. but if you have tumor present in 1,2 or 
3 lobes you know there is likely microscopic disease in all the lobes.


slides: liver cancer in older dog - liver was mobilized - mass was in 
left lateral lobe which was really ideal since these lobes have nice long 
pedicle for ligature. there are a few techniques to try to remove large 
hepatic masses. this is difficult and challenging surgery. if you can 
create a pedicle on the mass, down to the hepatic hilus, you can use a 
surgical stapling gun around it - this is easiest and safest way to 
resect a liver lobe. usually use vascular staples that close to 1 mm and 
put in a triple row of staples. this provides very good hemostasis. the 
other technique - and this slide isn't so great - this is another 
solitary tumor, hepatocellular carcinoma - look at the edge, you see the 
parenchyms has been ruptured. this is called "finger fracture" and you 
can do it with your fingers, or with a suction tip, or even with an 
ultrasonic aspirator, which helps you to find the major vessels and 
ligate them individually. this is relatively safe, but you can 
accidentally rupture vessels. but if you are careful you can do this 
fine.

so, large hepatic tumors can be removed. most common are as above. 
unfortunately, px for these carcinomas is not good. the hepatomas and 
cholangiomas do have a good prognosis, and percentage of solitary masses 
that are benign are about 50% so you can't condemn the dog for having a 
liver mass. you should at least biopsy it.

hepatic trauma: in brief
can 
be result of blunt abdominal trauma - which may also affect urinary 
tract, spleen, GI tract. 
massive blunt abdominal trauma resulting in 
hemoperitoneum should give you cause to question all the parenchymous 
organs. 
hemorrhage - massive hemorrhage occurs from traumatized liver

toxemia - liver contains clostridia and coliforms and can cause 
peritonitis
bile duct system trauma - can cause chemical peritonitis or 
septic if was infected.

diagnosis of hepatic trauma:
history of trauma

guarding of abdomen
radiography - local or general loss of contrast

abdominocentesis - blood or bile, inflammatory exudate
abdominal u/s - to 
dx hepatic fracture
shock - hypovolemic or septic

if animal has massive 
hemoperitoneum, pursue exploratory surgery, don't do an ultrasound :). 
two dogs have come in here with massive hepatic trauma and hemorrahge, 
both have died. 

Portosystemic disorders: 
management of portosystemic 
shunts in small animals: 
classification of PSS: single or multiple, 
intrahepatic or extrahepatic, congenital vs acquired.

slide: human 
alcoholic patient with multiple extrahepatic shunts. alcohol --> 
cirrhosis --> portal hypertension --> acquired, extrahepatic shunts.


most patients we see are those with congenital portal vascular anomalies 
- a single extra or intra hepatic shunt. clinical features are similar. 


most patients have neurological signs:
CNS: lethargy, depression, stupor, 
circling, ataxia, blindness, personality change, seizures, head pressing.


we also see significant numbers of animals presenting not with CNS signs 
but GI signs: anorexia, vomiting, ptyalism - common in cats, diarrhea


since liver isn't functioning well, we see urinary problems due to urea 
cycle problem and urate urolithiasis: UTI, pu/pd, urolithiasis

finally a 
group of other presenting signs: poor anesthetic tolerance - used to be 
most common presenting sign, animal would take 2 weeks to wake up from 
spay. also wt loss, ascites, pyrexia, epistaxis, pleural effusion.


pathology is usually a large single vessel from portal system to systemic 
circulation, bypassing the liver. these animals are smaller than 
littermates, they have poor body condition, may have seizures, we get 
some animals with GI signs or uroliths (radiolucent).

clinical 
pathology:
CBC: microcytic anemia due to reduced ferritin, 
hypoproteinemia, leukocytosis, coagulopathy can all be present, but 
usually the CBC is normal
CHEM: reduced BUN, hypoalbuminemia, 
hypoglycemia, ALP elevation due to hepatic necrosis from poor perfusion, 
hypocholesterolemia
UA: ammonium biurate crystalluria always present, 
hyposthenuria or isosthenuria, urate urolithiasis may be present

when 
you suspect liver dysfunction in a young dog, it's highly suggestive you 
have some congenital portovascular anomaly. to get closer to this dx:

serum bile acids
serum ammonia levels
both are good liver function tests 
- main difference in practice situation b/w the two tests is that serum 
bile acids are stable and can be shipped, wheras ammonia is labile and 
requires rapid transfer to lab. 
BSP retention is classic liver function 
test (not done anymore?)

diagnostic imaging: to figure out why liver 
isn't working
plain rads - not that helpful - usually you see 
microhepatica and renomegaly
contrast rads - give definitive anatomical 
info: angiograms, intraoperative mesenteric portography, 
splenoportography, cranial mesenteric arteriography - but all require sx 
placement of cath.
u/s exam - very sensitive for finding intrahepatic 
shunts, not sensitive for extrahepatic shunts
nuclear scintigraphy is 
great for telling you if shunt exists, but not where it is.

slides: 

radiographs - lat rad, plain film, very small liver.
plain film - lat 
abd, renomegaly present

best anatomical study is by placing cannula into 
mesenteric vessel and getting angiogram. 

here we see flow of contrast 
into mesenteric vein, directly into caudal vena cava. this dog has a 
single, extrahepatic shunt.

here is a portogram of a cat - contrast in 
portal vein, and contrast going directly into caudal vena cava. some 
contrast also going into liver. single extrahepatic shunt is present.


u/s slides: most dogs we suspect of having shunts get a u/s done. 


scintigraphy - this involves placement of radiopharmaceutical into colon 
- we look at the dog and watch the agent move from colon to liver - liver 
should be first to light up. then with time, agent should leave colon, 
light up liver, and eventually you should see heart and lungs light up. 


affected dog - most blood bypassing liver - we see the agent in the 
colon, the first thing we see lighting up is heart and lungs. eventually 
we see a little bit lighting up the liver. 

Medical therapy for 
stabilizing the portosystemic shunt patient:

low protein diet like hills 
K/D, pasta and cottage cheese
lactulose to make osmotic diarrhea, trap 
ammonium in intestine
oral abx - neomycin, metronidazole

tx of choice is 
surgery 
slides: sheltie with single extrahepatic portocaval shunt. you 
dissect around the shunting vessel, place ligatures around it. you can't 
always just completely ligate the vessels. these animals do not have 
normal portal circulation - they have underdeveloped circulation. so you 
have to try to slightly occlude the shunt and wait for collateral portal 
circulation to develop.

another approach: ameroid band constrictors - 
neat things
if you find the shunting vessel, put the band around it. 
these are hygroscopic bands, of compressed casein within surgical steel. 
when immersed in fluid it gradually expands and will eventually occlude 
the lumen of the shunt. so gradual occlusion should permit gradual 
dilation of portal vasculature. 

slides: multiple portosystemic shunts - 
acquired. these dogs have chronic fibrosing hepatopathy causing portal 
hypertension and now there are tons of new blood vessels going from 
portal vein to the caudal vena cava. 

shunt ligation: maximum portal 
pressure: 20 cm H2O
monitor CVP, arterial pressure, color of pancreas and 
bowel, bowel peristalsis, and surface oximetry.

that's that for the 
shunts. it's not a complete description, if you want that you have to 
take 8501.

same is true for biliary system.
indications of surgery of 
biliary tract are few and far between. remember, we have different 
components making up biliary tract - gall bladder, hepatic ducts coming 
from different divisions of liver, joining cystic duct from gall bladder, 
going to the common bile duct. 

the system is a little different in man 
- one large hepatic duct from all the lobes then joins cystic duct. in 
dogs there are 4 or 5 hepatic ducts joining the cystic duct. 


evaluation: history, PE, clin path, rads, u/s.

radiology: limited use

plain films show liver size, cranial abdominal detail
cholangiography: 
give contrast agent that is cleared by biliary system - these do not work 
well when animal is jaundiced, and usually when surgery is indicated the 
animal is jaundiced. 

u/s:  of common bile duct, hepatic duct - probably 
much more useful
radionucleotide scans: useful, you do get good 
resolution in presence of jaundice. it isn't specific but it is sensitive 
for biliary obstruction. 

jaundice is, by the way - yellowing. can be 
prehepatic or hepatic.
indications for biliary tract surgery: 
extrahepatic obstruction (neoplasia, choleliths, etc), rupture of duct, 
infection unresponsive to medical therapy (rarely)

cholelithiasis - 
common in people but rare in their pets. when we see these in gall 
bladder or common bile duct, 50% are calcium bilirubinate - some of those 
are radioopaque. but most are not. so we see them on u/s or at surgery.

formation may be due to chronic biliary stasis and distillation of Ca+ 
salts in bile. these create disease when they migrate down into bile duct 
and obstruct it. u/s shows us dilation of biliary tree only, sometimes, 
as the only indication of the obstruction. if you don't see the stones, 
you might think this might be due to neoplastic obstruction. 

surgically 
we want to flush out any calculi from common bile duct back into gall 
bladder and then resect the gall bladder. resecting the gall bladder 
hopefully ensures the biliary stasis will not recur. to resect the gall 
bladder, we need to ligate the cystic artery, and usually in small 
dogs/cats we do this while ligating the cystic duct. the ggall bladder 
must be elevated from its fossa, then we ligate and clamp the artery and 
duct. 

slide: red rubber cath going through major duodenal papilla into 
duct, to flush stones back. 

chronic fibrosing pancreatitis is another 
cause of obstruction of bile duct - treatment for this is to simply 
rather than remove the pancreas, to divert the biliary flow via a 
cholecystoduodenostomy, opening the gall baldder into the duodenum. now 
bile can flow right into the intestine.


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