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wilkins
peritonitis in horses

handout has all the info you 
need for the exam. 

Peritonitis:
-inflammation of the peritoneum 
(semipermeable mesothelial lining of peritoneum)
-also serosal covering 
of abdominal viscera
-mechanisms resulting in peritonitis are designed 
for protection - to localize whatever the cause of irritation or 
inflammation is; if exuberant, cause harm

peritonitis is usually 
secondary to something else

primary peritonitis - does occur, but is 
rare. often these are just cases where we do not find the primary cause. 
can be "idiopathic" or "idiotpathic"

secondary peritonitis - more common

can be focal or diffuse - if focal, inflammation has done its job - more 
common in cows than horses. diffuse more so in horses
usually is 
secondary to:
bacterial contamination
vascular insults
trauma
chemical 
insults
neoplasia
viral infections

slide: postmortem of horse with 
peritonitis - note serosal surfaces are rough, red, most of the time when 
you see fresh tissue the surfaces are smooth and glistening, but these 
are dull from fibrin deposition. can get edema, fibrin strands mature 
into fibrous adhesions, etc. 

Etiology: trauma

-rectal tear in horse: 
anyone who does rectals on horses will eventually cause one of these 
tears. hopefully minor. it comes with the territory.
-enterotomy

-trocharization
-needle biopsy
-enterocentesis
-castration
-vaginal 
perforation: not common but can occur if exuberant stallion
-foreign body 
penetration: running into fence, being shot
-blunt trauma: big bruise in 
abdomen
-splenic tear
-birth injuries

etiology: urogenital injuries: 
urinary types cause chemical peritonitis, not septic

-ruptured urinary 
bladder (foals)
-ruptured ureter or renal capsule
-fenestrated ureter 
(congenital)
-ruptured uterus (parturition- explosive in mares - 20 min)

-ruptured uterine artery - another problem in dam b/c of large blood loss 
- can get huge hematoma in broad ligament - this hematoma or free blood 
in abdomen can result in peritonitis.

etiology: vascular accidents:

horses love these

verminous arteritis - rare now - parasite emboli 
seeding smaller vessels, causing ischemic necrosis of supplied tissue 
(bowel)
intestinal strangulation
infarction
thromboembolism

intussusception (primarily foals) - no peritonitis early, but if affected 
bowel starts to die, septic peritonitis occurs
vasculitis - immune 
mediated, viral, parasitic

etiology: infectious
more common
septicemia

bowel perforation - horses very sensitive to antitoxin, get really really 
sick.
focal intestinal necrosis, intestinal accidents, NSAID toxicity 
(right dorsal colitis; gastroduodenal ulcers in foals)
foreign body 
perforation
intestinal mural abscess/neoplasia (LSA most common GI 
tumor)(SCC of stomach occurs too)
strep zoo abscess - bastard strangles

r.equi abscess - foals can get huge mesenteric LN abscesses. 
pyometra

enteritis with full thickness necrosis: salmonella, clostridia, fungal.


etiology: other:
bile peritonitis - cholelithiasis, cholangitis - 
generally ascending biliary infection in older horses. if they get big 
enough stones can obstruct. no gall bladder in horses. 
pancreatitis - 
not commonly reported but does exist in horses.
neoplasia - primary or 
metastatic
ascarid impaction in foals - does still occur - even in adult 
can occur.

clinical signs - LOCAL peritonitis:
mild/severe abdominal 
pain
unusual postures - may stretch out, may stand with one leg twisted, 
elbows out, etc.
tachycardia (60)
ileus
adhesions with extramural 
obstruction of bowel
low volume frequent diarrhea - classic sign - small 
amounts, almost constantly
weight loss - may be only sign!
intermittent 
fever
anorexia
ventral edema
exercise intolerance

signs: diffuse 
peritonitis - more overwhelming, acute
these animals are very sick, 
present in shock
increased PCV (60-70)(from splenic reserve), decreased 
TP(protein going into peritoneum)
abdominal splinting, pain

endotoxic/hypovolemic shock: hypothermia, tachycardia, tachypnea, cold 
distal limbs (poor perfusion), ears and nose cold, red/purple mucous 
membranes, significantly increased CRT, ileus, diarrhea (higher volume)


dx local peritonitis:
abdominocentesis: fluid has increased cell count, 
increased protein, abnormal cytology, +/- culture (don't be surprised if 
culture is negative in the presence of bacteria on cytology - there are 
bacterial growth inhibitors in the inflammatory exudate)
laparoscopy

hematology: anemia of chronic dz (depending on how long lasting), 
hyperproteinemia (increased globulin fraction), hyperfibrinogenemia 
(unless starting DIC), variable leukocytosis (depends on how long it has 
been going on, etc)
exploratory laparotomy if you are unsure

dx diffuse 
peritonitis:
abdominocentesis fluid usually diagnostic but may be 
misleading
signs of shock with no other cause being seen
exploratory 
laparotomy

treatment local peritonitis: tx infection w/broad spectrum 
abx; tx adhesions via exploratory laparotomy; correct inciting cause.


treatment diffuse peritonitis: 
treat shock: fluids, electrolytes, 
plasma, colloids
treat toxemia: low dose flunixin meglumine, hyperimmune 
anti-endotoxin plamsa, polymyxin B (investigational)
treat infection: 
broad spectrum antibiotics - commonly Pen, Gentamicin
correct inciting 
cause

Gastric and Duodenal Ulcers in horses:

Peptic ulcers: 
ulcers 
form, and some of you are probably on meds for this, etc - 
anyway they 
form when protective mechanisms are overcome by aggressive factors.
cycle 
begins with acid back diffusion to the mucosa
clinically significant 
ulcers are relatively *uncommon* in horses
bleeding ulcers are 
*rare*rare*rare*rare* in horses - not a cause of anemia.
you can get 
gastric blood loss from other things - eg gastric SCC.
ulcer cycle:

mucosal barrier somehow broken --> H+ back diffusion --> cell damage --> 
histamine release --> increased H+ release --> back diffusion of H+


barrier can be broken by a foriegn body or a number of other things. FB 
could be very rough hay stems, or something stuck in the hay. 

again, 
gastroscopic abnormalities in horses are very very common - usually you 
do see some type of ulcer. but signs associated with them are not common.

ulcers and erosions along the margo plicatus are most common. if you find 
a horse stomach that does NOT have a single erosion or ulcer along the 
margo plicatus, Dr Wilkins will buy you coffee.
clinically relevant 
ulcers are usually large, extending dorsally into the squamous fundic 
region.

five categories of ulcers:
1. clinically silent to vague signs 
(ADR)
2. bleeding ulcers
3. incomplete or slowly perforating
4. complete 
perforation with generalized peritonitis
5. chronic ulceration - 
fibrosis, stricture, obstruction, dysfunction

slide: ulcers in horses 
stomach - tiny ones along the margo plicatus. note also some bots in 
there. 
slide: bleeding ulcer, not perforating all the way through. in 
mucosal portion of stomach, not squamous portion
slide: severe ulceration 
in squamous portion of stomach - very severe - incomplete to slowly 
perforating. 
slide: perforated gastric ulcer
slide: duodenum from foal 
who had obstruction due to fibrous scarring - this syndrome used to be 
more common in late 80s early 90s, sort of disappeared now though. more 
rare now. maybe was caused by unidentified infectious agent or was caused 
by NSAIDs we stopped using. 

ulcers in foals:
1% of all foal deaths are 
due to perforating ulcers of stomach or duodenum.
non perforating ulcers 
of squamous epi commonly seen at post mortem - adaptive change? usually 
multiple small ulcers confined to the squamous or glandular areas. these 
are probably developmental in most foals.

gastric ulcers in foals:
non 
glandular mucosal most commonly affected - desquamation without 
ulceration in foals 35-50 days old probably developmental
glandular 
mucosal ulcers - associated with stress (illness, overcrowding, maternal 
rejection)
perforating and non-perforating: peforation is uniformly fatal 
in foals. 

duodenal ulcers in foals:
possibly associated with immaturity 
of acid regulation and protective mechanisms. 
preceeds gastric 
ulceration in many cases due to delayed gastric emptying.
perforation 
uniformly fatal
stricture may occur - results in delayed gastric emptying 
and may result in gastric rupture.

etiology: stress, trauma, NSAIDs, 
infectious agents - bacterial (salmonell, clostridia, maybe 
helicobacter), viral (rotavirus, coronavirus)

signs of ulcers 
(nonperforating) in foals:
colic, bruxism, ptyalism (triad)
depression, 
anorexia, variable fever, ileus, diarrhea
lying on back.
slide: foal with 
ptyalism - foaming at mouth, drooling

signs of perforating ulcers

depression, pain 
bruxism
dyspnea
injected mms
profuse salivation
diffuse 
peritonitis

signs of duodenal stricture
gastric stasis, dilatation

esophageal reflux
esophagitis
esophageal dilation

slide: rads - barium 
swallow - fluid pooling in esophagus, with air distension above.

adults: 
ulcers of esophageal region:
common along margo plicatus, associated with 
musculoskeletal dz (pain? drugs?)
large erosions of squamous region 
common with septicemia, toxemia
chemical irritants can cause that too

gasterophilus intestinalus near the margo plicatus

ulcers in glandular 
mucosa:
may cause abdominal pain
rarely perforates
chronic fibrosis, 
pyloric obstruction: intermittent colic, severe pain, association with 
eating/drinking b/c stomach fills up. mimics duodenal stricture or 
habronemia

dx: endoscopy, peritoneal fluid analysis, contrast rads, u/s 
exam, exploratory laparotomy, gastric cytology

tx: 
antacids, H2 
blockers (cimetidine, ranitidine), proton pump blockers (omeprazole), 
gastric protectants (sucralfate), metoclopramide, erythromycin, 
metronidazole-ampicillin-bismuth salts


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Ross:

Large animal 
hernia repair

hernias are boring. 
once a foal came down from ICU. he 
had infected umbilical remnant removed. sometimes hernias are complicated 
by infxn, too. 
Dr Ross did this surgical resection of remnant and out 
pops the ileum. he went to stick it back in and saw Meckel's diverticulum 
(yolk sac remnant - very very rare, only ever seen in 2 yr old with colic 
before). so he decided to take it off to prevent colic later. it was 
small so he took it off, did inverting pattern - two days later foal was 
colicky b/c he had intussusception at that site. oops. he surgically 
reduced it. it recurred and foal had to be euthanized. moral of the 
story? well, had he not removed the diverticulum, the horse would have 
developed surgical colic in 2-3 yrs anyway, so maybe he saved the owners 
the training expense. other moral: don't try to play god.

what is a 
hernia? protrusion of organ or tissue through abnormal opening. we see 
internal and external hernias. internal ones occur when bowel goes 
through diaphgragmatic tear, epiploic foramen, etc. external ones occur 
when a piece of something protrudes through body wall opening.  

slide: 
2 yr old palomino QH admitted for surgical repair of "umbilical hernia" 
that was freely reducible, one hand width in length, along ventral body 
wall. that's what he came in for. think about it and we'll bring it up 
later.

most umbilical hernias we see are in foals, calves - most common 
type.
also inguinal, scrotal - in foals, or adult horses, or congenital 
in pigs.
"ventral hernia" means any hernia of the abdominal wall that 
doesn't involve a normal opening like inguinal canal or umbilicus.so this 
could be on the lateral body wall or whatever.
incisional hernia - 
something you do not want to deal with b/c you probably made the incision 
in the first place. most common reason for these is b/c the original 
incision is infected and there is weakening, or delayed fibroplasia. 
sometimes due to frank suture breakage but that usually occurs 
immediately and causes acute dehiscence. 

other terms - 

reducible/non-reducible
strangulated
uncomplicated
complicated

hernia 
can contain anything from abdominal cavity but most often the small 
intestine, omentum, rumen/abomasum in cattle. 

reducible means you can 
put it back into place freely.
nonreducible or incarceration means you 
can't put it back, but it's not strangulated.
strangulated means blood 
flow is cut off - emergency
uncomplicated = simple, reducible, no problem

complicated - involves some kind of infection or something else 
complicating it.

Umbilical hernia in foals: 
very common, generally 
congenital, may be hereditary - a predisposition clearly exists in TB 
fillies. some horse people claim that hernias can develop as a result of 
breakage of the cord too soon or too short. foals can look normal at 
birth and get the hernia showing up a few mos later. probably b/c as foal 
grows, he outgrows the strength of the body wall - most likely the defect 
is there at birth but not noticed. PE findings are most important - could 
also do u/s or radiography. most often though just a good PE, palpation 
of the area. in foals usually 1 finger to greater than one hand wide. 
smaller defects sort of are worse because a piece of intestine will get 
down there through a small defect and then have a higher chance of being 
strangulated. with a large hernia, stuff doesn't strangulate. 

if you 
have a small umbilical hernia, that is uncomplicated, freely reducible - 
what do you do? fat, peritoneum, small intestine is probably what is in 
the hernia, most often, by the way. anyway, small ones can close 
spontaneously. or, some people advocate scarification/irritation of ring; 
trying to reduce it a few times a day, chronic bandaging - doesn't work 
in male foals or in calves. chronic bandaging alone doesn't seem like it 
would work w/o some kind of irritation of the hernia ring. one other 
technique is sort of effective although also sort of barbaric - the use 
of hernia clamps.

hernia clamp - take a dowl rod - split it down the 
middle and put some wing nuts in it - put it around the hernia sac and 
crush it for 10-14 days and let it slough. ugh. you are trying to cause 
ischemic necrosis of skin, sq tissue and hernia sac. when it falls off, 
you hopefully have a healed defect. but that's disgusting. well, it works 
well and is used often on large breeding farms where there are a larger 
number of hernias. you tranquilize the foal, roll it over, clip and prep 
the site, take your allis tissue forceps and clamp skin and sac, pick it 
up and make sure there is no intestine or anything in there - foal is on 
his back so you wouldn't expect it to be - apply your hernia clamp, 
squeeze it down...tighten it the next day - also may need to give 
flunixin meglumine or other analgesic because this is painful. anyway, 
10-14 days later it will slough and you have a hopefully healed defect. 
works well. Dr R favors surgical repair, however. 

surgical repair - 
best done b/w 3-6 mos of age though 1 month to 3 years is ok. probably 
best done after weaning. this is mandatory if colic is associated with 
the defect, or if complications like swelling or infection are present. 
how do you do it? well, you may be asked to do it in a less than 
desirable situation such as in the stall, in the barn, whatever. well, 
jeez...you don't want to send it to the referral center...and usually you 
don't ahve a problem with the surgery per se, but the anesthesia and 
restraint are a real problem if you're alone out there. the parasurgical 
issues are more important than the actual surgical issues.

surgical 
technique: clip, prep, drape for sx. wear gloves and gown. make 
elliptical/spindle shaped incision but do not take off all that extra 
skin. leave as much skin as you need - better to have more than not 
enough. if there is infection there you run into a lot of blood vessels 
that may require clamping/ligation. remove and discard the extra skin. 
then you either poke the sac into the body and close the defect - without 
opening the abdomen - or you open the sac. the sac is thick fibrous 
tissue that should have been body wall but isn't. optimally, incise 
around the defect so you have a nice fresh edge to suture closed. if you 
stray too far laterally and see muscle, what would you see? rectus 
abdominus. remember holding layer is the ventral fascia. when you open 
the sac like this, you see small intestine sitting there. this is the 
problem with the closed technique - you could accidentally stick the 
intestine. 
close the defect with simple appositional technique, number 1 
or 2 dexon or something. if you're used to dog spays and you are used to 
small suture it can feel weird. "vest over pants" mayo mattress suture is 
written up in literature - not required. this is an overlapping technique 
where you put one side of the body wall over the top. this is weaker than 
simple appositional by the percent overlap. so simple appositional is 
better. preplace your sutures about 1 cm apart and 1 cm back from edge of 
ring. suture subcu tissue with one or two layers of absorbable suture 
like vicryl. then close skin with whatever you want - staples are ok but 
to get those out that would kind of be a pain - only use these if you do 
not like the referring vet. so maybe put absorbable sutures in. they can 
cause a reaction but when sutures are in a place that it is hard to get 
them out, it's probably the lesser of two evils. 

when you've done this 
repair, you want it to heal, so give foal 3 weeks rest in stall with hand 
walking only, then 3 weeks of turnout in the paddock. do not put him out 
with his mom b/c he will follow mom all over the place no matter what she 
does. also give foal abx - TMP/sulfa or something. it's almost impossible 
to do sx on a foal without some sign of infection. they almost always 
have runny nose, or fever, or cough, or high WBC, or something. 

in 
calves, similar but one difference - umbilical hernia in calves more 
often have complications associated with them b/c many of these calves 
have umbilical abscesses or some infxn of umbilical remnant ** more 
likely to find complications in calf, infection in calf. if you want to 
repair these in calves you **must** remove hernia sac, not invert it as 
is possible (but not recommended) to do in the foal. 

your PE is 
important at all time. farmer might bring calf in for umbilical 
herniorrhaphy, and you might feel nonreducible lump on one side, or 
nonreducible abscess, or whatever. PE is really important. hernias in 
calves are congenital, probably hereditary. some folks think they are 
secondary to some kind of phlebitis. could be. or, hernia could be there 
to start with and they show up as calf grows. but infxn of umbilical 
remnant occurs more often in calf. if you have u/s you might do that more 
often in calves than in foals. 
inside an umbilical hernia in calf expect 
fat, omentum, abomasum, and rumen. could be adhered to there. another 
reason why you have to open the hernia sac. 


slide: infected umbilical 
vein surgery - urinary bladder is present, we see thickened umbilical 
vein heading all the way up to the liver. 

in the calf remember much 
more likely to have complications than the foal so please give 
antibiotics. other methods of management do not usually work in calf 
(other than surgery, that is) - shape doesn't allow chronic bandaging, 
defects tend to be very big.

slide: horse with big ventral swelling. 
incisional hernia. most common reason for this is infection. it's unusual 
to see an incisional hernia without infection. you can have acute or 
sudden dehiscence from suture or body wall failure, usually right after 
surgery. that's technically a hernia but we call it dehiscence and it 
requires acute management. but when you see hernia 30-60 days postop, 
usually it's b/c there was infection, delayed fibroplasia, etc. 

slide: 
affected cow with ventral swelling. often when these occur after ventral 
midline exploratory you can repair it primarily with no synthetic mesh. 
when it's off the midline after paramedian incision, you can't b/c it 
makes too much tension, so you have to augment your repair with double 
plastic mesh called proxplast - most economically reasonable, strong 
piece of mesh. if you have too much tension you have to use mesh. some 
large hernias you can't appose the edges and only the mesh spans the 
distance.

slide; large ventral hernia in broodmare - looks like prepubic 
tendon rupture. but you can feel nice defined hernia ring the size of a 
watermelon. can't repair this primarily. you have to cover it with mesh. 
can be really hard to repair, requiring lengthy surgery and big implant. 


slide: big ventral hernia  2x2 feet.

slide: that palomino QH with the 
alleged umbilical hernia. the *owner* said this horse needed umbilical 
hernia repair. however, it is not located at the site of the umbilicus. 
it is more cranial. this is a ventral hernia. and it isn't along the 
midline. also there is a scar there. this is a traumatically induced 
hernia. this has a well defined hernia ring but you can not appose the 
edges so you need to put in a mesh. this costs more b/c of mesh, longer 
surgery, and antibiotics.

comments - inguinal hernias - we see inguinal 
hernias mainly in horses - two categories: foal with congenital hernia - 
sometimes a large amt of small intestine will be down in the vaginal 
tunic and will still be asymptomatic. remember that foals just like with 
umbilical hernias can grow out of a weak spot or something in this area. 
some of these foals are probably born with a muscle weakness in this 
area, and as they get bigger bowel falls through it. sometimes benign 
neglect cures them. they have no clinical signs and are doing fine - 6 
mos later the swelling is gone. they just spontaneously correct, perhaps 
by gaining muscle integrity. however if a LOT of intestine is down there, 
it can rupture through vaginal tunic and cause colic. if foals are colicy 
you have to operate. that's the second category - horses or foals 
admitted with colic referable to inguinal herniation (indirect). acquired 
form in adults is more frequent in STB, morgan. associated with colic. 
adults with this would be expected to show clinical signs. 

when we see 
these as colic, or surgical emergency post castration (evisceration) - 
indirect hernia through vaginal ring into vaginal tunic - but if ventral 
aspect of tunic was removed via castration you get evisceration. 
realize 
- as we talked about before, when you have inguinal herniation in 
domestic animals it is indirect - that means the bowel goes into the 
vaginal tunic through vaginal ring. in people, as you grow, you lose the 
internal inguinal ring. so you get a direct hernia, directly through the 
body wall. most common organ to go there btw is ileum.


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