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medsurg3
11/23/98

Whitlock: Vagal Indigestion

this is a 
chronic indigestion syndrome - broken into types I - IV

history is 
similar for each type:

anorexia (off feed)
decreased milk production

gradual weight loss
percieved gradual abdominal enlargement * key 
clinical sign! **

chief complaints:
weight loss
decreased milk 
production
abdominal distension
bloat - free gas bloat - at any stage of 
lactation, with any subtype of VI.

slide: cow with a distended abdomen

she's off feed, decreased milk production, distended. this is an advanced 
VI case - very big full abdomen, bilateral. 
also rumen distension - full 
of fluid and/or gas

slide: tucked up looking cow; rumen contracted down; 
abdomen small. normal forestomach motility and function; cow is off feed 
for some other reason. no abdominal distension.

slide: same cow - can 
see the concavity from rib cage to femur. 

Other key features of vagal 
indigestion:

-abdominal distension * key feature (interpret in light of 
history - not necessarily round, but fuller than should be for anorexic 
cow
-ruminal distension * fluid/gas
-rumen motility - variable, often 
increased. when ausculting dorsal sac, listen for rate and strength of 
contractions. cows with VI have increased rate of contraction >2/min, but 
decreased strength of the contractions.
-rumen consistency - more fluid 
than normal, or bloat/gas
-heart rate normal to bradycardia - < 60/min - 
about 25% of VI cows bradycardic.
-above are *main signs*. also may see:

-hypogalactia
-decreased fecal output
-localized abdominal pain in the 
xipoid region - but may be hard to elicit in these cattle. pain is b/c 
many of these are due to traumatic reticulitis, abscess - but pain is 
more obvious in acute phase, this is more chronic.
again: key dx feature 
is history of anorexia with suggestion of abdominal fullness.
- feces may 
be mucoid, pasty; long plant figbers may be seen due to poor abomasal 
function
-rectal exam - distended rumen distended ventral sac forms an L 
shape
-"papple" cow - apple on left (bloat), pear on right

again, b/c 
process is chronic, hard to elicit pain @ xiphoid even if traumatic 
reticulitis is cause.

Type I Vagal Indigestion (VI-I): Failure of 
eructation
a chronic, free-gas bloat. excessive gas in rumenoreticulum; 
cow presents distended high on left side. problem is NOT excessive gas 
production but rather failure of eructation. easy to remove gas via 
stomach tube. animal will bloat again when fed. dx usually based on 
confirmation of free gas bloat (non-frothy) which is easily relieved by 
stomach tube.  when you pass the tube, there's no excessive fluid in the 
rumen. just gas. 
most of these are young heifers, but also some adult 
cows. 

Type II VI: Omasal Transport Failure (VI-II: OTF)
rumen 
consistency is "splashy" or fluid. diffuse peritonitis, abomasal 
volvulus, lactic acidosis (grain overload).
hay particles in feces often 
very large, indicating loss of omasal function causing increased fluid in 
rumen and failure of reticular omasal orifice to regulate the size of 
particles reaching the abomasum. 
plasma chloride is normal, no metabolic 
alkalosis
dx confirmed by exploratory laparotomy
if the problem is in the 
omasum, there is no chloride reflux from the abomasum. this is why cows 
with OMT have normal chloride. the HCl goes distal and is absorbed 
normally. with impactions, there is reflux and chloride is trapped in 
rumen. So chloride level differentiates b/w VI-II and abomasal impaction.


Type III vagal indigestion: abomasal impaction (VI-III: AI)
similar to 
OTF clinically
these cattle have abomasal reflux and hypochloremia
rumen 
chloride often > 25 mEq/L (normally nder 20)
normal plasma chloride 
95-105; these cattle 50-95 mEq/L

type IV vagal indigestion: indigestion 
of advanced pregnancy: VI-IV: IAP
may be adhesions interfering with 
forestomach motility
pregnancy becomes advanced, puts pressure on 
adhesions
abdomen becomes distended in addition to fetus
omasal/abomasal 
dysfunction
hypochloremia usually present, but chloride is variable.

Lab 
Data in general for VI:

dehydration: increased PCV and TP
TP increased 
due to chronic infection, abscesses, or pneuonia - normal 6.5-7.5 gm/dl

hyperfibrinogenemia due to chronic infxn
hypocalcemia due to GI stasis, 
decreased feed intake
hypochloremia esp with type III and IV, abomasal 
reflux

pathophysiology:

I: failure of eructation - localized 
peritonitis ventral and left reticulum. most common cause in young 
heifers is calf pneumonia - reactive lymphadenopathy adjacent to vagus 
nerve may cause vagal neuritis. chronic bloat is rarely if ever caused by 
excessive fermentation so antifermentatives are not very useful. it is a 
failure to eructate normally. 

slide: adult cow with massive distension. 
pass a tube, it will go away. dx is easy. most of it is all free gas.

slide: rumen that has gotten huge, extended ventrally to the right - can 
feel a cleft b/w sacs, sort of L shaped. gas extends dorsally to the 
left.

Free gas bloat: cause: not excessive gas production but decreased 
eructation - failure to clear cardia. antifermentatives are not 
appropriate. must establish means to get rid of gas via rumen fistula.


II: OMT: omasum normally acts as a pump, moving rumen contents into 
abomasum, acting as particle sizer. any lesion interfering with this may 
cause omasal dysfunction - abscess, tumor, foreign body, anything.  
obstructive lesions in omasal canal will cause omasal dysfunction: LSA in 
omasum or abomasum. abscess most common cause - can occur on right wall 
of the reticulum in particular. most common cause of OMT.

OMT can be 
secondary to liver abscess as well: signs - distended left paralumbar 
fossa (free gas bloat), bradycardia in 5/8 cows, scant feces, enlarged 
distended rumen by rectal palpation. 

slide: papillomas blocking omasal 
canal

Mycotic omasitis: secondary to septic mastitis or metritis, or 
rumenitis. characteristic lesions occur - fungal plaques. 
Omasal 
Impaction: Dr Whitlock believes this does not occur. he thinks problem is 
usually omasal dysfunction, failure of pump. postmortem dx - omasal 
contents very dry - but normally the omasal contents are dry and when 
there are problems, they get soft and atonic, so this is questionable. 

slide: normal omasum - dry contents - as expected. if you palpate omasum 
of cow with OMT expect soft, easily kneadable omasum. dry contents are 
normal and not a sign of impaction. 

so space occupying lesions etc can 
cause OMT type II VI.

type III - abomasal impaction - two major 
classifications of these - 
primary abomasal impaction, or secondary. 
most cases of VI are secondary to some other lesion. primary abomasal 
impactions occur in beef cattle, out west - water restricted cattle fed 
coarse, dry roughage = predisposed. 
secondary abomasal impaction is 
usually sequel to traumatic reticulitis, etc. slide: huge distended 
abomasum, secondarily impacted due to an abscess distally. 
when cows get 
abomasal impaction, either type - prognosis is very poor, they usually 
recur. 

type IV: IAP: adhesions, enlarged uterus pushing forward on 
reticulum, omasum, etc. 

Vagus Nerve:
90% sensory activity
10% motor 
activity - very important - stimulates mostor function of rumen, 
reticulum, omasum, and abomasum and stimulation of the nerve may cause 
bradycardia.

dz of vagus nerve:
traumatic reticuloperitonitis (90%)
LSA 
of mediastinal LNs (rare)
diaphragmatic hernia (rare)
dry pleuritis with 
adehsions around esophagus; chronic pneumonia with enlarged LNs
hypoderma 
larvae (rare) - migrate internally sometimes near vagus nerve.


Diagnostic ruleouts: 

type I - free gas bloat: a single animal dz


ruminal tympani due to other causes:
-complete esophageal obstruction due 
to FB like potato, tuber, apple pear (rare)
-esophageal compression from 
neoplasm or LN abscess
-frothy bloat: springtime, alfalfa, multiple 
cattle affected.

type II-IV

chronic rumen tympani (bloat) - pass tube

displaced abomasum - percuss for ping
cows with type I VI do NOT have a 
ping associated with the distension!
hydrops allantois or amnii - rectal 
exam
ascites - rare, ballotte
ruptured bladder -rare in cow, more common 
in feedlot cattle

5Fs of abdominal distension:
fetus (rectal)
fat 
(inspect)
feces (rectal)
flatus (inspect)
fluid (ballottement)


Diagnostic plan:
when presented with a cow with potential VI:

pass a 
stomach tube
determine consistency of rumen contents - firm, dull if only 
free gas;, if fluid, consider types II-IV VI
PE of esophagus for FB, 
stricture
plasma chloride concentration to tell type II from type III 

rectal exam - for pregnancy and rumen size, position
TP: hyperproteinemia 
--> chronic infection
BLV titer - if positive, could have LSA, if not, 
could not have adult LSA
radiograph reticulum to see hardware, FB (rare 
in practice, $$$)
serum calcium - often mildly hypocalcemic - 6-8 mg/dl 
(normal 10) - correct w/subcu calcium injections

Treatments:

type I: 
failure of eructation:
a) rumenotomy - explore reticulum - establish a 
rumen fistula by surgically suturing rumen to skin, place trochar (Buffs 
screw trochar) - use local anesth, make hole, place thing in there. most 
cows after 2-3 weeks will regain ability to eructate so you can remove 
the trochar. or, make small incision and suture skin to rumen, making a 
small rumen fistula that will remain open as long as cow needs to pass 
gas through it. as she regains ability to eructate, will granulate 
closed.
b) long term abx especially w/ chronic pneumonia
c) not 
antifermentatives

type II: OMT
first, determine value of animal - if 
she's not valuable, send to salvage, if she is, surgery: first, 
rumenotomy to determine lesion - many are abscess - if abscess, drain 
with needle and tube or if very adherent to rumen/retic, blindly incise 
through reticulum into abscess and let it drain into reticular lumen. 
gross. if mass is neoplastic, send to salvage. if FB (placenta, plastic 
sheeting, whatever), remove it. fibropapillomas are not easy to remove.

Abscess usually on R side of reticulum. make sure it is an abscess before 
you blindly incise. 

slide: a nail that was removed in surrounding 
abscess tissue, scar tissue

cows with liver abscess - have big masses 
adjacent to reticulum, sometimes adherent to diaphragm and right 
abdominal wall. drain with tube through abdomen.

type III: AI
correct 
alkalosis and dehydration with IV fluids, NaCL or NaCl and KCl, 20-40 L. 
if she's not pregnant or valuable, send to salvage b/c poor prognosis, 
maybe 20% survive. rumenotomy if economically feasible - if abomasum is 
huge, px grave. if only end of pylorus is distended, can infuse w/epsom 
salts, mineral oil, dss, try to break up impaction.

type IV: IAP


depends on value of fetus - 6 or 7 mos gestation, abortion is required to 
save cow. in last month, medical therapy may help before parturition, or 
can induce. 

economics: if animal is valuable, rumenotomy is considered. 
if not valuable: send to salvage.

General medical therapy:
for all types 
of vagal indigestion:
oral cathartics (except for type I), mineral oil, 
epsom salts, anything to stimulate GI evacuation
subcu calcium gluconate 
to correct mild hypocalcemia - four sites under skin so it lasts and 
prevents relapse
abx if abscess present
parasympathomimetics - esp with 
type IV - may be of value. neostigmine q 4-6 hrs but stimulates spastic 
contractions, not normal, so not the whole answer.
force feeding hay a 
few times a day may encourage to chew cud - if she chews and swallows, px 
better than if she drops it (duh)
oral electrolytes - eps KCl a few doses 
a day

client education:
type I: rumen fistula will heal closed in time, 
animal will get better, regain ability to eructate. prognosis excellent

type II: px for life guarded, 50-70% survive
type III: px poor, 20-50%

type IV: px depends on stage of gestation -better if closer to 
parturition.
---break---

Clinical problems associated with liver disease 
in large domestic animals:

Icterus (jaundice) in large animals:

adult 
sheep: chronic copper poisoning is the prime diagnostic rule out ***

Cattle: icterus is very very rare, consider hemolysis first!
Horse: 
icterus is very common - fasting hyperbilirubinemia is the first 
consideration; also consider hepatocellular disease if any CNS signs are 
present.

History:
neonatal calves - suspect use of anaplasmosis vaccine 
- hemolytic crisis if vaccinated for anaplasmosis in southern US occurs.

neonatal foals - suspect neonatal isoerythrolysis or rhinopneumonitis 
(herpes infection of the fetus; w/liver failure secondary to virus)
sheep 
- chronic copper poisoning

slide: foal with neonatal isoerythrolysis - 
moderate icterus, pigment in urine, sclera icteric, injected.

PE: 
icterus is best recognized in the sclera, oral, and vaginal mms
lab data: 

hemolytic crisis: increased indirect pigment, decreasing PCV

hepatocellular dz
major increase in direct reacting pigment w/liver 
failure expcep horse; more when [slide confused me][see handout]

obstructive disease - rare or uncommon, sometimes in horse with 
gallstones, sometimes in pig with parasites

enzymes:
alkaline 
phosphatase - not liver specific - also in bone, intestinal mucosa, 
biliary tree, placenta - use this enzyme in horse with biliary cirrhosis

*aspartate aminotransferase AST nonspecific (liver or muscle), indicates 
acute injury, common test
*CPK - muscle specific - run with AST, if CPK 
normal when AST high suggests liver dz. (creatine phosphokinase)
(ast, 
cpk most common tests; bovine and equine)
LDH lactate dehydrogenase - 
very nonspecific, increases with liver, muscle, heart dz. rarely used

OCT: liver specific but most labs do not run. 
bile acids - only useful 
in horse with chronic liver disease
SDH sorbital dehydrogenase - liver 
specific but very labile, need to test w/in 2-3 hrs of obtaining sample

cholesterol - ester, free, and total - cattle with fatty liver - 
inversely correlates with fat infiltration of liver. as infiltration 
increases, cholesterol decreases
GGT gamma-glutamyltransferase: routine 
in large animals, looks for injury to biliary epithelium. not liver 
parenchymal disease.

diagnostic rule outs:
obstructive jaundice - RARE 
rare rare in cattle and horse
hepatocellular disease:
cirrhosis - plant 
toxicosis
Theiler's dz
Hemolytic crisis in cattle - only rarely:

-anaplasma vaccine
-leptospirosis in young calves (rare in adults)

-postparturient Hburia - PO4 deficiency in beef cattle
-onion poisoning 
(rare)
-anaplasmosis (rare in our area)
-bacillary Hburia - clostridium 
hemolyticum

hemolytic crisis in horse: 
red maple leaf
onion poisoning

foal neonatal isoerythrolysis

Fatty liver syndrome p 4
patient profile: 
overconditioned cattle (body score 4 or 5), periparturient period 
postcalving
history: 
herd problem: overconditioned, high energy rations 
in corn silage, high moisture corn
or
individual problem: peripartum 
disaese present - milk fever, DA, metritis, mastitis, twins, etc - these 
cows can get anorexic and fatty liver disease

chief complaints: ketosis, 
decreased milk production, weight loss, "off feed" - all nonspecific. 
occurs in early postpartum period - w/in 2 mos of calving.

again- think 
of lactation curve - no lactation until calving, then early postpartum 
period - rapid rise in milk production. this is when you see ketosis, 
fatty liver disease. the prerequisite thing in history that has to almost 
always occur to induce fatty liver is in addition to not eating much, 
there is an extra drain on energy - lactation. if cow isn't lactating, it 
is rare to develop fatty liver. also is rare during drying off. anything 
that causes her to go off feed during early lactation can predispose to 
fatty liver. the lipid in her body stores is mobilized and it goes into 
the liver, which can't process it fast enough, so the hepatocytes get 
engorged with lipid. it becomes more and more fatty. ultimately fails. 
picture cow with lots of milk production, decreased energy intake, early 
postpartum period.

ketosis almost always occurs with fatty liver. 

slide: cow dull, depressed, ears down a bit, BLV negative, lactating, 
very advanced fatty liver

predisposing factors: 
failure to restrict 
concentrate after peak lactation - cow gets obese. cows obese in dry 
period, then calve, etc
dary cows with prolonged dry periods
other 
diseases during periparturient period
slide: cow with displacement of 
abomasum

PE: good body condition, normal vital signs
hypophagia, 
hypogalactia - gradual decrease over days/week
**weight loss -- key point 
** 100-200 pounds over 7-15 days
predisposition to periparturient disease

head held high, "odd stare" in advanced case
the greater the decrease in 
weight since calving, the likelier to be fatty liver.

lab findings - 
mild ketosis
cholesterol is low (under 50, normal 90-140)
leukopenia esp 
terminally, increased bands
hypoglycemia (normal is 45)
increased blood 
ammonia (CNS signs)

slide: cow with relatively subtle signs of fatty 
liver.

fatty liver vs ketosis - when you see ketosis, there is usually 
some fatty liver with it; may or may not be significant clinically, do 
cholesterol level.
necropsy: fat accumulation, soft yellow liver, etc
see 
handout

something about nervous ketosis? have abnormal metabolite in 
blood that makes them chew on themselves, act nervous, be hyperexcitable. 
tx glucose, usually respond.

slide: pink/yellow liver, huge, disgusting, 
pale.liver like this can't function.

lipid chokes out hepatocytes, 
animals die of liver failure. see foci of neutrophils...liver can't 
detoxify endotoxin, loss of kuppfer cell function.

ketosis, abomasal 
displacements, mastitis, metritis all predispose to fatty liver.

tx of 
fatty liver - therapy: inquire about history, make clinical judgement - 
if significant wt loss, probably has fatty liver. if clinically 
significant,
maintain in positive energy balance 
provide energy by 
giving glucose
propylene glycol, sodium proprionate (3 carbon moieties, 
metabolized in rumen to form glucose -- they are glucose precurosors)

steroids - azium , dex. these decrease milk production, change energy 
balance.

note that prednisolone (Predef, Upjohn or whoever) should be 
used cautiously in postpartum cattle - may predispose to profound 
hypokalemia and hypophosphatemia
and downer cow syndrome and death.


glucose, force feeding, rumen transfaunation, forced exercise, abx for 
infxn, lipotrophic agents like choline chloride, methionine - minimal 
value but used as adjunctive therapy

client education: 
limit energy 
intake in dry period
concentrate intake limited after peak lactation
feed 
7-8 lbs hay during dry period
good reproductive management to maintain 
12-13 month calving interval

fatty liver common, often secondary to 
other postpartum diseases
key point - how much weight cow has lost in 
past few weeks.

Liver abscess in cattle:
patient profile - any age
more 
common in feedlot beef animals
also in dairy cattle
history variable, 
depending on type of abscess

four categories of these. actually, five.

see page nine.

1. clinically silent found at necropsy
2. associated with 
weight loss, anorexia
3. acute anaphylactic respiratory distress
4. 
thrombosis of caudal vena cava
5. recurrent epistaxis

the first type is 
just an incidental finding. associated with actinomyces pyogenes - thick 
white pus. some have secondary necrophora (?) organism.

type 2, some 
have pain in ventral cranial abdomen and don't ventroflex like cow with 
traumatic reticulitis. hard to dx antemortem though. 
most have profound 
hyperproteinemia

type 3 - these cows have ruptured abscess in vena cava 
causing shower of septic emboli to the lungs. cow suddenly can't breathe, 
may die acutely. this is the closest thing a cow has to a heart attack. 
she's fine, then she's dead a few minutes later. 
slide: cow looking 
really scared, tryign to breathe, eye sunken back, breathing fast, head 
sticking out.

slides of gross lungs with interestitial and interlobular 
emphysema
you can't do much for these cows with type 3.

type 4, chronic 
diarrhea and weight loss due to thrombosis of posterior vena cava. 
distended subcutaneous abdominal veins (superficial epigastric) jugular 
vein is normal, though. so not a heart problem. high total protein >8.0 
due to high gamma globulin, chronic antigenic stimulation. the abdominal 
veins are very full, very turgid. blood normally going to posterior vena 
cava and heart are now going this alternate route to the azygous into the 
chest. 

[it is now 11:50 on the nose]

liver, showing congestion

posterior vena cava - complete septic thrombus - looks gross - yellow, 
pasty, fibrinous.

type 5 - recurrent epistaxis. this syndrome also has a 
liver abscess but it breaks through posterior vc, creates septic thrombi 
that break and cause lung abscesses, presenting clinically with 
epistaxis. most common cause of recurrent epistaxis in cows are liver 
abscesses!!** can bleed a few hundred ml at a time. cows lose wt, poor 
px. generally lung abscess secondary to liver abscess.
slide: horrible 
lung, multiple small abscess present, eroding into bronchial arteries 
causing hemoptysis and epistaxis. can percuss dull areas in chest.


diagnostic rule outs - middle of pg 11.
they present with weight loss so 
rule out:
parasites in young animals (usually many animals, liver abscess 
usually one)
malnutrition (low TP, with liver high TP)
other chronic 
infection (also high TP)
heart failure (would have jugular distension)

Johne's dz - emaciation, chronic diarrhea (herd history)

diagnostic 
plan:
TP
alb/glob ratio (low, < 0.5)
enzymes little value for abscess 
(best for acute problems)
liver sonogram can detect space occupying 
lesions
laparotomy right flank

treatment: prognosis sucks
isoniazid 3-5 
mg/lb body wt per os - this is used for chronic infections in cattle, is 
relatively cheap
rifampin orally with abx, very expensive
send to 
slaughter

poor px for life.
minimize by feeding diets that do not cause 
lactic acidosis.

not in handout:
slide: liver of cow with big distended 
gall bladder full of bile. this is to show you that if you have an animal 
which dies suddenly and you do a necropsy and this is all you find, and 
bile is very thick, then you know she's been sick for days/week. if bile 
is thick, it's chronic. thin bile is normal. thick bile indicates 
chronicity. b/c of no CCK secretion, bile stasis.

---break---
regarding 
pathogenesis of liver abscesses:

make sure you understand, the cause is 
usually secondary to rumenitis.
how does rumenitis occur? most of that is 
secondary to lactic acidosis. when there is too much grain eaten, the 
rumen pH goes down, mucosa is damaged. normal flora die, new bacteria 
proliferate, animal gets dehydrated because of high starch intake with 
lots of branched chain CHO being digested by enzymes and stuff, producing 
fermentable CHO which lowers pH while increasing osmotic draw of rumen 
contents, pulling fluid into the rumen. this causes distension. the 
papillae get vesicles forming on them due to hydropic degeneration. 
bacteria get in there, leading to bacterial rumenitis. anaerobes, 
aerobes, and fungi, all together there.if it isn't a severe rumenitis it 
scars and heals. if it is significant rumenitis, blood supply from rumen 
drains to liver, carrying bacteria, setting up metastatic liver abscess. 
he mentions in handout, there are actinomyces pyogenes and necrophorus 
something organisms also in a high proportion - both can occur together. 
the main one is the sporophorus, but there can be secondary actinomyces 
pyogenes. other abscesses are almost always actinomyces - ones in other 
parts of the body. but in bovine liver abscess, 90% are spherophorus 
necrophorus (that's what it says in handout)(fusobacterium necrophorum?). 
if fungi set up in the rumen, mucor or aspergillus, cow usually dies of 
mycotic rumenitis.

once you get the liver abscess, it can invade 
posterior vena cava, cause acute respiratory distress, septic emboli with 
pulmonary abscessation and epistaxis, complete vena cava obstruction with 
chronic diarrhea, etc etc.

Theiler's disease - horses - serum hepatitis, 
acute hepatitis, acute serum hepatitis.

patient profile: adult horses, 
rarely in horse under 2yrs old. classic syndrome, often on nat'l boards 
***
history: equine serum based biologic: TAT (tetanus antitoxin) or PMS 
(pregnant mare serum) - used in at least 50% of horses with Theiler's. 
usually was given about 2 mos prior to signs. 

PE:
marked icterus

hepatic photosensitivity (photodermatitis in 10-15% of horses)
defective 
hemostasis - petechial to ecchymotic hemorrhages
hepatic encephalopathy 
** the key thing. CNS hyperexcitability is the main thing with this. 
without hepatic encephalopathy present, probably your dx is wrong. 
incoordination, compulsive walking, maniacal behavior; bizarre 
unmanageable behavior - walks through walls, very strong and weird 
behavior. may resemble intense abdominal pain and mimic colic; sluggish 
pupillary light reflex. hepatic encephalopathy occurs with more than 80% 
of horses with Theiler's, but only 30% of horses with megalocytic 
hepatitis. CNS signs are a poor prognostic sign.

100% of cases have 
icterus
44% will have hemoglobinuria (intravascular hemolysis) - West 
coast only!
67% have hepatoencephalopathy in one study
22% have 
photodermatitis (must have white skin area)

CNS signs: dullness, 
depression, muscle tremors, dysmetria, maniacal behavior, head pressing, 
pushing walls or fences or gates over. this compulsive behavior is not 
100% specific for Theiler's but is very characteristic of it. could also 
see with brain abscess (strangles), brain tumor

maniacal behavior ddx: 
Theiler's disease, rabies, encephalitis, urea poisoning. the main way to 
tell from rabies is that horses with rabies are usually not icteric. 


slide: horse with bad sunburn on nose - solar dermatitis - 2 horses in 
this barn in last 10 days died of Theiler's, then this horse had a 
sunburn so they checked his liver and found some subclinical necrosis.


photodermatitis:
primary: st john's wort/other plant
secondary: 
accumulation of phylloerythrin as with Theiler's dz.

lab findings:

bilirubin increased massively
liver enzymes increased - AST, GGT, other

fibrinogen decreased < 2-300 mg/dl
glucose decreased to normal - 100 
mg/dl - some maniacal behavior is due to hypoglycemia
prothrombin time 
increased to normal - 10-12 sec
liver bx definitive - 12-13 intercostal 
space, right side
blood ammonia increased
BUN decreased, often under 10 
mg/dl (should be 15-20)

liver looks atrophied, histologically massive 
hepatocyte necrosis and washout.
slides: histological preps of affected 
livers showing necrosis

plan: 
diagnostic rule outs:
rabies
viral 
encephalidites (dull, depressed, lethargic)
leukoencephalomalacia from 
moldy corn (dull, depressed)
plant toxicosis - yellow star thistle 
(california, oregon)
CNS parasites can sometimes cause bizarre behavior

protozoal myelitis (ataxia, not excitement)

plan:
blood glucose  (low)

liver enzymes (very high)
BUN (low)
ammonia (high)

tx: 
give glucose ** 
if nothing else, give IV glucose. at least a liter of 50% glucose and if 
they respond, repeat in a few hours. 
some horses respond to that well.

sedation - to control maniacal behavior - chloral hydrate, xylazine, 
other
oral laxatives to reduce GI ammonia: Mg sulfate, mineral oil 
(gallon)
lipotrophic agents - choline chloride  minimal value
oral 
neomycin - decrease microbial ammonia production in gut - not so helpful

fluid and electrolytes to correct acidosis.

elizabeth asked about using 
chloral hydrate. it's the old "mickey finn" from the movies. 

There is 
no particular agent associated with Theiler's - thought to be a virus but 
no one has been able to find a virus associated with the TAT or PMS or in 
these horses. but in the literature there is a frequent association w/ 60 
days previous administration of these products, and specific lots have 
lots of dz associated with it. but we think it is a virus. also, TAT is 
commonly used in foals after they're born but we do not see Theiler's in 
foals. only in horses over 2 yrs and even more so in really old mares 
-sometimes outbreaks of disease in mares over 15 yrs old, seasonal, 
highest incidence september, october, november.

prognosis not good 
unless seen early. some will survive with early intervention.

Finally - 
hyperlipemia

patient profile: obese horses, especially ponies and 
pregnant mares (90% of ponies are pregnant mares) (??); hx of high energy 
diet in excess of energy needs.
animal overweight, anorexic, off feed, 
pregnancy = energy drain, dull, depressed, injected mms, abortion, 
staggering gait, death occur.

lab data: leukopenia, hyperlipemia **, 
acidosis, hemoconcentration
this is like fatty liver in cows, but in 
horses they get hyperlipemia instead. 

assess - is animal pregnant? not 
eating? losing weight? dx by blood sample.
rule out anything causing 
anorexia
plan: measure lipids, enzymes, electrolytes - main thing is to 
see serum lipids. can see in PCV tube. 

treatment: force feed, IV 
dextrose, heparin, supportive other. need to give energy source. heparin 
is used b/c it stimulates lipoprotein lipase and moves lipid from blood 
to tissues. 

prognosis is poor, esp in severe case. to save these 
animals requires extensive therapy, fluids, electrolytes, repeat force 
feeding, until foal delivered or aborted.
reduce obesity, rule out/treat 
concurrent disease, many will develop secondary dz like salmonellosis 
which complicate the problem. 

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