3 CE

CREDITS CE Article 2

Treating Acute Colitis*

❯❯ R
 . P. Atherton, BVSc, Abstract: Acute colitis is a therapeutic challenge for equine veterinarians. A plethora of therapies
MSc, DACVIM, MRCVS are available, but treatment may vary because a definitive diagnosis may be elusive. In addition,
Lingfield Equine Vets, Chester
treatment of horses with acute colitis is intensive and often costly. This article discusses (1) a
Lodge, Felbridge, Surrey,
United Kingdom logical approach to treatment and (2) the therapeutic options available to equine clinicians. The
prevention and treatment of complicating sequelae, such as laminitis and endotoxemia, are dis-
❯❯ H
 . C. McKenzie III, cussed and must be considered in the patient’s prognosis.
DVM, MS, DACVIM
❯❯ M
 . O. Furr, DVM,
PhD, DACVIM

F
Marion duPont Scott Equine or many equine diseases, the goal Fluid Therapy
Medical Center, Virginia- of treatment is to target the under- When the integrity of the gastrointestinal
Maryland Regional College of lying etiology; however, in cases of (GI) barrier is compromised, fluid shifts
Veterinary Medicine acute colitis, a definitive diagnosis may from the intravascular compartment to
not be determined and was made in only the interstitial compartment, which can
At a Glance 35% of cases in one report.1 Appropriate have catastrophic effects. Depending on
diagnostic tests may identify specific time to clinical assessment and the sever-
Fluid Therapy
Page 416 infectious organisms, but often not in a ity of disease, signs of hypovolemia may
timely manner. Because the condition be apparent only within the intravascular
Electrolyte Supplementation
can be fatal, treatment must be initiated space (i.e., poor systemic perfusion and
and Correction of Acid–Base
before results are obtained. The primary pulse quality) or may manifest as clinical
Derangements
Page 418 treatment goals for acute colitis are as hypovolemia (TABLE 1). In cases of mild to
follows: moderate hypovolemia of short duration
Colloidal Support
Page 419
M
 aintenance of fluid and electrolyte
Antiinflammatory Therapy
Page 420
balance TO LEARN MORE
P
 reservation of colloid oncotic pressure
Analgesic Therapy and replacement of plasma protein
Page 420
C
 ontrol of local and systemic inflammation
Antidiarrheal Therapy P
 romotion of tissue perfusion
Page 421
P
 romotion of mucosal repair
Probiotics N
 utritional management
Page 421

Antimicrobial Therapy All patients with acute colitis require

Page 421
intensive care, and even if the primary
Treating Common Sequelae treatment is effective, sequelae associated
of Acute Colitis with the disease can limit a horse’s future
Page 422
performance or can be severe enough to  onsultant’s Corner: How Do
C
Nursing Care and Nutrition require euthanasia. The cost of treatment I Diagnose and Manage Right
Page 424 can rise quickly, and the total bill may Dorsal Colitis? (Winter 2006)
Response to Therapy easily approach that for colic surgery.
Page 424 Related content on
*Companion articles on the patho­physiology and
Prognosis and Outcome noninfectious causes as well as the infectious CompendiumEquine.com
Page 425 causes appeared in the October 2009 issue.

416 Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com
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Treating Acute Colitis CE

table 1 Clinical Assessment of Hypovolemia

Degree of Hypovolemia
Parameter Mild Moderate Severe
Skin turgor Good to fair Fair Poor
Mucous membrane Good to fair Tacky Dry
moisture
Capillary refill time 1–2 sec 2–4 sec >4 sec
PCVa 40%–50% 50%–65% >65%
Total plasma proteina 6.5–7.5 g/dL 7.5–8.5 g/dL >8.5 g/dL

Heart rateb 40–60 bpm 60–80 bpm >80 bpm

Pulse quality Good (easily palpated Fair (slightly weak with Poor (weak/thready and
and turgid) decreased tone) difficult to palpate)
a Normal packed cell volume (PCV) depends on the horse’s breed and level of athletic training. Thoroughbreds and
Standardbreds in training have normal PCVs up to 45%. The normal PCV of draft breeds can be 25%–30%. Splenic
contraction and hypoproteinemia may affect PCV and total protein, respectively.
bHeart rate is also affected by the horse’s pain level.

without continued GI dysfunction and ongoing quantitative means of accurately determining

losses, simple replacement of the calculated
fluid deficit with an isotonic crystalloid solution
may be adequate to restore fluid and electro-
lyte homeostasis (BOX 1). Typically, a polyionic,
isotonic, crystalloid fluid (e.g., Normosol-R
[Baxter Healthcare], lactated Ringer’s solution)
can be used as an initial replacement fluid.2
The volume of fluid to administer should be
estimated based on the replacement deficit/
degree of hypovolemia, maintenance require-
ments, and anticipated ongoing losses.
A general guide for fluid replacement dur-
ing initial resuscitation is 10 to 20 mL/kg/h,
but rates of 20 to 45 mL/kg/h might be indi-
cated in a profoundly hypovolemic patient.
These high rates of fluid administration should
be used only for the first 2 to 3 hours of treat-
ment, during which the goal is to replace the
calculated fluid deficit. Once a fluid volume
equal to the calculated fluid deficit has been
administered, ongoing fluid losses must be
assessed and the fluid rate switched to a main-
tenance rate that accounts for the patient’s
basal metabolic needs and ongoing losses.
Prolonged fluid administration at a rate above
10 to 20 mL/kg in a patient without substan-
tial fluid losses may result in edema, especially
because many colitis patients have hypopro-
teinemia and diminished colloidal oncotic
pressure. During colitis, fluid is lost into the
colon wall and the GI lumen, so there is no
ongoing fluid losses, which can be as high as
150 mL/kg/d.3 Frequency, consistency, and vol-
ume of diarrhea per episode are useful subjec-
tive indicators; high-volume, high-frequency,
watery diarrhea indicates that a large volume
of fluid has been lost from the colon.
Most cases of acute colitis require a fluid
rate two to three times the maintenance rate
once the deficit has been replaced due to
ongoing water loss through diarrhea; however,
this rate varies from patient to patient and can
be reduced with clinical improvement. Close
monitoring of the patient’s hydration status
by assessing capillary refill time and cardio-
Box 1
Calculating Fluid Deficit and Formulating
a Fluid Replacement Plan
Replacement fluid volume (L) = Body weight (kg) × % Hypovolemia ÷ 100 (L/kg)
Replacement fluid rate = 10–20 mL/kg/hr
Maintenance fluid volume = 50–100 mL/kg/day
Rate of maintenance fluid administration = 2–4 mL/kg/hr
Example:
A 500-kg horse is 5% hypovolemic.
Replacement fluid volume (L) = 500 kg × 5% Hypovolemia ÷ 100 = 25 L
Replacement fluid rate (hr) = 10–20 mL/kg/hr × 500 kg/1000 mL/L =
5–10 L/hr for 2.5–5 hr
Maintenance fluid volume (L/day) = 50–100 mL/kg/24 hr × 500 kg/1000 mL/L =
25–50 L/day
Maintenance rate (L/hr) = 2–4 mL/kg/hr × 500 kg/1000 mL/L = 1–2 L/hr

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CE Treating Acute Colitis
vascular parameters (e.g., heart rate, pulse
quality) is essential to ensure an appropriate
fluid rate. Indirect blood pressure monitoring
is also useful for assessing response to treat-
ment. Measurement of packed cell volume
(PCV) and total protein concentration (TP) is
quick, inexpensive, and clinically useful for
monitoring hydration status. However, while
increased PCV and TP suggest hypovolemia,
these values may be lower than expected due
to intravenous fluid therapy and hypoproteine-
mia secondary to colitis. In very mild cases
of acute equine colitis, the volume of each
fecal episode and the frequency (e.g., five to
six times per day) of diarrhea are only moder-
ate, so the patient can maintain an acceptable
hydration state without supplementary intra-
venous crystalloid fluid therapy.
When a fluid therapy plan is designed, it
is important to remember that sodium-con-
taining fluids rapidly exit the vasculature to
CriticalPo nt equilibrate with extracellular fluid, and only
25% of these fluids remain in the intravascu-
Fluid therapy is lar space. Therefore, if ongoing fluid losses
the most important are significant, adequate colloidal support
treatment for acute (e.g., plasma) and electrolyte supplementation
equine colitis. must be provided.2 In severely hypovolemic
equine patients, hypertonic saline (1 to 2 L of
7% sodium chloride [NaCl]) can expand intra-
vascular blood volume, increasing systemic
blood pressure and cardiac output. Circulating
fluid volume can be rapidly increased as fluid
moves from the extracellular space into the
vascular compartment in response to hyper-
tonic solution in the vascular space.4 However,
after administration of hypertonic saline, it
is imperative to quickly administer crystal-
loid fluids to replenish fluid from the extra-
cellular space and maintain intravascular fluid
volume.
Electrolyte Supplementation and Correction
of Acid–Base Derangements
Horses with colitis often have marked electro-
lyte deficiencies, which can be exacerbated by
aggressive fluid therapy. Diminished absorp-
tion and increased secretion via the GI tract
lead to a net loss of serum sodium, chloride,
potassium, calcium, and bicarbonate into the
colonic lumen. Clinical signs do not adequately
predict the patient’s need for electrolyte
supplementation, so this should be deter-
mined from measured plasma concentrations.
418 Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com
Ongoing monitoring throughout the course
of the disease is also essential. The recom-
mended supplementation rate differs for each
ion. Potassium is typically supplemented using
potassium chloride (KCl). The starting supple-
mentation rate should be determined from the
serum potassium concentration after clinical
rehydration of the patient, and the clinician
should be careful to account for the ongoing
loss of potassium, especially in an inappetent
patient. In most cases, adding KCl to intrave-
nous fluids at a concentration of 20 mEq/L
is appropriate for replacement therapy. More
severe hypokalemia can be treated by increas-
ing the KCl concentration to 40 mEq/L, but
care must be taken not to exceed an adminis-
tration rate greater than 0.5 mEq/kg/h.5
Hypocalcemia is usually treated with intra-
venous administration of 23% calcium gluco­
nate solution. Daily administration of 100 to
300 mL (2.14 to 6.42 g) is typically required
in equine patients with ongoing GI losses, but
the amount depends on the severity of dis-
ease and the patient’s nutritional intake.6 The
calcium gluconate solution is typically added
to the intravenous fluids that the patient is
already receiving, but calcium-containing so­lu­
tions cannot be used concurrently with bi-
carbonate-containing solutions because this
results in formation of calcium carbonate pre-
cipitate. Some horses with severe colitis remain
hypocalcemic despite aggressive calcium sup-
plementation, so ongoing monitoring of the
ionized calcium concentration is indicated.
Excessively rapid calcium administration may
result in cardiovascular complications, particu-
larly in septic horses, which may be more vul-
nerable to toxic effects of calcium. However, a
calcium dose of 1 to 2 mg/kg/h is considered
safe, and Toribio et al7 have induced hypercal-
cemia in horses with rapid administration of
calcium gluconate with no obvious complica-
tions. Concurrent administration of fresh-fro-
zen plasma or blood results in a transient fall
in the number of divalent cations as a result of
chelation by citrate.8
Magnesium is typically supplemented using
magnesium sulfate (MgSO4). A recommended
dosage of intravenous MgSO4 in adult horses is
25 to 150 mg/kg/d (12.5 to 75 g/d for a 1100-lb
[500-kg] horse), and MgSO4 can be added to
the crystalloid fluids that the horse is already
receiving.9 Magnesium is already added to some

crystalloid fluids (e.g., Normosol-R), so this
must be considered when calculating the rate
of magnesium supplementation.
When sodium is supplemented beyond
what is contained in primary resuscitation flu-
ids, it is important to remember that in other
species, rapid correction of sodium deficits
has been shown to cause demyelination of
pontine and extrapontine neurons, resulting
in severe neurologic dysfunction.10 This con-
cern is greatest when the patient is profoundly
hyponatremic (serum Na+ concentration: ≤120
mEq/L). A simple guideline for clinical use is
to calculate the sodium deficit using the fol-
lowing equation:
Normal serum sodium concentration –
Actual serum sodium concentration =
Sodium deficit (mEq/L)
The result can be used as a guideline; for
example, a deficit of 20 mEq/L should be
replaced over no fewer than 20 hours and
a deficit of 15 mEq/L over no fewer than
15 hours. Hypertonic saline (5%) or sodium
bicarbonate (5% or 8.5%) solutions are used
for sodium supplementation; NaCl may be
used when hyponatremia is accompanied by
hypochloremia, and sodium bicarbonate may
be used when the serum chloride concentra-
tion is normal or increased. To avoid excessive
or overly rapid correction of the serum sodium
concentration, the plasma sodium concentra-
tion should be carefully monitored. We rec-
ommend taking a repeat blood sample 6 to 8
hours after initiating corrective fluid therapy
and every 12 hours thereafter until the sodium
concentration is within normal limits.
Acid–base disturbances in colitis patients
are primarily corrected by addressing the
primary disease process and the associated
sequelae, such as hypovolemia. Metabolic aci-
dosis frequently accompanies acute colitis due
to (1) the colon’s failure to resorb bicarbonate
and (2) lactate buildup in the tissues second-
ary to poor tissue perfusion and anaerobic
metabolism associated with endotoxemia. Cor-
rection of hypovolemia is an important com-
ponent of therapy for acid–base disorders
in diarrheic patients. If correction of hypo­
volemia is not accompanied by correction of
acid–base abnormalities, additional therapy
will be required to correct plasma imbalances.
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Treating Acute Colitis CE
For example, hyponatremia leads to metabolic
acidosis, so sodium supplementation should
help resolve acidosis. Similarly, albumin is a
weak acid, so severe hypoalbuminemia may
contribute to metabolic alkalosis or mask con-
current metabolic acidosis; therefore, protein
supplementation should correct the acid–base
imbalance.11 Persistence of acidosis despite
correction of oral or intravenous supplemen-
tation should prompt the clinician to reassess
the source of the pH abnormality (i.e., Is it
respiratory or metabolic acidosis?). In addition,
the clinician should address the underlying
cause of this physiologic imbalance by treat-
ing the primary disease process.
Oral administration of fluids is an effective
and economical adjunct to intravenous fluid
administration. Once severe electrolyte or acid–
base disturbances have been corrected, horses,
if given a choice, often elect to drink a solution
containing the electrolyte in which they are
deficient. The following “water buffet,” includ-
ing an assortment of electrolyte-supplemented
CriticalPo nt
water solutions, can be offered free choice: Many adjunctive
anecdotal thera-
P
 lain water pies are available
W
 ater with 6 to 10 g/L Lite Salt (iodized NaCl for treating acute
and KCl; Morton)
colitis, but clinical
W
 ater with 10 g/L baking soda (sodium
bicarbonate)
evidence supporting
W
 ater with 6 to 10 g/L plain salt (NaCl)
their use is limited.
Colloidal Support
Because of GI losses and serum albumin
catabolism, many horses with acute colitis
are hypoproteinemic. Additionally, absorption
of bacterial products may induce systemic
inflammatory response syndrome (SIRS), lead-
ing to increased vascular permeability and low
plasma oncotic pressure. A large volume of
crystalloid fluids causes hemodilution, contrib-
uting to decreased plasma oncotic pressure.12
In contrast, colloids preserve colloidal oncotic
pressure, resulting in more effective volume
expansion.2 Commercial colloids include plas­-
ma, dextran 40, dextran 70, hydroxyethyl
starch (hetastarch), and polymerized bovine
hemoglobin. The duration of oncotic support
provided by a colloid is affected by the severity
of inflammation in the colon and by resultant
molecular loss from the circulation. Hetastarch
(up to 10 mL/kg/d) has been shown to increase
colloidal oncotic pressure for up to 24 hours in
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CE Treating Acute Colitis
hypoproteinemic horses. Experimental studies
suggest hetastarch may be superior to plasma
in stopping endotoxin-induced increases in
vascular permeability.2 This is due to the larger
molecular size of polymers in hetastarch and,
perhaps, to its ability to attenuate permeabil-
ity dysfunction associated with endotoxemia.
Caution is indicated, as higher doses of het-
astarch (>20 mL/kg total cumulative dose) may
prolong bleeding by altering von Willebrand’s
factor function.2
Intravenous administration of plasma pro-
vides protein (albumin and globulins) as well
as other beneficial elements, such as coagula-
tion factors. Acute colitis is probably the most
common disease associated with disseminated
intravascular coagulation (DIC) in horses. In
one study, the 1-year incidence of subclini-
cal DIC in horses with acute colitis was 32%.13
There is no published dose of plasma for cor-
rection of hypoproteinemia in adult horses;
CriticalPo nt however, as a guideline, equine patients with
acute colitis require 10 to 15 mL/kg of plasma
Prevention and to raise their TP approximately 1 g/L. Close
treatment of the monitoring of the patient’s plasma protein is
devastating seque- essential, as ongoing GI losses may require
lae of acute colitis repeated doses of plasma. Fresh-frozen com-
mercial equine plasma is readily available from
are crucial to opti-
various sources. Adverse effects of plasma
mizing a patient’s administration in horses are uncommon but
chance of survival. may include immune-mediated reactions and
changes in hemostatic variables.14
Antiinflammatory Therapy
The NSAIDs typically used in equine patients
inhibit cyclooxygenase (COX) 1 and 2, which
are responsible for producing vasoactive and
proinflammatory prostanoid compounds, such
as prostaglandin I2 (PGI2), prostaglandin E2
(PGE2), and thromboxane. Suppression of this
process can help break the self-perpetuating
inflammatory cycle within inflamed colonic
mucosa and allow GI mucosa to heal. However,
evidence suggests that certain prostaglandins,
such as PGI2 and PGE2, are cytoprotective to
GI mucosa and critical for mucosal repair;
therefore, using COX inhibitors to block pros-
taglandin production in these tissues may
exacerbate GI pathology.15 It is unclear whether
the benefits of NSAID therapy outweigh the
limitations; however, many horses with colitis
may initially require analgesia. Similar to the
standard dose of flunixin meglumine (1.1 mg/
420 Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com
kg IV q12h), the low dose (0.25 mg/kg IV q8h)
has been shown to decrease eicosanoid pro-
duction and ameliorate some clinical signs of
systemic inflammation following exposure to
intravenous endotoxin. The low dose is also
thought to be less likely to impair tissue blood
flow in the GI mucosa; therefore, the low dose
may be safer than the standard dose.16
Other antiinflammatory therapies for equine
acute colitis include the free radical scavenger
dimethyl sulfoxide (DMSO; 1 g/kg IV q12–24h
as a 10% solution), the antimicrobial metro­
nidazole (20 mg/kg PO q8h; 10–25 mg/kg
PO q6–12ha; 15–25 mg/kg PO q6hb),17,18 the
prokinetic and analgesic lidocaine (1.3 mg/
kg over 15 min, then 0.05 mg/kg/min), and
the PGE1 analogue misoprostol (5 µg/kg q8h).
Experimental evidence for these therapies is
limited, but they may be of clinical value.
Analgesic Therapy
Many horses with acute colitis develop mild
to severe signs of abdominal discomfort from
gas and fluid distention of the colon, colonic
is­chemia, and infarction. NSAIDs are com-
monly used, particularly flunixin meglumine
(1.1 mg/kg IV or PO q12h) because of its anti-
inflammatory effects compared with the effects
of phenylbutazone or ketoprofen.16,19 However,
NSAIDs impair prostaglandin production by
the kidneys, inhibiting normal renal blood
flow. Overdosage or misuse of NSAIDs, espe-
cially in hypovolemic patients, can lead to
renal crest necrosis and may increase the risk
of acute tubular nephrosis during hypovolemia
or aminoglycoside administration. Therefore,
low-dose flunixin meglumine may be better to
use than the standard dose in some patients.
Alternative analgesics include lidocaine,
α2-agonists (e.g., xylazine, detomidine), and
opioids (e.g., butorphanol). These are all con­
sidered to be short acting, but constant-rate
in­fusion may be used to provide sustained clini-
cal analgesia. However, opioids and α2-agonists
decrease GI motility, so patient comfort and
fecal output should be monitored.
aIn:Robinson NE, Sprayberry K, eds. Current Ther-
apy in Equine Medicine. 6th ed. Philadelphia: WB
Saunders; 2008.
bSweeney RW, Soma LR, Woodward CB, Charlton
CB. Pharmacokinetics of metronidazole given to
horses by intravenous and oral routes. Am J Vet Res
1986;47(8):1726-1729.

Antidiarrheal Therapy
Bismuth Subsalicylate
Bismuth subsalicylate is commonly adminis-
tered orally to equine patients with colitis to
decrease inflammation and secretion in the
colon. In a double-blind, placebo-controlled
study in children with acute diarrhea, this drug
was shown to significantly decrease the time
to the last watery stool.20 The precise mecha-
nism of action of bismuth subsalicylate in any
species is unclear, but the salicylate moiety
may have an antisecretory action in the large
colon, where it stimulates fluid and electrolyte
absorption.21 In addition, salicylic acid inhibits
prostaglandin synthesis, which is responsible
for intestinal inflammation and hypermotil-
ity, and modulates oxidative stress in colonic
mucosal cells.22 Furthermore, the drug and
its intestinal reaction products, bismuth oxy-
chloride and bismuth hydroxide, appear to be
bacteriocidal in vivo and in vitro.21 Based on
extrapolation from human medicine, the dose
required in adult horses is large (3 to 4 L by
stomach tube q4–6h)20; however, the drug
is also available as a concentrated paste. In
humans, bismuth subsalicylate is considered
extremely safe. A feeding trial in which mice
were fed 60 times the maximal recommended
human dose did not result in adverse effects,
and no histopathologic lesions were noted
in the brains on postmortem examination.23
Bismuth subsalicylate toxicosis in horses has
not been reported.
Di-Tri-Octahedral Smectite
Di-tri-octahedral smectite is a natural hydrated
aluminomagnesium silicate with a lamel-
lar structure. It binds to digestive mucus and
increases intestinal resistance to bacterial dam-
age.24 The drug has been shown to increase
water and electrolyte absorption in rabbit
intestinal loops in the presence of Escherichia
coli infection; a preliminary study in horses
reported that administration of di-tri-octahe-
dral smectite prevented lincomycin-induced
colitis in four horses, whereas four untreated
horses died or were euthanized due to severe
colitis.24,25 In vitro studies have shown that di-
tri-octahedral smectite can bind Clostridium
difficile toxins A and B as well as Clostridium
perfringens enterotoxin and endotoxin.26 The
current recommendation for a 1000-lb (454.5-
kg) horse is administration of a solution of 1 lb
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Treating Acute Colitis CE
of Bio-Sponge (Platinum Performance) and 3 L
of water via nasogastric tube q6–12h.
Probiotics
Restoring the microbial ecology of the colon
has recently attracted experimental interest,
leading to the use of many different agents
(e.g., commercial probiotic pastes, live-culture
yogurt) and techniques (e.g., transfaunation).
In transfaunation, freshly harvested colonic or
cecal contents (5 to 6 L) or a slurry of fresh
feces from a healthy horse is administered via
nasogastric tube to the patient to restore nor-
mal GI flora. Transfaunation has had reported
clinical success in cattle but has not been
reported in diarrheic horses.27
There is little supportive evidence for the
use of commercial probiotic pastes in horses,
and one study in foals found the pastes to be
detrimental.28 In comparison, Saccharomyces
boulardii is a nonpathogenic yeast that has
been used prophylactically and therapeuti-
cally as an antidiarrheic agent in humans since
CriticalPo nt
1962.29 Experimentally, the yeast has been In a double-blind,
found to survive within the equine GI tract, and placebo-controlled
the severity and duration of acute enterocoli- study in children
tis were significantly decreased in horses that with acute diarrhea,
received S. boulardii compared with horses
this drug was shown
that received a placebo.29 S. boulardii has been
found to release a protease that can digest C.
to significantly
difficile toxins A and B; additional mecha- decrease the time
nisms of action include an immunoprotective to the last watery
effect attributed to promoting the release of stool.
secretory immunoglobulins within the intes-
tine or activation of the reticuloendothelial
and complement systems.30,31 Because phar-
macokinetic studies with S. boulardii have not
been performed in horses, the equine dose is
extrapolated from the human literature. One
study reported the use of an S. boulardii dose
of 25 g (10 × 109 yeast cells) PO q12h for 14
days in horses with acute colitis, resulting in
no clinical adverse effects and in significant
improvement in the severity and duration of
GI disease compared with a placebo group of
horses.29
Antimicrobial Therapy
Antimicrobial therapy is hotly debated in
many cases of acute colitis. In cases with
concurrent neutropenia, it is thought that the
host’s defenses may be weakened sufficiently
to render the horse susceptible to organisms
421
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that breach the mucosal barrier; therefore,
some clinicians recommend broad-spectrum
antimicrobial coverage. However, antimicro-
bials can have adverse GI effects in horses.32
Antimicrobial administration has been reported
to prolong shedding of Salmonella spp in
experimentally infected ponies, and there are
many reports of antimicrobial-induced diar-
rhea in horses.32
For certain infectious causes of acute colitis
in horses, such as Potomac horse fever (equine
monocytic ehrlichiosis) and Clostridium infec-
tions, antimicrobial therapy is required to
address the underlying cause. Neorickettsia
risticii, which causes Potomac horse fever, is
highly sensitive to tetracyclines (e.g., oxytet-
racycline dosed at 6.6 mg/kg IV q24h for 5
days).33 Clostridium spp, namely C. difficile
and C. perfringens, have been shown to be
eradicated using metronidazole (minimum
inhibitory concentration: ≤4 mg/mL34; com-
CriticalPo nt monly used dosage: 20 mg/kg PO q8h), and
in vitro evidence suggests efficacy of chloram-
Experimentally, the phenicol (50 mg/kg PO q6h).35 Antimicrobial
yeast has been use must be decided on a case-specific basis,
found to survive with consideration for the most likely etiol-
within the equine GI ogy, including the most common agents in the
area, the season of the year, and the history
tract, and the sever-
and clinical presentation.
ity and duration of
acute enterocolitis Treating Common Sequelae of Acute Colitis
were significantly Because of the severity of systemic illness asso-
decreased in horses ciated with acute colitis, complicating issues
that received S. are frequently encountered, the most common
boulardii compared of which are endotoxemia, thrombophlebitis,
with horses that and laminitis. Preventive or therapeutic mea-
sures must address these sequelae to optimize
received a placebo.
the patient’s chance of survival.
Endotoxemia is a well-recognized com-
plication of GI disease, particularly diseases
involving GI inflammation or ischemia, such
as acute colitis. A horse’s intestinal tract nor-
mally contains a large number of gram-nega-
tive bacteria that release endotoxin when they
die or multiply rapidly. The endotoxin is nor-
mally restricted to the intestinal lumen by an
efficient intestinal mucosal barrier; however, if
some endotoxin crosses the mucosal barrier,
it enters the portal system and is removed by
hepatic mononuclear phagocytes without initi-
ating systemic signs in the horse.36 If the intes-
tinal barrier is impaired (e.g., inflammation,
ischemia), endotoxin translocates more sig-
422 Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com
nificantly into the circulation, and the hepatic
clearance mechanism becomes overwhelmed,
leading to endotoxemia as well as synthesis
and release of inflammatory mediators.
Four therapeutic approaches should be
considered when addressing endotoxemia.
The first approach is to prevent absorption of
endotoxin into the circulation by treating the
primary cause of the GI disease. The second
approach is neutralization of endotoxin before
it interacts with inflammatory cells. Polymyxin
B has shown some promising endotoxin-neu-
tralization effects in vitro and in vivo, appear-
ing to be clinically useful in decreasing the
inflammatory response to endotoxin expo-
sure.37 However, polymyxin B must be used
judiciously due to its inherent toxic effects
on neural and renal tissues.38 Polymyxin B
is administered at a rate of 1 mg (6000 U)/
kg diluted in 1 L of sterile saline solution IV
q8h and is typically discontinued after 1 or
2 days of therapy39; however, many clinicians
administer the drug every 12 hours to prevent
adverse effects. Doses below 6000 U/kg may
be effective and less nephrotoxic.40 Although
few experimental data are available to sup-
port the in vivo use of antilipopolysaccha-
ride (anti-LPS) hyperimmune equine plasma,
it provides antibodies that target the endo-
toxin and appears to have bacteriocidal activ-
ity.40,41 The third approach is prevention of the
synthesis, release, or action of inflammatory
mediators that follow endotoxin exposure and
are responsible for SIRS. This approach has
included the use of NSAIDs, corticosteroids,
monoclonal antibodies directed against cyto­
kines, platelet-activating factor receptor antag-
onists, pentoxifylline, and naturally occurring
nontoxic endotoxins. However, all of these
interventions have demonstrated only limited
efficacy,42 and only flunixin meglumine has
become clinically accepted. The fourth and
most clinically important approach to endo-
toxemia is appropriate supportive care. This
helps minimize organ dysfunction second-
ary to severe SIRS, which is characteristic of
endotoxemia.
Abdominal pain associated with colitis may
result in stall rolling, excessive catheter move-
ment, and contamination or disconnection of
the intravenous line. Patients with acute coli-
tis can be at high risk for thrombophlebitis
(inflammation of the vein with thrombus for-

mation) because of associated general debili-
tation, lowering of the head for prolonged
periods, and placement of an indwelling cath-
eter for several days or weeks.43 In addition, a
large volume of intravenous fluids and intrave-
nously administered drugs can cause turbulent
blood flow and irritate vascular endothelium
at the catheter tip. Patients with colitis may be
predisposed to venous thrombosis because of
endotoxemia-associated loss of anticoagulants
in the bloodstream and systemic activation
of procoagulants.44 No studies have proven
that type of catheter material is a risk factor
for thrombophlebitis in horses, but polyure-
thane, over-the-wire catheters are assumed to
have less risk. If thrombophlebitis develops,
the use of topical antiinflammatory therapies
(e.g., DMSO), systemic anticoagulants (e.g.,
aspirin), and antimicrobials is advisable but
has not been experimentally confirmed to be
beneficial.
Laminitis is the primary reason for eutha-
nasia in many colitis cases.44 Prevention and
treatment of laminitis are controversial, pri-
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Treating Acute Colitis CE
marily because the exact pathophysiology of
the condition is unclear. To effectively prevent
laminitis, clinicians must be aware that patients
with colitis are at high risk of developing it.
Preventives include vasodilator administration,
CriticalPo nt
corrective hoof trimming and shoeing, deeply For certain infec-
bedded stalls, and frog support. Many of these tious causes of
measures are also used therapeutically. acute colitis in
Venodilatory therapy, namely low-dose ace­- horses, such as
promazine (0.03 to 0.06 mg/kg IM q6–8h),
Potomac horse
isoxsuprine hydrochloride (1.2 mg/kg PO
fever (equine mono-
q12h), or topical glyceryl trinitrate cream
(2-cm strip applied to the back of the pas- cytic ehrlichiosis)
tern of the affected feet q6–8h), should the- and Clostridium
oretically reduce venous resistance in the infections, antimi-
feet, decrease capillary pressure, and dimin- crobial therapy is
ish abnormal fluid movement within laminar required to address
tissue.45 Conversely, blood flow to the feet the underlying
can be decreased or altered by dramatically cause.
cooling the feet with ice-packed boots. The
associated mechanism of action is thought
to be induction of hypometabolism of lami-
nar tissue, thereby decreasing proteolytic and
neutrophil enzyme activities, inflammatory
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CE Treating Acute Colitis
Box 2
Technician Tips
Many hospitals provide frequent supportive
care and intensive care unit checks.
Examples of supportive care checks
Is the patient eating well?
Are there signs of deterioration?
Examples of intensive care unit checks
Are there signs of colic (pawing, rolling)?
How much is the patient drinking?
Is there fever?
Is the heart rate or respiratory rate in-
creased?
Are there signs of inflammation or infection
at the intravenous catheter site?
What is the frequency and consistency of
diarrhea?
Are there signs of laminitis?
cytokine activity, and metalloproteinase activ-
ity, which have been found to be increased
in laminitic feet.46 Applying supportive pads
to the feet, trimming the hooves, and using
soft bedding may decrease mechanical shear
forces on the laminae, limiting the predisposi-
CriticalPo nt tion to or exacerbation of laminitis. Inhibiting
neutrophil adhesion to endothelial cells with
Because of the the use of pentoxifylline, lidocaine, or flunixin
severity of systemic meglumine could also have some prophylactic
illness associated value.47,48 If a horse with acute colitis develops
with acute colitis, laminitis, treatment should be directed at pain
complicating issues control and ongoing correction of the underly-
ing cause. Historically, phenylbutazone (2.2 to
are frequently
4.4 mg/kg IV or PO q12h) has been regarded
encountered, the
as the best NSAID for treating pain and inflam-
most common of mation associated with laminitis; however, it is
which are endotox- important to consider using available COX-2–
emia, thrombophle- selective NSAIDs such as firocoxib (Equioxx,
bitis, and laminitis. Merial) and meloxicam (Metacam, Boehringer
Ingelheim). Further research may show COX-2
inhibitors to be superior and safer.49 Lateral
radiographs of the feet illustrating rotation
or sinking of the pedal bone in addition to
response to analgesic therapy are key prog-
nostic indicators in laminitic cases.
Nursing Care and Nutrition
Good nursing care and nutrition are essential
to a successful outcome for equine patients
with acute colitis (BOX 2). The goal of enteral
424 Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com
nutrition should be to avoid overloading the
poorly functioning colon; this can be achieved
by feeding small, frequent meals with a pre-
dominantly pellet base. Feeds with greater
digestibility decrease the amount of undi-
gested concentrate that reaches the cecum,
where fermentation may exacerbate diarrhea.
Hay can be fed but should be high-quality
grass hay. Feeding hay may help produce
volatile fatty acids (propionate, butyrate, ace-
tate) within the colon; these compounds are
important for normal functioning of colonic
mucosa. Because many colitis patients are
anorectic and the severity of the disease can
result in catabolism, corn oil can be added to
the diet to increase caloric intake. If a patient
remains anorectic for longer than 3 to 4 days
despite therapy, parenteral nutrition should
be provided. In addition, gastroprotectants
such as sucralfate (1 g/45.5 kg PO q6–8h) and
omeprazole (4 mg/kg PO q24h) are useful for
improving appetite and treating gastric ulcers,
if present, due to inappetence.
Response to Therapy
Response to therapy is determined by frequent
monitoring of clinical signs, clinicopathologic
data, and fecal water content. Signs of improve-
ment are decreased fever, stability of serum
electrolyte concentrations, acid–base balance,
and improved appetite. Clinicopathologically,
one of the earliest signs of improvement can
be a decreased number of morphologically
“toxic” neutrophils. Decreases in fecal water
content and frequency of diarrhea suggest
clinical improvement. Acute colitis can have
an infectious cause, so equine patients may
continue shedding the infectious agent even
when diarrhea has resolved, thereby putting
other horses at risk.50 Repeated diagnostic test-
ing should be considered before removing a
horse from isolation. Because salmonellosis
patients shed Salmonella spp intermittently,
a series of five fecal cultures obtained on
different days should have negative results
before isolation protocols are discontinued.50
Alternatively, three consecutive fecal samples
can be obtained 24 hours apart and submitted
for polymerase chain reaction (PCR) testing
to test for Salmonella spp. This method can
provide a level of confidence similar to that
obtained by testing five samples by culture.51
Because watery feces are difficult to culture

for Salmonella spp due to a dilutional effect,
samples for culture or PCR testing should con-
tain at least 5 to 10 g of feces. The usefulness
of repeat testing in clostridiosis cases has not
been critically evaluated, but obtaining nega-
tive results from a fecal sample following reso-
lution of diarrhea helps ensure that the risk of
shedding has decreased. Because salmonello-
sis is highly contagious, many hospitals have
an infectious disease, environmental monitor-
ing protocol.
Prognosis and Outcome
The substantial mortality rate and treatment
expense associated with acute enterocoli-
tis underscore the importance of identifying
equine patients with a poor prognosis for sur-
vival. Patients that recover from acute colitis
typically show clinical improvement within
3 to 6 days after treatment begins.5,52 The
following clinical signs suggest a guarded
prognosis: azotemia, clinicopathologic find-
ings consistent with hemoconcentration and
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Treating Acute Colitis CE
hypoproteinemia (e.g., a persistent PCV >50%
and TP <6.2 g/dL), and failure to show demon-
strable signs of improvement after 10 days of
therapy.5,52 Certain types of colitis, including
necrotizing enterocolitis and antimicrobial-
associated diarrhea, have been associated with
low survival rates.52 If a horse survives acute
colitis without developing sequelae such as
laminitis, ongoing health issues are unlikely.
Conclusion
Managing equine patients with acute coli-
tis can be challenging due to the intensity of
care involved and the concerns regarding dis-
ease transmission. Many different treatments
are available for this condition; although the
efficacy of some treatments is unclear, clini-
cians have the opportunity to explore different
therapeutic approaches, making acute colitis
rewarding to treat. It is important to remember
that if the patient responds to therapy in the
first few days, the prognosis for a full recovery
is favorable.
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CE Treating Acute Colitis
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22. Drew JE, Arthur JR, Farquharson AJ, et al. Salicylic acid modu-
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23. Bierer DW. Bismuth subsalicylate: history, chemistry, and safe-
ty. Rev Infect Dis 1990;12(suppl 1):S3-S8.
24. Rateau JG, Morgant G, Droy-Priot MT, et al. A histological, en-
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coprotective clay, on experimental infectious diarrhoea in the rabbit.
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25. Herthel D. Treatment of clostridial colitis with smectite. Proc 6th
Annu Colic Res Symp 1998:12.
26. Weese JS, Cote NM, deGannes RV. Evaluation of in vitro prop-
erties of di-tri-octahedral smectite on clostridial toxins and growth.
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27. Rager KD, George LW, House JK, et al. Evaluation of rumen
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myces boulardii for treatment of horses with acute enterocolitis. JAVMA
2005;227:954-959.
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32. Papich MG. Antimicrobial therapy for gastrointestinal diseases.
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Treating Acute Colitis CE
3 CE
CREDITS CE Test 2 This article qualifies for 3 contact hours of continuing
education credit from the Auburn University College of Veterinary
Medicine. Subscribers may take individual CE tests online and get real-time
scores at CompendiumEquine.com. Those who wish to apply this credit to fulfill
state relicensure requirements should consult their respective state authorities
regarding the applicability of this program.
1. Which fluid would not be appropriate
to administer to a hypovolemic equine
patient?
a. hypertonic saline
b. lactated Ringer’s solution
c. plasma
d. dextrose 50%
e. 0.9% saline
2. Which serum level is not typically low in an
equine patient with acute colitis?
a. sodium d. potassium
b. chloride e. bicarbonate
c. lactate
3. Which statement regarding equine acute
colitis is false?
a. Prostaglandins such as PGI2 and PGE2 may
be cytoprotective to GI mucosa.
b. Flunixin meglumine must be administered
at 1.1 mg/kg IV q12h to decrease produc-
tion of tumor necrosis factor and other
inflammatory cytokines in the GI mucosa.
c. Horses with severe colitis have profound
hypoproteinemia.
d. Metronidazole use is indicated in cases of
C. difficile infection.
e. DMSO and lidocaine may be used as anti-
inflammatories in horses with acute colitis.
4. Which statement regarding bismuth subsali-
cylate is true?
a. The anecdotal dose of liquid bismuth
subsalicylate for horses is large, requiring
passage of a stomach tube every 6 to 8
hours. Alternatively, a concentrated paste
can be administered.
b. Several cases of associated toxicosis in
horses have been reported.
c. Adverse cardiac signs were reported in a
person with suspected bismuth subsalicy-
late toxicosis.
d. It has a prokinetic mechanism of action.
e. No studies support its use in humans.
5. Which commonly used therapy lacks experi-
mental support as a beneficial treatment of
equine acute colitis?
a. bismuth subsalicylate
b. metronidazole
c. di-tri-octahedral smectite
d. S. boulardii
e. probiotic pastes
6. Which disease and treatment combination
for equine patients is incorrect?
a. C. difficile infection; metronidazole
b. Potomac horse fever; oxytetracycline
c. C. difficile infection; S. boulardii
d. antimicrobial-associated colitis; ceftiofur
sodium
e. right dorsal colitis; misoprostol
November/December 2009 | Compendium Equine: Continuing Education for Veterinarians®
FREE
7. Which statement regarding colloid therapy
in equine patients is true?
a. Administering plasma is beneficial only if
the volume is adequate to replace all pro-
tein loss.
b. Hydroxyethyl starch should not be admin-
istered to horses with diarrhea.
c. Hypertonic saline has short-term colloidal
action.
d. Plasma administration reduces the chance
of developing laminitis.
e. Colloid administration decreases plasma
oncotic pressure.
8. Which statement regarding fluid therapy for
equine acute colitis is false?
a. Fluids should not be administered until
clinicopathologic test results are available.
b. Calcium supplementation is often required
due to reduced feed intake and increased
GI loss.
c. Ongoing fluid losses must be considered in
addition to maintenance requirements and
replacement of lost fluid when determining
an appropriate fluid plan.
d. Potassium should be supplemented
carefully.
e. Sodium bicarbonate administration is
appropriate for correcting hyponatremia in
some cases.
9. Which statement regarding equine acute
colitis is false?
a. Many components of treatment are the
same regardless of etiology.
b. Fluid therapy is crucial to all treatment
plans.
c. Antimicrobial therapy should not be rou-
tinely administered in colitis cases.
d. If complications do not occur and diarrhea
resolves, the patient should have no long-
term effects.
e. Laminitis is an uncommon sequela of
acute colitis.
10. Which statement regarding treatment of
equine acute colitis is false?
a. Treatment with COX inhibitors should be
routine because they limit the chance of
developing intestinal ulceration.
b. The volume and frequency of diarrhea are
good subjective indicators of fluid loss
and should be considered when devising a
fluid therapy plan.
c. There is limited evidence to support the
use of transfaunation.
d. Antimicrobial therapy may prolong bacte-
rial shedding in salmonellosis cases.
e. Oxytetracycline is an appropriate therapy
for Potomac horse fever.
427