C H A P T E R

67

Anterior Enteritis

RODNEY L. BELGRAVE

nterior enteritis (AE) is a syndrome of acute inflam

mation and subsequent ileus affecting the proximal
to middle segments of the small intestine. It is
also referred to as duodenitisproximal jejunitis, proximal
enteritis, and gastroduodenojejunitis. The disorder is charac
terized by inflammation of the duodenum, proximal part
of the jejunum, or both and generates copious volumes of
nasogastric reflux, leading to intestinal distension and
abdominal pain.
The exact cause of this malady is yet to be elucidated;
however, organisms such as Salmonella spp, Clostridium perfringens, and Clostridium difficile have been implicated. The
detection of these organisms in the gastric fluid or feces of
diseased horses is neither consistent nor limited to horses
with the condition. Prevalence rates vary from 3% to 22% of
all small intestineassociated colic cases, and prevalence
varies with geographical location, with a greater incidence
and severity of disease seen in the southeastern United States.

PATHOPHYSIOLOGY

The inciting factors involved in AE remain unknown. The

isolation of C difficile and C perfringens strains from reflux
fluid in limited numbers of affected horses, compared with
those with small intestinal strangulating obstruction, sug
gests that either of these organisms may initiate the inflam
matory response seen in the small intestine. Feeding practices,
such as giving rations with a high grain content, have also
been proposed as a contributing cause. However, to date,
only a weak association between ration and AE has been
reported. Regardless of the cause, an inflammatory response
mediated by endotoxin and inflammatory mediators, such
as eicosanoids, ensues and leads to small intestinal stasis.
These mediators also account for hypersecretory mecha
nisms, which account for the accumulation of fluid in the
affected portions of intestine.
The serosa of affected segments may have petechial to
ecchymotic hemorrhages, and the mucosal surfaces are
usually diffusely hyperemic with varying degrees of petechia
tion or ulceration. The fluid contents of the affected small
intestine may be red-brown.

CLINICAL PATHOLOGY

The clinicopathologic changes seen in horses with AE stem

from a combination of inflammation and endotoxemia as
well as accumulation of fluids within the proximal gastroin
testinal tract (a third space). As a result, affected horses are
characteristically azotemic, hemoconcentrated (high PCV),
hyperlactatemic, and hyperproteinemic. Of these, the sever
ity of hemoconcentration and azotemia are negatively asso
ciated with survival. White blood cell counts vary from
leukopenia to leukocytosis.
Metabolic acidosis with a large anion gap character
ized by enteric bicarbonate loss, hypochloremia, and

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hyperlactatemia is often observed. An anion gap greater

than or equal to 15 mEq/L has been associated with a
high mortality rate in affected cases.
Horses with AE are at greater risk for sustaining hepatic
injury relative to horses with other forms of small intestinal
obstruction. High values for -glutamyl transferase (GGT),
alkaline phosphatase (ALP), and aspartate aminotransferase
(AST) are commonly seen. These increases may be incited by
ascending infection through the common bile duct and con
comitant endotoxemia. Horses with AE were 12 times as
likely to have high values for GGT activity as horses with a
small intestinal strangulating obstruction. Use of serum GGT
activity greater than 22U/L as a cutoff point was only mod
erately sensitive at differentiating horses with AE from those
with obstruction in one study, but this cutoff was highly
specific and had a high positive-predictive value.
Peritoneal fluid accumulates secondary to serosal inflam
mation and distension of affected small intestine segments.
High peritoneal fluid protein concentration (>3.5g/dL) and
mild to moderate increases in peritoneal white cell count
may be observed. Analysis of peritoneal fluid may aid in
determination of the prognosis. High fluid total protein con
centration is significantly associated with death in horses
with AE.

CLINICAL MANIFESTATION OF DISEASE

The primary challenge faced in evaluating horses with AE is

differentiating the condition from forms of small intestinal
obstruction, which may require surgical intervention. Signs
of abdominal discomfort in horses with AE typically abate
upon gastric decompression, in contrast to the unrelenting
pain often observed in those with strangulating or obstruc
tive lesions. In the southeastern United States, differentiating
the disease from ileal impactions can also be challenging.
Horses with AE typically are presented with mild to
severe abdominal discomfort; the heart rate is typically high,
ranging from 60 to 100 beats/minute in accordance with
severity of the condition, and horses are often also tachy
pneic. Many are febrile at the time of presentation (tempera
ture >101.5F [38.6C]); mucous membranes may appear
congested, and a toxic rim can be observed in horses with
endotoxemia. Capillary refill time is often prolonged. Gas
trointestinal borborygmus is generally decreased, and in
severe cases, the horse may have spontaneous reflux at the
nares. Patients may also present with concurrent laminitis or
may develop laminitis over the course of treatment. The
incidence of laminitis in horses with AE ranges from 7.5% to
28.4%. Other secondary complications include pneumonia
and thrombophlebitis.

DIAGNOSIS

A definitive diagnosis of AE can only be made at the time

of surgery or necropsy. A tentative diagnosis may be reached


on the basis of clinical progression and response to gastric
decompression, along with the clinicopathologic changes
previously described. Rectal palpation before nasogastric
intubation may reveal turgid, distended loops of small
intestine. Palpation of an impacted ileum may rule out a
diagnosis of AE.
Nasogastric intubation typically yields large volumes of
reflux, usually reddish brown to bloody in appearance. Signs
of abdominal pain subside until fluid reaccumulates in the
stomach.
Abdominal ultrasound may provide useful information to
support a diagnosis of AE. Evidence of gastric distension is
provided by the presence of anechoic fluid along with a
gasfluid interface within the stomach, which may extend
beyond the 12th intercostal space, in the cranial and lateral
aspect of the left side of the abdomen. A distended duode
num with poor or absent motility may be seen coursing
caudodorsally around the caudal pole of the right kidney.
The distended duodenum and more distal portions of small
intestine may exceed 5cm in diameter. Wall thickness of the
small intestine can also be assessed and may become increas
ingly thick as the disease persists. Patients with small intes
tinal strangulating obstructions characteristically have more
significant wall thickening and edema in affected portions
of bowel than horses with AE. The lungs in the cranioventral
aspects of both hemithoraces should be evaluated for pneu
monia secondary to aspiration.
Ultrasonography should also be used to assess the pres
ence, volume, and character of peritoneal fluid. In general,
horses with strangulating obstructions have more substantial
increases in fluid total protein than those with AE. Patients
with an abdominal total protein of 3.5g/dL or greater were
four times as likely to succumb to AE as horses having an
abdominal PF total protein of less than 3.5g/dL in one study.

MEDICAL THERAPY

Medical treatment of horses with AE is advocated over surgi

cal management, which does not decrease the volume or
duration of nasogastric reflux. The primary goal of medical
therapy is gastric decompression. Once in place, the nasogas
tric tube should be left indwelling and the patient reassessed
for reflux every 2 hours. The tube should be capped between
checks to better quantitate the volume of reflux being
produced. Production and sequestration of reflux may con
tinue for 3 to 5 days, depending on the severity of the insult
to the bowel. Evacuation of reflux under gastroscopic guid
ance may allow for more accurate quantification of reflux
and more thorough evacuation of the stomach and duode
num and is recommended for horses in which reflux has
been protracted. The stomach and duodenum can also be
assessed at the same time. Diffuse erosive ulceration of the
squamous mucosa has been seen on endoscopic examination
of these patients. Prolonged or repeated nasogastric intuba
tion can give rise to complications such as pharyngitis and
esophagitis.
Fluid therapy with a balanced polyionic solution is the
mainstay of therapy. Aggressive fluid therapy is required to
restore extracellular fluid volume, correct existing acid-base
and electrolyte abnormalities, and enhance renal perfusion.
The use of 7% hypertonic saline (HSS; 4 to 6mL/kg given as
a bolus over 15 to 20 minutes) or hydroxyethyl starch (HES;
10mL/kg) is recommended to initially address hypovolemic
shock. These fluids allow for more rapid correction of intra
vascular volume deficits than does crystalloid fluid adminis
tration. The administration of HES results in a better cardiac
index than HSS. The presence and degree of endotoxemia in

CHAPTER

67 Anterior Enteritis

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these cases may dampen the effects of both HES and HSS,
when combined or administered individually, on the cardiac
output, blood lactate concentration, and mean arterial pres
sure. Small-volume resuscitation with HSS or HES should
be immediately followed by administration of a balanced
electrolyte solution. Estimation of the initial fluid require
ments should be based on hydration status. A moderately
(8%) dehydrated 500-kg horse may have a deficit approach
ing 40L. A second large-bore intravenous catheter may be
needed to facilitate timely administration of such a large
deficit. Large volumes of fluids, upward of 60L/day, may be
required to replace fluids continually being sequestered in
the gastrointestinal tract. A fine balance between fluids
lost and fluids administered must be maintained to limit
overhydration, which may lead to increased third-space
accumulation of fluid within the gastrointestinal tract. This
balance is best achieved by frequently and collectively moni
toring the quantity of the reflux being obtained, the hydra
tion indices derived from serial physical examination and
serial assessment of plasma protein concentration, blood
lactate, and blood urea nitrogen concentration. Supplemen
tation of polyionic fluids with additional electrolytes may be
necessary.
Because affected horses have enteric protein loss, oncotic
pressure must be maintained by administration of colloids,
either HES (10mL/kg/day) or fresh or thawed frozen plasma
(12mL/kg/day). Low oncotic pressure may contribute to
both peripheral dependent edema and bowel edema. Devel
opment of these signs or a decline in blood total protein
or albumin concentrations should prompt colloid adminis
tration. Combination colloid therapy with HES and plasma
is generally more cost effective than treating solely with
plasma.
Nonsteroidal antiinflammatory drugs such as flunixin
meglumine (0.25 to 0.5mg/kg, IV, every 8 hours) or firocoxib
(0.1mg/kg, IV, every 12 hours) should be administered for
their antipyretic and analgesic effects, as well as to attenuate
the effects of endotoxemia on the cardiovascular system.
Flunixin meglumine is thought to be a more efficacious anal
gesic, but given its contribution to delayed mucosal healing
and the possibility of nephrotoxicosis in volume-depleted
animals, administration of firocoxib should be considered.
Butorphanol, an opioid agonist-antagonist, may also be
administered for its analgesic effects as a constant-rate
infusion (13g/kg/hour).
The use of polymyxin B (3000U/kg, IV, every 12 hours)
and pentoxifylline (7.5mg/kg, IV, every 8 to 12 hours)
should also be considered to counteract the effects of
endotoxemia.
Antimicrobial therapy in horses with AE remains contro
versial. The putative association of some species of clostridia
with AE may support the use of antimicrobials such as potas
sium penicillin G (22,000 to 44,000U/kg, IV, every 6 hours)
or metronidazole (20mg/kg, per rectum, every 6 hours).
Addition of a fluoroquinolone such as enrofloxacin should
be considered to provide broader spectrum antimicrobial
coverage and limit complications associated with bacterial
translocation across the compromised bowel. Gentamicin
may be considered in place of enrofloxacin, provided renal
function is adequate.
The efficacy of various prokinetics on inflamed bowel
remains questionable. However, intravenous lidocaine
(2mg/kg loading dose, given IV over 15 minutes, followed
by infusion of 50g/kg/minute) may be beneficial for the
added analgesic relief that it provides. In one report, use of
lidocaine in AE and postoperative ileus cases resulted in a

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SECTION

VI Gastrointestinal Disease

significant decrease in the volume of reflux obtained and

decreased the duration of hospitalization of affected patients.
Metoclopramide, a dopamine antagonist, may also be given
at a rate of 0.04mg/kg/hour. It increases peristalsis of the
jejunum and duodenum, increases tone and amplitude of
gastric contractions, and relaxes the pyloric sphincter to
facilitate gastric emptying. Extrapyramidal side effects such
as akathisia may be seen with its use.
In horses experiencing an extended period of fasting
because of persistent reflux, the use of total or partial paren
teral nutrition should be considered. A negative energy
balance ensues within 24 hours of fasting and is accompa
nied by an increase in triglycerides and total bilirubin. Use
of total parenteral nutrition results in an improved nutri
tional status in horses undergoing small intestinal resection
and anastomosis, and a similar benefit should be seen in
those with AE.

SURGICAL THERAPY

Surgical therapy is indicated if abdominal discomfort and

tachycardia persist and a mechanical obstruction cannot be
ruled out. Increases in the volume and character of perito
neal fluid, as well as changes in the nucleated cell count and
total protein of the fluid, may also support a decision to
perform an exploratory celiotomy. Surgery may be more
useful as a diagnostic aid than as a treatment; a more rapid
reduction in the volume and duration of nasogastric reflux
was not seen in horses with AE that had surgical intervention
versus cases that were managed medically. Various bypass
methods to circumvent the affected portions of bowel and
restore transit of ingesta and fluid to the cecum have been
described. A 95% survival rate with a combined medical
(intravenous metronidazole and procaine penicillin) and sur
gical approach involving manual evacuation of the small
intestine into the cecum has been reported; this approach
plays on the theory that clostridial species are at the root of
the disease, and its success is possibly a result of geographical
differences in disease etiology.

PROGNOSIS

Survival rates vary and have been reported to be anywhere

from 25% to 95%. Historically, medically managed cases
have had higher survival rates than those managed surgi
cally. However, many of the surgically treated cases likely
involve horses whose condition was more severe and refrac
tory to medical therapy. Recurrence of the disease is rare.
Collectively, the anion gap, blood lactate concentration,
and abdominal fluid total protein concentration are useful
prognostic indicators when used in the early stages of hos
pitalization. Complications that may affect prognosis include
development of laminitis and pneumonia.

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