Postoperative Management of The Large Colon Volvulus Patient

Vet Clin Equine 20 (2004) 167–197
Postoperative management of the large

colon volvulus patient
Louise L. Southwood, BVSc, PhD
University of Pennsylvania, New Bolton Center, 382 West Street Road,
Kennett Square, PA 19348, USA
Prognosis, pre- and intraoperative considerations, and the importance

of postoperative critical care
Overall, the prognosis for horse with large colon volvulus (LCV) is
generally considered to be guarded to fair (approximately 30%–60% short-
term survival) [1–3]. Encouragingly, a recent study [4] reported a short-term
survival of 83%; however, horses in that particular practice are referred and
operated on soon after the onset of clinical signs compared with horses in
other practices. In contrast, we have recently evaluated the short-term
survival of horses with LCV (Fig. 1) [3], and although the survival improved
significantly (P = 0.01) over the 10 years of the study, it was still less than
70%. Although the results of these studies emphasize the importance of
immediate referral and surgical intervention, many horses are not observed
regularly and are housed several hours from a surgical facility [3,4].
Prolonged venous or arteriovenous strangulation causes extensive colonic
damage, and these patients require intensive postoperative management.
Some horses with LCV are euthanized before or during surgery (see Fig.
1). Euthanasia is often performed for economic reasons. When economics
are not a major influential consideration, the surgeon is left with the decision
of whether to correct the volvulus and recover the horse, perform a large
colon (LC) resection and anastomosis, or euthanize the horse for humane
reasons. There has been recent anecdotal evidence that an extensive LC
resection can decrease the morbidity and mortality for horses with a LCV
[5–7]. The improved prognosis is thought to be a result of reduced
inflammatory mediator and endotoxin absorption and the mucosa having
a smaller surface area over which to regenerate. There have been no
controlled studies, however, evaluating the benefit of LC resection for
horses with LCV. Although LC resection is clearly indicated in horses with
E-mail address: southwoo@vet.upenn.edu
0749-0739/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.cveq.2003.12.004
168 L.L. Southwood / Vet Clin Equine 20 (2004) 167–197
Fig. 1. The association between the year in which the horse had a large colon volvulus (LCV)
and outcome. The year the horse had a LCV is shown on the x-axis, and the percentage of horses
is shown on the y-axis. Cases in which the owner declined treatment are excluded. Induction,
horses that died before surgical intervention; table, horses that were euthanized on the table;
postop, horses that died or were euthanized after surgery; discharge, horses that were discharged
from the hospital. Cases are from a retrospective study performed at Colorado State University
(Data from Southwood LL, Bergslien K, Jacobi A, Stashak TS, Frisbie DD, Trumble TN. Large
colon displacement and volvulus in horses: 495 cases (1987–1999). In: Proceedings of the Seventh
International Equine Colic Research Symposium. Manchester, UK; 2002, p. 32–3).
obvious focal ischemic necrosis, most horses with LCV do not have a visible
line of demarcation between viable and nonviable intestine, and it can be
difficult to differentiate those horses that will survive from those that will not
if the LC is left in situ [8].
Criteria that have been used to predict survival and determine whether a
LC resection or euthanasia is indicated include the duration of colic [7]. This
can be unreliable, however, because the duration of actual severe colic can be
variable (ie, horses show mild to moderate signs of colic for several hours,
possibly associated with a nonstrangulating obstruction or gas distention,
and then become acutely and severely painful with a strangulating
obstruction); and many unobserved horses are found with signs of colic,
with the actual duration being unknown. In a retrospective study of horses
with LCV, we found that heart rate (HR), hematocrit, glucose concentration,
creatinine concentration, chloride concentration, anion gap, peritoneal fluid
total protein (TP), and mean arterial pressure (MAP) under general
anesthesia (anesthesia score) were useful for predicting survival and may be
used to decide whether or not to leave the LC in situ, perform an LC resection,
or euthanize the horse (Fig. 2) [3]. Interestingly, although most horses in the
study had an increase in liver enzymes (sorbitol dehydrogenase [SDH] in 80%
of horses, gamma-glutamyl transferase [GGT] in 55% of horses, bilirubin in
L.L. Southwood / Vet Clin Equine 20 (2004) 167–197 169
Fig. 2. The association between physical examination and laboratory measurements and
outcome. The measurement is shown on the x-axis, and the percentage of horses is shown on the
y-axis. Heart rate (A), hematocrit (B), glucose concentration (C), creatinine concentration (D),
anion gap (E), chloride concentration (F), and anesthesia score (G) calculated by measuring the
amount of time (minutes) that the horse spent with the mean arterial pressure under 30, 40, 50,
60, or 70 mm Hg. Cases in which the owner declined treatment are excluded. Induction, horses
that died before surgical intervention; table, horses that were euthanized on the table; postop,
horses that died or were euthanized after surgery; and discharge, horses that were discharged
from the hospital. Cases are from a retrospective study performed at Colorado State University
(Data from Southwood LL, Bergslien K, Jacobi A, Stashak TS, Frisbie DD, Trumble TN.
Large colon displacement and volvulus in horses: 495 cases (1987–1999). In: Proceedings of the
Seventh International Equine Colic Research Symposium. Manchester, UK; 2002, p. 32–3).
63% of horses, and aspartate aminotransferase [AST] in 75% of horses), most

likely as a result of endotoxemia and marked LC distention, there was no
association between any of these measurements and outcome [3]. MAP under
general anesthesia can be difficult to interpret, because improved anesthetic
techniques and medical management can result in improved cardiovascular
status despite severe LC damage. Other studies have found a divergence of
Fig. 2 (continued )
Fig. 2 (continued )
hematocrit (>50%) and TP (\4.5 g/dL) and fever to be associated with

a poor prognosis for survival [5]. These measurements can be used in
conjunction with visual assessment (eg, serosal or mucosal color, hemorrhage
at the enterotomy or decompression site, edema resolution, motility, palpable
pulse) or other methods to assess intestinal viability, if available (eg, surface
oxygen tension, laser Doppler, Doppler ultrasonography, intraluminal pres-
sure, fluorescein dye, histology), to determine the best possible surgical
management [9]. Horses with a short duration of severe pain that have
a relatively normal physical examination and laboratory measurements and
whose LC serosa and mucosa are pink at surgery have a good prognosis with
minimal postoperative management (eg, fluid and electrolyte therapy,
flunixin meglumine, perioperative antimicrobials). In a considerable number
of horses, however, this is not the situation.
In many horses, the LC may seem to be viable grossly and the mucosa
considered being capable of regeneration; however, the damage is more
severe or extensive than thought to be the case based on initial assessment.

These horses require intensive postoperative management and, often,
euthanasia 12 to 72 hours after surgery. When there is extensive mucosal
damage from ischemia, reperfusion, and oxidant injury, the horse may be
unable to survive the massive systemic insult from the increase in permeability
of the damaged mucosa or the mucosa is unable to regenerate adequately
(Fig. 3). In other horses, the colonic vessels are so damaged that thrombosis
and segmental ischemic necrosis result in euthanasia several days after
surgery (Fig. 4). The major cause of postoperative morbidity and mortality
for horses with LCV is endotoxic shock and loss of intravascular oncotic
pressure as a result of absorption of endotoxin and loss of albumin from the
damaged LC as well as an increase in vascular permeability leading to
circulatory collapse and severe pulmonary edema. Horses with LCV require
intensive postoperative monitoring and treatment directed toward these
anticipated postoperative complications. Despite intensive postoperative
management, many horses do not survive (see Figs. 3 and 4), and future
studies directed at treating endotoxemia and enhancing colonic perfusion and
mucosal regeneration are needed.
Postoperative monitoring
General considerations
Horses undergoing surgical correction of LCV, with or without pelvic
flexure enterotomy or LC resection and anastomosis, should be monitored
closely for signs of postoperative complications. Common postoperative
complications include severe endotoxemia, continued ischemic necrosis of the
LC, hypoproteinemia, and diarrhea. Postoperative endotoxemia may be mild
to severe and, if severe, can lead ultimately to multiple organ dysfunction
syndrome (MODS). Signs of endotoxemia include ileus, tachycardia,
tachypnea, fever, injected or toxic mucous membranes, and increased hema-
tocrit. A generalized lack of colonic viability or focal ischemic necrosis may be
indicated by signs of moderate to severe abdominal pain, lack of gastro-
intestinal tract sounds, abdominal distention, persistent or severe tachycardia
(HR >80 beats per minute [bpm]), and an inability to maintain serum protein
concentrations above 4 g/dL. These indicate a poor prognosis for survival.
Unfortunately, there have been no prospective or retrospective studies
evaluating postoperative indicators of survival in horses with LCV. Further,
accurate assessment of the true survival of horses is limited by economic
constraints and the veterinarian’s ability to euthanize patients humanely.
Physical examination
The horse should be monitored for improvement in attitude, appetite,
abdominal pain and distention, fecal production and consistency (especially
absence of fecal production or diarrhea), and urination. The HR, respiratory
Fig. 3. Gross appearance of the serosal (A) and mucosal (B) surface at the enterotomy site and
histologic section (C) from a 17-year-old Quarter Horse gelding 3 days after surgical correction
of a large colon volvulus (LCV). Before surgery, the horse had a heart rate (HR) of 84 beats per
minute (bpm), a hematocrit of 69%, a creatinine concentration of 3.1 mg/dL, a chloride
concentration of 88 mg/dL, and a lactate concentration of 12.7 mmol/L; however, at surgery,
the large colon (LC) appeared viable based on serosal and mucosal color as well as motility, and
the horse was doing well under general anesthesia (mean arterial pressure >50–60 mm Hg).
Therefore, the decision was made to leave the LC in situ and recover the horse. The horse
seemed to do well reasonably well for 24 hours after surgery with a HR of 54 to 76 bpm,
hematocrit of 48%, total protein of 4.7 g/dL, gastrointestinal tract sounds present, and
development of hemorrhagic diarrhea. Nevertheless, the horse became more severely
tachycardiac (HR of 84–96 bpm) and tachypneic (respiratory rate of 70–90 breaths per
minute), developed severe laminitis, and was euthanized. The tachycardia and tachypnea were
thought to be associated with the severe laminitis. Grossly and histologically, the submucosa,
muscularis, and serosal surface were viable; however, there was extensive mucosal damage.
Laminitis is a complication of endotoxin absorption from the intestinal mucosa. It is unknown,
however, whether or not the mucosa could have regenerated with the severity of damage or
whether an LC resection might have improved the prognosis.
Fig. 4. Gross appearance of a 5-year-old Quarter Horse mare 4 days after correction of a large
colon volvulus (LCV). The horse had a duration of colic of less than 2 hours. Before surgery,
the horse had a heart rate (HR) of 76 beats per minute (bpm), a hematocrit of 50%, a creatinine
concentration of 2.5 mg/dL, a chloride concentration of 90 mg/dL, and an anion gap of 27
mEq/L. At surgery, the large colon (LC) appeared viable based on serosal color, and the horse
was doing well under general anesthesia; therefore, the decision was made to leave the LC in situ
and recover the horse. The horse seemed to do well for 24 hours after surgery, with a HR of 52
to 80 bpm, hematocrit of 48%, total protein of 4.7 g/dL, gastrointestinal tract sounds present,
and development of diarrhea. Four days after surgery, the horse’s HR increased to 120 bpm and
the horse was euthanized. At necropsy, there was a segment of left dorsal colon adjacent to the
pelvic flexure that was not viable. It is possible that this horse may have survived if an LC
resection had been performed at the initial surgery.
rate, rectal temperature, gastrointestinal tract sounds, oral membrane color

and moisture, and capillary refill time should be monitored every 2 to 6 hours
depending on the duration of time after surgery and severity of LC damage
(Fig. 5).
Horses are often dull immediately after surgery; however, attitude and
appetite should improve over 12 to 24 hours after surgery. Inappetence or
anorexia (particularly if the horse is hand grazed or offered fresh grass),
persistent abdominal pain, increasing abdominal distention, and absence of
fecal production are poor signs and usually indicate extensive or severe LC
damage. A nasogastric tube should be passed and the horse checked for reflux
if there are signs of gastrointestinal tract dysfunction, because endotoxemia
can cause generalized ileus. A rectal examination should also be performed in
horses showing signs of abdominal pain or distention to determine the degree
of LC distention, anatomic abnormalities, and any other possible causes of
abdominal pain. Horses with LCV commonly develop diarrhea after surgery.
Fecal cultures for Salmonella spp (and Clostridium spp and toxin) should be
taken, and horses with diarrhea should be managed with barrier nursing or be
isolated.
Horses are usually mild to moderately tachycardiac (50–70 bpm) for the
first 12 to 24 hours after surgery; however, the HR should rapidly decrease
Fig. 5. Examples of monitoring and treatment sheets used for postoperative colic patients at
Colorado State University (A,B) and New Bolton Center, University of Pennsylvania (C,D).
after surgery. Severe or prolonged tachycardia (>80–90 bpm for longer than
24 hours) indicates a poor prognosis. Respiratory rate can be variable, and
trends for increased respiratory rate can indicate pain (eg, abdominal pain or
laminitis) or secondary respiratory tract complications (eg, pleuropneumo-
nia). The cause of an increase in rectal temperature should be determined and
treated appropriately. Possible sources of fever include endotoxemia, focal
ischemic LC necrosis, colitis, peritonitis, septic thrombophlebitis, incisional
Fig. 5 (continued )
infection, pneumonia, and placentitis or endometritis in broodmares. After

identification of the source of the fever, culture and sensitivity tests should be
performed before treatment with antimicrobials. Indiscriminant use of anti-
microbials is inappropriate in a horse with a postoperative fever. Oral mucous
membrane color may initially be bright red (injected membranes); however,
membrane color should improve during the 24 hours after surgery, and
mucous membranes should be moist and capillary refill time less than 2
seconds in adequately hydrated horses. Gastrointestinal tract sounds may
Fig. 5 (continued )
initially be reduced but should improve during the first 24 hours after surgery.
Absence of gastrointestinal tract sounds in combination with signs of
abdominal pain and increasing abdominal distention is an indicator of a poor
prognosis for survival.
Horses with endotoxemia, diarrhea, fever, and generalized debility are
predisposed to thrombophlebitis, particularly if catheterization is prolonged
[10,11]. The catheter site should thus be monitored for signs of heat, pain,
swelling, and drainage. The use of silastic or polyurethane material for long-
term (>72 hours) intravenous (IV) catheterization is recommended (Arrow,
Arrow International, Reading, PA; Milacath, Mila International, Coving-
ton, KY) [12]. The celiotomy incision should also be monitored closely for
drainage and treated locally if mild drainage occurs. If the incisional
infection is persistent or severe, culture and sensitivity testing should be
performed and the horse treated with appropriate systemic antimicrobials.
Many horses with LCV are pregnant [3]. The abortion rate of horses after
abdominal surgery is approximately 20% and was much higher in horses
that had a severe medical colic; therefore, this complication should be
discussed with the owner, and mares should also be monitored for signs of
complications associated with pregnancy [13]. The horse’s body weight
Fig. 5 (continued )
should also be monitored several times a week, particularly in horses that

develop postoperative complications and in pregnant or lactating mares.
Laboratory data
Hematocrit and plasma TP should be monitored every 6 to 12 hours for the
first 24 to 72 hours after surgery. An increase in hematocrit with a concurrent
decrease in TP is an indicator of a poor prognosis. It is not uncommon for the
hematocrit to remain high (>40%–50%) and the TP to be low (\5 g/dL) for
24 to 48 hours after surgery; however, the hematocrit and TP should converge

during recovery. Most horses are leukopenic after surgery, most likely as
a result of endotoxemia, and there is usually neutropenia (segmented
neutrophils) and left shift (increase in band neutrophils). Mild to moderate
hyperfibrinogenemia is also common in all horses after abdominal surgery.
Low fibrinogen or a sudden decrease in the fibrinogen can be an indication of
a coagulopathy. Coagulopathies are not uncommon before or after surgery in
horses with LCV and should be treated aggressively. Electrolytes and acid-
base measurements should be monitored closely and corrected as necessary,
particularly ionized calcium, magnesium, and potassium, which are often low
in horses after colic surgery as a result of endotoxemia. The creatinine
concentration should be monitored; if it is above the normal concentration
range before surgery, it should decrease rapidly with fluid therapy after
surgery. Persistently high or increased creatinine concentration after surgery
may indicate inadequate fluid therapy or renal damage and should be
followed up with urinalysis or fluid challenge. Urination frequency should be
monitored. If the horse has an increased creatinine concentration and oliguria
or anuria, diuretic therapy (dopamine, 3–7 lg/kg/min; mannitol, 0.25–1 g/kg;
or furosemide, 1–2 mg/kg every 2 hours [14]) should be considered; however,
the prognosis is poor.
Treatment
Fluid therapy
Crystalloids
Polyionic isotonic fluid therapy (lactated Ringer’s solution, Baxter
Health Care Corporation, Deerfield, IL; Plasmalyte A, Baxter Health Care
Corporation; or Normasol-R, Abbott Laboratories, North Chicago, IL) is
the mainstay of postoperative supportive treatment for horses with LCV
[15]. In addition to the facts that the patient has lost large volumes of
immeasurable fluid through sweating and at surgery and has not been taking
in oral fluids and that gastrointestinal tract disturbances inherently cause
fluid and electrolyte abnormalities, endotoxemia causes severe hemody-
namic and cardiovascular disturbances [15]. Although endotoxemia results
in an initial transient hyperdynamic phase with an increase in cardiac output
(CO) and low peripheral vascular resistance (PVR), this is followed by
a hypodynamic phase often seen after surgery in horses with LCV [15]. The
hypodynamic phase of endotoxic shock is characterized by a decrease in
plasma volume [16], decrease in CO [17,18], increase in PVR and pulmonary
arterial pressure (PAP) [17], and hypotension [19], with a subsequent
increase in plasma lactate [18] and metabolic acidosis as well as hypoxemia
[16].
Sterile polyionic isotonic fluids should be administered intravenously at
approximately 10 to 100 mL/kg/h (0.5–5 L/h for a 500-kg horse) to manage
the cardiovascular effects of endotoxemia [15]. The fluid rate can be

increased if the horse is showing severe signs of hypodynamic endotoxic
shock, particularly tachycardia (HR >80 bpm) and increased hematocrit
(>50%). Care should be taken with rapid administration of large volumes
of fluids, because the decrease in plasma volume resulting from endotox-
emia is not associated with a decrease in extracellular or total body fluid
volume but is actually a consequence of an increase in vascular
permeability, with loss of fluid and protein from the vascular space and
shunting of blood from the arteriovenous to lymphatic circulation [16].
Therefore, although fluid therapy is critical to maintain CO and peripheral
perfusion, excessive and rapid fluid administration should be avoided,
because hypoproteinemia from intestinal loss and an increase in vascular
permeability can result in edema formation in the lung, digit, brain, and
intestine. Fluid therapy can be monitored by assessing mucous membranes
and capillary refill time, urination and azotemia, and development of
peripheral or pulmonary edema as well as hematocrit and TP. Central
venous pressure (CVP) is used in small animal critical care medicine to
monitor fluid therapy; however, there have been no studies evaluating the
use of CVP or MAP after surgery for assessing fluid requirements,
perfusion, and prognosis in horses with LCV [14]. Although the use of
inotropic or pressor therapy (eg, dopamine, dobutamine, vasopressin) in
combination with fluid therapy to manage cardiovascular abnormalities is
common during anesthesia in horses as well as in critically ill small animals
and foals, this type of treatment has not been evaluated clinically in horses
with LCV and is not commonly used. Dopamine (5 lg/kg/min), however,
was found to increase CO, cardiac index, and MAP and to decrease
diastolic PAP, PVR, and total pulmonary resistance compared with
untreated horses given endotoxin experimentally [20]. Dopamine did not
improve arterial oxygen tension, leukopenia, or acidosis associated with
endotoxin administration [20].
Electrolyte disturbances are also common in horses with LCV. In one
study evaluating preoperative serum calcium and magnesium concentra-
tions in horses undergoing abdominal surgery, 17% and 54% of horses had
low total and ionized magnesium, respectively, and 57% and 86% of horses
had low total and ionized calcium, respectively [21]. Ionized calcium and
magnesium were lower in horses with strangulating lesions compared with
those with nonstrangulating lesions [21]. Similarly, a retrospective study of
horses with LCV found that 69% of horses were hypocalcemic (total
calcium), 23% were hyponatremic, 54% were hypochloremic, and 3% were
hypokalemic before surgery [3]. Electrolyte disturbances in horses with
LCV can be a result of decreased intake, diuresis, endotoxemia,
gastrointestinal losses, and acid-base abnormalities [22]. Although calcium
may exacerbate oxidant injury, disturbances in calcium and potassium can
contribute to postoperative ileus; therefore, supplementation is recommen-
ded. Ionized calcium should be measured, because total calcium concen-
tration is affected by albumin concentration. Extracellular electrolyte

deficits (eg, sodium, chloride, calcium) may be estimated by the following
equation:
Deficit ðmEqÞ ¼ Normal ðmEq=LÞ Measured ðmEq=LÞ BWT 0:3
where BWT is body weight (kilograms). Calcium should be given if calcium

concentration decreases to less than 10 mEq/L or ionized calcium levels are
less than 1.2 to 1.5 mmol/L (4–5 mg/dL). Calcium is usually given as
calcium gluconate solution in the fluids at a rate of 50 to 100 mL (23%) per
5 L of fluids after surgery [22]. Potassium is an intracellular ion, and body
status for potassium is difficult to determine from serum measurements.
Between 10 and 20 mEq/L (25–50 mL [2mEq/mL KCl] per 5-L bag) of
potassium chloride is usually added to polyionic isotonic fluids [22]. Serum
concentrations of other electrolytes should be monitored closely, and
supplementation should be provided as needed.
Base deficits exist in occasional cases, and these deficits can be calculated
once bicarbonate (HCO3) and total carbon dioxide (TCO2) levels are
measured. Although almost all base deficits self-correct with fluid adminis-
tration, exogenous sodium HCO3 may be necessary when these deficits are
severe or persistent, which may occur if the horse develops diarrhea.
Treatment with exogenous HCO3 is not uncommonly reserved for cases in
which the base deficit is greater than 10 mEq/L, HCO3 is less than 15 mEq/
L, or pH is less than 7.2, although earlier treatment may be indicated. The
HCO3 deficit is calculated by the following equation:
Base Deficit 0:3 BWT ¼ HCO3 Deficit ðmEqÞ
One half of the estimated deficit may be replaced rapidly, with the
remainder being given over 12 to 24 hours. Interestingly, only 5% of horses
with LCV were found to have metabolic acidosis (decrease in TCO2 or
HCO3) before surgery, despite most horses (61%) having an increase in
anion gap (lactate) [3]. This was attributed to severe hypochloremia, thought
to be associated with intestinal obstruction, resulting in hypochloremic
alkalosis with alkalosis and lactic acidosis in balance [3].
Hypertonic saline (7% sodium chloride [NaCl]) has been shown to
increase CO and stroke volume (SV) and to decrease PVR and resulted in
serum lactate concentration returning to normal more rapidly after
administration of endotoxin compared with isotonic saline [17,23].
Supporting theses findings, horses with experimental LCV treated with
7.5% NaCl and 6% dextran 70 had improved CO, MAP, SV, oxygen
delivery, oxygen consumption, pH, and HCO3 compared with untreated
horses [24]. Similar effects were also observed with a combination of 25%
NaCl and 24% dextran 70 in anesthetized normovolemic horses, but some
horses developed transient and severe intravascular hemolysis and
hemoglobinuria [25]. In addition to potential complications, the benefits of

hypertonic saline are transient, and CO, SV, and PVR were decreased
compared with pretreatment values after 1 to 2 hours in horses administered
endotoxin [23]. Therefore, hypertonic saline (7% NaCl at 4 mL/kg [14])
should only be used in emergency resuscitation of horses with endotoxic
shock and should always be followed with polyionic isotonic fluids. The
serum sodium concentration should be monitored closely when hypertonic
saline is administered.
Synthetic colloids
Colloids are solutions containing molecules of large molecular weight that
increase the plasma oncotic pressure and, subsequently, the plasma volume.
An increase in plasma volume improves CO, SV, MAP, and oxygen delivery
(see section on hypertonic saline). The main indications for the use of
synthetic colloids are (1) plasma volume expansion of horses with
endotoxemia and (2) increase in oncotic pressure in horses that are
hypoalbuminemic (low TP). It is recommended that TP be maintained at
4 g/dL or greater to maintain intravascular oncotic pressure, because extra-
vascular fluid retention (edema) may occur at levels less than 4 g/dL [22].
It may not be possible to maintain adequate TP and oncotic pressure in
some patients with LCV. If with fluid delivery at a level required for volume
maintenance, the TP is too low, plasma or plasma expanders, such as dextran
70 (eg, 6% dextran 70 in 5% dextrose or 0.9% sodium chloride, Abbott
Laboratories, at 5–10 mL/kg/h) [14] or hetastarch (eg, 6% hetastarch in 0.9%
sodium chloride, Abbott Laboratories; Hespan, DuPont Pharma, Wilming-
ton, DE, at 10–20 mL/kg) [14,26] may be required. Dextran 70 has been
associated with adverse effects on coagulation (inhibition of platelet and
leukocyte aggregation) and histamine release with anaphylactoid reactions
[26]. The plasma half-life of dextran 70 is 3 to 12 hours. Hetastarch (10 and 20
mL/kg) was found to increase colloidal oncotic pressure and to decrease
hematocrit, TP, and fibrinogen concentration as well as to decrease
prothrombin time and activated partial thromboplastin time (APTT). There
were no adverse effects, except for a dose-dependent decrease in von
Willebrand factor antigen and factor VIII:C, which did not result in
a significant increase in bleeding time, although there was a trend observed at
20 mL/kg [27]. Other authors have used hetastarch at 5 to 15 mL/kg without
adverse effect [26]. The half-life of hetastarch in horses is unknown but
is approximately 7 days in dogs, and 13 days in human beings [26]. Hetastarch
is stable for 1 year at room temperature. If treatment with hetastarch is
indicated, the cost of therapy should be considered.
Plasma
Plasma, a natural colloid, can be administered to increase the TP; to
provide active proteins, such as acute-phase proteins, complement, clotting
factors and antithrombin III (ATIII); and to provide antibodies to endotoxin.

Therefore, plasma has several advantages over the synthetic colloids. The
amount of plasma to administer to increase the TP can be calculated
ðTPg TPrÞð0:05 BWTÞ=TPd
where TPg is the goal plasma protein concentration, TPr is the recipient
plasma protein concentration, and TPd is the donor plasma protein con-
centration [21]. Assuming no ongoing loss, 2 to 4 mL/kg (1–2 L for a 500-kg
horse) is usually needed to maintain plasma protein at greater than 4 g/dL
[21], or a minimum of 7 L of plasma is required to increase plasma pro-
tein by 1 g/dL in a 450-kg horse [26]. There are several disadvantages to
using plasma as a colloid compared with synthetic colloids: (1) risk of
anaphylactic reaction; (2) time taken to thaw frozen plasma; (3) expense; (4)
frequent requirement for large volumes; and (5) albumin is the primary
colloid in plasma and is likely to become extravasated, making plasma the
least effective of colloids for expanding the plasma volume [26]. The use of
plasma to treat coagulopathy is discussed elsewhere in this issue.
One of the major uses of plasma for postoperative treatment of horses with
LCV is for its antiendotoxic effects [14]. Endotoxin is the lipopolysaccharide
(LPS) component of the outer cell membrane of gram-negative bacteria and is
released during rapid bacterial proliferation or death [14]. Endotoxin consists
of inner hydrophobic lipid A and core polysaccharide components, which are
well conserved between bacterial species, and an outer O-specific poly-
saccharide, which varies between bacterial species [28]. Plasma from horses
vaccinated against mutant rough strains of either J5 Escherichia coli or the Re
mutant of Salmonella spp, which have lost their ability to attach O-specific
polysaccharide side chains and thus have the core polysaccharide exposed,
contains antibodies directed against the core polysaccharide [14]. Although
some studies have found that treatment with core polysaccharide hyperim-
mune plasma either clinically [29] or experimentally [30,31] improved clinical
signs and reduced hospitalization time and mortality (13% versus 47%
mortality) [29], other studies failed to demonstrate benefit after experimental
administration of endotoxin [32,33]. The author routinely uses plasma during
surgery and after surgery for horses with LCV, however, and in a survey of
diplomats of the American College of Veterinary Internal Medicine
(ACVIM) and American College of Veterinary Surgeons (ACVS), 64%
and 65% of respondents reported that they used hyperimmune plasma (1–2
L) for prevention and treatment of endotoxemia, respectively. Forty-five
percent of respondents thought that hyperimmune plasma was effective in
treating or preventing signs of endotoxemia, 45% were unsure of its
effectiveness, and 10% thought that it was ineffective [34]. Horses should be
monitored closely for signs of an anaphylactic reaction during plasma
administration, and plasma should always be administered through a blood
administration set.
Antimicrobials
The importance of the preoperative administration of antimicrobial
therapy is well recognized in human and veterinary medicine [35].
Antimicrobial treatment should be administered within 2 hours of incision
to ensure adequate tissue levels during surgery [35]. In a recent survey of
ACVS members, 97% of surgeons used antimicrobials in horses undergoing
abdominal surgery and 84% used potassium penicillin and gentamicin [36].
Aminoglycoside antimicrobial drugs are nephrotoxic and should be used with
caution in horses with LCV, because many of these horses are azotemic.
Preoperative ceftiofur or enrofloxacin can be used instead of an aminoglyco-
side drug in horses with moderate to severe azotemia. Other reported
complications with the use of aminoglycosides include neuromuscular
blockade, cardiovascular depression, and apparent inhibition of gastrointes-
tinal tract motility, which may be restored with administration of calcium
[37]. These other reported complications are uncommonly recognized clini-
cally in horses with LCV. Metronidazole can be added to the antimicrobial
regimen in horses with severe abdominal contamination.
Discriminant postoperative antimicrobial use is important for the in-
dividual patient as well as for the surgical facility. Postoperative antimicro-
bials should never be used in place of meticulous aseptic surgical technique.
The use of antimicrobials has been associated with postoperative diarrhea;
Salmonella and Clostridium spp are the most common causes [37,38]. In
a study identifying risk factors for salmonellosis, horses treated with pa-
renteral antimicrobials (6.4 times increased risk), horses treated with pa-
renteral and enteral antimicrobials (40 times increased risk), horses with colic
(4.3 times increased risk), and horses having a nasogastric tube passed (2.9
times increased risk) were at increased risk compared with nonaffected or
nontreated horses [38]. Clostridium spp have also been associated with
antimicrobial-induced diarrhea, and this syndrome carries a high mortality of
approximately 40% [39]. Careful use of antimicrobials is also important for
minimizing antimicrobial resistance and subsequent nosocomial infections
with multiresistant bacteria.
Appropriate postoperative use of antimicrobials is important, however, to
prevent many serious complications. In human surgery, several studies have
found no benefit to prophylactic postoperative antimicrobial use for longer
than 24 hours after surgery [35]. There have been no studies evaluating the
need for postoperative antimicrobial therapy for horses undergoing
abdominal surgery. In a survey of ACVS members, 72% to 78% of
respondents used antimicrobials for 1 to 5 days (most for 24 hours) after
surgery if there was no intestinal penetration or intestinal decompression
only; 100% of respondents used antimicrobials for 1 to 10 days if an
enterotomy or enterectomy was performed; and 88% of respondents used
antimicrobials for 1 to 10 days (most for 5 days) if there was intestinal
ischemia or LCV [36]. Many horses with LCV are leukopenic after surgery,
and it is unknown whether horses that are leukopenic require antimicrobials

after surgery. Interestingly, 50% of ACVS members used antimicrobials for 1
to 5 days (most for 3 days) in horses that were leukopenic or until the
nucleated cell count returned to within normal limits, and 34% did not use
antimicrobials or discontinued the use of antimicrobials in leukopenic horses
[36]. Further clinical studies are required to evaluate the use of postoperative
antimicrobials in horses undergoing abdominal surgery, because it is possible
that antimicrobial therapy is being overused. Postoperative monitoring of
hospital infection rates and identification of the cause of an increase in
infection rate (eg, visceral retainer or inadequate skin preparation) are
important. Culture and sensitivity testing should be performed for any
source of infection (eg, incisional or catheter site infections, peritonitis) to
ensure that the patient is being treated with the appropriate antimicrobial
therapy and to identify common hospital pathogens and their sensitivity
patterns.
Flunixin meglumine
Flunixin meglumine (1.1 mg/kg administered IV every 12 hours) is
routinely administered to horses undergoing exploratory celiotomy for
analgesia as well as for its anti-inflammatory and antiendotoxic effects.
Flunixin meglumine was used by 86% of ACVIM and ACVS respondents at
0.25 to 1.1 mg/kg for prevention or treatment of endotoxemia [34]. Flunixin
meglumine is a nonsteroidal anti-inflammatory drug (NSAID), which
inhibits cyclooxygenase (COX) and subsequent prostaglandin synthesis.
Endotoxin administration results in an increase in thromboxane B2 (TXB2)
and 6-keto-prostaglandin F1 (PGF1) [17]. Numerous early studies showed
that flunixin meglumine (1.1 mg/kg administered IV) prevented clinical signs,
cardiovascular and hemodynamic alterations, arterial hypoxemia, and lactic
acidosis after experimental administration of endotoxin [40–45]. Flunixin
meglumine (1.1 mg/kg) also suppressed the increase in TXB2 and PGF1 after
endotoxin administration compared with untreated horses [44]. The
commonly used ‘‘antiendotoxic dose’’ or ‘‘low dose’’ of flunixin meglumine
(0.25 mg/kg administered IV) was also shown to suppress the increase in
TXB2 and PGF1 as well as hyperlactatemia after administration of endotoxin
to horses [46]. The low dose is not commonly used in the postoperative
management of horses with LCV, because flunixin meglumine is used as an
analgesic as well as for its antiendotoxic effects, but it is recommended for
horses with persistent or severe azotemia.
Commonly recognized complications associated with the use of flunixin
meglumine include gastric ulceration and renal crest necrosis [47]. More
recently, in vitro studies have indicated that the use of nonspecific COX
inhibitors, such as flunixin meglumine, which inhibits COX induced by
inflammation or endotoxin (COX-2) as well by as the constitutively pro-
duced COX (COX-1), may inhibit repair of ischemic-injured intestine and
reduce intestinal motility [48,49]. In the future, the use of specific COX-2
inhibitors for horses after abdominal surgery may be possible.
Other NSAIDs, such as phenylbutazone and ketoprofen, have been
evaluated for use in horses with gastrointestinal tract disease; however, their
use has not gained widespread acceptance. A large dose of phenylbutazone
(10–15 mg/kg administered IV every 6 to 12 hours) inhibited clinical signs,
hemoconcentration, hyperlactatemia, hyperglycemia, and acidosis after ad-
ministration of endotoxin to ponies; however, three of the five ponies died [50].
Phenylbutazone (4.4 mg/kg administered every 8 hours for 12 days) caused
hypoalbuminemia, gastric and colonic ulceration, jejunal edema, and renal
crest necrosis. Therefore, based on these studies, phenylbutazone is not ideal
for postoperative management of horses with LCV [47,50]. Ketoprofen
(1.1–2.2 mg/kg administered IV every 24 hours) was reported to be less
nephrotoxic and less ulcerogenic compared with phenylbutazone and flunixin
meglumine and was found to be an adequate analgesic for mild to moderate
abdominal pain, similar to flunixin meglumine [47,51].
Polymixin B
Polymixin B is a cyclic cationic polypeptide that has a high affinity to the
lipid A portion of endotoxin [52]. Lipid A is the toxic portion of the LPS
molecule [28]. Once polymixin B is bound to endotoxin, a stable complex is
formed and the conformation of endotoxin is altered, preventing binding to
cell receptors and cell activation [15]. When endotoxin enters the systemic
circulation, it binds to an acute-phase reactant protein (LPS-binding protein),
which facilitates endotoxin binding to and activation of endothelial cells,
platelets, neutrophils, and mononuclear inflammatory cells [15]. Activation
of these cells results in the release of numerous proinflammatory mediators,
including tumor necrosis factor (TNF) and interleukins (ILs), in addition to
arachidonic acid metabolites (TXB2 and PGF1) and procoagulant mediators
(tissue factor [TF]), which have already been discussed [15]. Early in vitro
studies demonstrated that endotoxin-induced production of TNF and lactate
by macrophages was inhibited by polymixin B [53]. Polymixin B significantly
reduced clinical signs (tachycardia, tachypnea, and pyrexia) and proin-
flammatory mediator (TNF and IL) responses of experimentally adminis-
tered endotoxin in horses in a dose-dependent manner [54–57]. A dose of 5000
U/kg had significantly beneficial effects, even when given 30 minutes after
endotoxin [55]. These studies have clearly demonstrated a favorable effect of
polymixin B on normal horses after exogenous administration of a single dose
of endotoxin. Polymixin B is usually administered at a dose from 1000 to 5000
U/kg in 1 to 3 L of isotonic fluids every 8 to 12 hours. There have been no
studies, however, evaluating the effects of polymixin B in clinical cases of
horses with LCV.
Polymixin B is potentially nephrotoxic and neurotoxic [52]. Nephrotox-
icity has not been documented in experimental studies in horses, even with
doses up to 36,000 U/kg [54,55,58]. Moderate reversible neurologic signs

(coughing and ataxia) were noted at doses of 18,000 and 36,000 U/kg but
not at doses of 10,000 U/kg or less [54,55,58]. Conjugation of polymixin B
with dextrans theoretically reduces the likelihood of toxicity at higher doses
[56]. In horses, the conjugate resulted in sweating, tachypnea, and increased
circulating TXB2, however, and these high doses do not seem to be
necessary to inhibit clinical signs of endotoxemia [54–57]. There are no clear
benefits of the dextran conjugate, and the dose that has been shown to
prevent clinical signs of endotoxemia does not seem to be nephrotoxic or
neurotoxic. Although studies have shown that polymixin B at recommended
doses for treating endotoxemia is relatively safe and effective, care should be
taken with its use in dehydrated or azotemic horses.
Pentoxifylline
Pentoxifylline, a methylxanthine derivative, improves red and white cell
deformability (rheology) and postepinephrine blood viscosity, decreases
platelet aggregation, enhances chemotaxis, decreases neutrophil adherence,
causes vasodilation, and may improve microcirculation [44,59,60]. In
addition, pentoxifylline inhibits TNF production and the effects of TNF on
leukocytes, decreases TXB2 concentration and tissue thromboplastin activity,
and increases PGF1, which suggests that it would be beneficial in the post-
operative management of horses with LCV [44]. Pentoxifylline is adminis-
tered orally at a dose of 8.5 mg/kg every 12 hours [59]. Many of the effects of
pentoxifylline are mediated by an increase in release of PGF1 and PGE2 [44].
PGF1 and PGE2 synthesis is inhibited by flunixin meglumine, suggesting that
pentoxifylline and flunixin meglumine could have a synergistic effect [44].
Pentoxifylline (8 mg/kg) was found to have a synergistic effect with flunixin
meglumine in inhibiting the deleterious hemodynamic effects after adminis-
tration of endotoxin to horses and was also shown to inhibit endotoxin-
induced increases in TNF and IL-6 activity and to decrease TF activity in vitro
[44,61,62]. There have been no deleterious effects associated with pentoxifyl-
line administration, and it is relatively inexpensive; however, it is reportedly
most efficacious when used before the onset of signs of endotoxemia, and
clinical studies assessing its benefits have not been performed [44].
Heparin
Heparin is an anticoagulant that may be used in horses with LCV because
of the predisposition of these horses to develop systemic coagulopathies as
well as focal ischemic necrosis in the LC (see Fig. 4). Heparin is an
endogenous sulfated glycosaminoglycan of varying molecular weight, which
is produced by mast cells and found in the highest concentrations in the
liver, lung, and intestine [63]. Commercially available heparin is usually
produced from bovine lung or porcine intestinal mucosa as either calcium or
sodium salts, and because of the large range of molecular weights in

unfractionated heparin, there is a large amount of variability in preparations
[63]. Unfractionated heparin binds to ATIII and platelets. The most
recognized action of heparin is as a catalyzer for the reaction between ATIII
and thrombin, which decreases the amount of thrombin being produced and
inactivates that already available. Heparin also inactivates factors IX, X,
XI, and XII as well as kallikrein. The low-molecular-weight fraction of
heparin binds to ATIII only and hence is associated with fewer side effects,
such as thrombocytopenia. Thrombocytopenia, thought to be associated
with binding of heparin to platelets or with an immune-mediated response in
human beings, does not seem to be a problem in the horse.
Plasma concentrations of heparin between 0.2 and 0.4 U/mL prolong
APTT 1.5 to 2.5 times normal limits and are considered to be in the
therapeutic range for anticoagulant therapy. This concentration also results
in a decrease in hematocrit. Lower doses can have antithrombotic rather
than anticoagulant effects, however, and should not prolong the APTT.
Antithrombotic or low doses of heparin increase inactivation of thrombin
and factor Xa by endothelium, inhibit activation of factors V and VIII by
thrombin, increase the activity of tissue plasminogen activator (tPA) and
decrease the activity of tPA inhibitor (PAI), increase phagocytosis by the
mononuclear phagocytic system, regulate complement, reduce the pro-
duction of TF by monocytes and increase TF inhibitor, and inhibit platelet-
activating factor (PAF) and platelet aggregation [63,64].
Heparin was used by 23% of ACVIM and ACVS respondents for
treatment of horses with endotoxemia [34]. The low dose of sodium heparin is
40 to 80 U/kg administered IV and then 40 U/kg administered sub-
cutaneously (SC) every 8 to 12 hours for 48 to 72 hours, at which dose there is
reportedly no increase in APTT or decrease in hematocrit [63,65]. Heparin
can be used alone when ATIII activity is greater than 60% of normal but
should be used with fresh-frozen plasma if ATIII activity is less than 60% of
normal. Heparin (plasma, 400 U/L of plasma) can be used to activate ATIII
and inhibit coagulation protein activation before plasma administration.
Calcium heparin is required at higher doses (150 U/kg administered SC
initially and then 120 U/kg administered SC every 12 hours), because the
calcium inhibits the reaction between heparin-ATIII-thrombin; however, at
these doses, there is an increase in APTT and a decrease in hematocrit [63].
Therefore, the use of sodium heparin is recommended.
Sodium heparin (80 U/kg administered IV) 30 minutes before LC
detorsion prevented systemic hypotension, the increase in colonic vascular
resistance, and the increase in thromboxane concentration in a pony LCV
model [64]. Sodium heparin also increased colonic blood flow during the
reperfusion period [64]. It did not alter the histologic appearance of the LC,
however, possibly because of reduced perfusion during heparin administra-
tion. Reduced production of bradykinin and TXB2 were thought to be
responsible for the findings in this study [64].
The author has routinely used heparin (40 U/kg administered IV

immediately before LC detorsion and then 40 IU/kg administered SC every
12 hours for 48 hours) clinically in horses with LCV. Subjectively, there was
an increase in LC perfusion, with the serosa becoming pink more rapidly
compared with horses not treated with heparin. The author has had one horse
treated with heparin develop focal ischemic necrosis of the LC after LCV;
therefore, in severe cases, heparin and aspirin therapy can be combined (5 mg/
kg administered orally every 48 hours for one or two doses). The benefit of
this treatment is unknown, and care should be taken using a combination of
heparin and aspirin, with the horse monitored closely. Complications
associated with the use of heparin in horses include a decrease in hematocrit
secondary to erythrocyte agglutination as well as incisional and abdominal
bleeding. The hematocrit appeared to decrease to less than 30% after 24 to
72 hours in horses with LCV treated with heparin, and horses did have
a tendency for incisional and abdominal bleeding after surgery. During
surgery, horses given low-dose heparin subjectively had more bleeding during
resection and anastomosis and abdominal wall closure. The use of low-dose
heparin should not cause hemorrhage; however, hypoproteinemia, altera-
tions in metabolism, and different concentrations of inflammatory and
coagulation proteins may have been associated with the low dose and these
signs. Therefore, heparin should be used with caution in horses with LCV,
and therapy should be monitored closely by evaluating the hematocrit every
6 hours as well as APTT and ATIII activity.
Low-molecular-weight heparin did not cause erythrocyte agglutination;
decreased hematocrit, hemoglobin concentration, red cell counts, or platelet
counts; or increased APTT and thrombin time, and it may be safer than
unfractionated heparin [66]. Low-molecular-weight heparin binds less avidly
to heparin-binding proteins and is thus more biologically active at lower
doses, resulting in more predictable activity. Currently, expense is a
major factor limiting routine use of low-molecular-weight heparin in equine
patients.
Free radical scavengers

Endotoxemia, ischemia and reperfusion, and tissue damage result in the
production of oxygen-derived free radicals. Inflammation, with the release of
free radicals from activated neutrophils and macrophages, is thought to be
a major cause of oxidant injury [67]. Free radicals produced include the
hydroxyl radical by the Fenton or Haber-Weiss reaction, hydrogen peroxide,
the superoxide radical by xanthine oxidase, and hypochlorous acid from
myeloperoxidase in neutrophils [67]. Initiation of lipid peroxidation by the
hydroxyl radical, for example, results in a chain reaction of free radical
production, oxidant injury, and tissue damage [67]. Malondialdehyde is
produced as a result of lipid peroxidation and can be measured in blood
and tissue. Endogenous enzymatic and nonenzymatic antioxidants include
superoxide dismutase, catalase, selenium, glutathione peroxidase, glutathi-

one, N-acetylcysteine, vitamin E, vitamin C, and several plasma proteins [67].
The author recently evaluated systemic oxidant injury in a few clinical
patients with LCV and colitis. There was a trend for horses with LCV or
colitis to have increased systemic malondialdehyde, decreased selenium, and
an increase in the ratio of reduced to oxidized glutathione compared with
healthy controls (L.L. Southwood, BVSc, PhD, unpublished data, 2001).
Only small numbers of horses have been evaluated, however, and measure-
ments in a large group of horses should be performed before making
conclusions. The use of antioxidants, such as dimethyl sulfoxide (DMSO),
allopurinol (xanthine oxidase inhibitor), manganese chloride (superoxide
scavenger), nonglucocorticoid aminosteroids (inhibit iron-dependent lipid
peroxidation), and superoxide dismutase, for treatment of horses with
endotoxemia and LC ischemia and reperfusion has been evaluated
experimentally in numerous studies. Results have been variable, however,
probably because of variability in doses, timing of administration, and
severity of the experimental model. Most of these treatments have not been
used in clinical cases of LCV, except for DMSO [34].
DMSO is a hydroxyl radical scavenger and prevents leukocyte adherence
to endothelium, decreasing neutrophil accumulation and lipid peroxidation
[68]. DMSO was used by 41% of ACVIM and ACVS respondents for
treatment of horses with endotoxemia [34]. Although data from studies in
laboratory animals evaluating DMSO for decreasing injury from ischemia
and reperfusion were favorable, results in horses have been less favorable
[69,70]. Horne et al [71] evaluated the effect of DMSO (1 g/kg IV) on the
histologic changes in the jejunum of horses subject to ischemia and
reperfusion and found no benefit of treatment. The authors proposed that
the lack of a response may have been associated with the severity of the
model, the timing of treatment, and poor perfusion to the mucosa (ie, many
studies showing a beneficial effect had instituted treatment before the onset
of ischemia) [71]. Although one study demonstrated that DMSO protected
the jejunum from the decreased PVR and oxygen consumption associated
with ischemia and reperfusion, other studies by the same authors showed no
effect of DMSO on oxygen consumption, potassium loss, intestinal motility,
or histologic changes (enterocyte detachment, fluid accumulation, and cell-
to-cell adhesions) [72–74]. DMSO prevented the decrease in PVR associated
with reperfusion, however [73,74]. Similarly, in the LC, there were no
beneficial or deleterious effects of DMSO (1 g/kg IV in a 20% solution) as
assessed histologically or by measuring the reduced-to-oxidized glutathione
ratio after experimental hemorrhagic or ischemic strangulating obstruction
[75]. Another study, however, found that DMSO (1 g/kg IV in a 10%
solution) resulted in more mucosal damage compared with controls in
a model of LC ischemia and reperfusion [68]. The authors recommended not
using DMSO at a dose of 1 g/kg for horses with LCV, but it may be safer
and efficacious a lower dose of 0.1 g/kg [68].
Corticosteroids
The use of the corticosteroids dexamethasone and prednisolone in shock,
particularly in endotoxic shock, is controversial. The major concerns
regarding the use of corticosteroids in horses with LCV are the risk of
laminitis and the risk of potentially increasing the susceptibility to infection as
a result of inhibition of neutrophil migration and bacteriocidal activity.
Although the benefit of corticosteroids has been evaluated experimentally,
there have been no studies evaluating the effects of corticosteroids on
structure or function of the LC after strangulation or on the survival of horses
with LCV [76–78]. Dexamethasone (1 mg/kg IV) was shown to reduce endo-
toxin-induced leukopenia, hyperlactatemia, and coagulopathy in anesthe-
tized ponies, and prednisolone sodium succinate (30 mg/kg IV) maintained
normal arterial oxygen tension and attenuated the decrease in SV after
administration of endotoxin, but it did not alter the PAP, PVR, or
hyperlactatemia and did not improve clinical signs [76,77]. In the same study
[77], flunixin meglumine (1.1 mg/kg IV) prevented the clinical signs of
endotoxemia, maintained arterial oxygen and carbon dioxide tension, and
prevented pulmonary hypertension and the increase in PVR and SV.
Similarly, in yet another study, neither dexamethasone (2 mg/kg IV) nor
prednisolone sodium succinate (10 mg/kg IV) altered clinical, hematologic, or
biochemical changes associated with endotoxin administration, but flunixin
meglumine (1.1 mg/kg IV) improved clinical signs and prolonged survival
[78]. Based on these studies, there seems to be no benefit to using corticos-
teroids compared with flunixin meglumine. The author has used a low dose of
dexamethasone (30–50 mg in a 450-kg horse every 24 hours for one or two
doses) in a few postoperative colic patients and has not observed any
deleterious effects; however, the use of dexamethasone on improvement of
clinical signs and survival in these patients has not been critically evaluated.
Progesterone
Many horses with LCV are broodmares, and we found that approximately
8% were recorded as being pregnant at the time of admission for LCV [3,4].
The abortion rate for horses with abdominal pain and undergoing ex-
ploratory celiotomy is approximately 20% and may be higher for horses with
LCV [13]. Endotoxemia causes a loss of luteal activity and, subsequently,
endogenous progesterone secretion as a result of increased PGF2a concen-
tration [79,80]. Low progesterone concentrations are associated with
abortion [79]. The use of altrenogest (44 mg or 20 mL) to compensate for
the low endogenous progesterone was found to be beneficial in preventing
fetal loss in the first 2 months of pregnancy [79]. Altrenogest (Regu-Mate;
Hoechst-Roussel Agri-Vet Company, Somerville, NJ) is commonly used at
0.044 to 0.088 mg/kg orally in pregnant mares undergoing abdominal surgery.
Flunixin meglumine was also found to prevent fetal loss after administration
of endotoxin; however, treatment early in the course of endotoxemia was

required [80].
Additional analgesia
Lidocaine
The routine use of intravenous lidocaine for postoperative management of
colic patients has been relatively recent. Lidocaine is generally used after
surgery as a motility stimulant; however, its analgesic and effects have
recently been recognized [81]. Side effects associated with lidocaine include
collapse and seizure, which are associated with higher doses or rapid infusion.
Seizures stop, and the author has not observed any persistent side effects once
lidocaine was discontinued. Other potential complications include increased
risk of incisional infection and laminitis, but the author has not observed
these problems. The author routinely uses lidocaine as a bolus (1.3 mg/kg IV),
followed by a constant rate infusion (0.05 mg/kg/min IV) administered using
a fluid pump without observed side effects.
Butorphanol
Constant rate infusion of butorphanol (13 lg/kg/h IV) was found to
decrease plasma cortisol concentrations, result in less weight loss, and result
in a shorter hospital stay compared with untreated horses [82].
Nutritional requirements
Adequate postoperative nutrition is important for a successful outcome.
Feed is usually withheld for 6 to 12 hours after surgery and then is gradually
reintroduced over 36 to 72 hours depending on the degree of LC damage and
whether or not the horse is showing signs of gastrointestinal tract disruption.
Hand grazing is our preferred method for initial reintroduction of feed. If the
horse develops complications, parenteral nutrition is recommended, and if
economics are not a concern, partial parenteral nutrition after surgery may be
beneficial in cases in which LC damage is severe and in pregnant or lactating
mares. Weaning of a foal should also be suggested to the owner because of the
large demands of lactation; in addition, the mare is unlikely to produced
adequate milk for the foal. Regular body weight measurement of the mare
and foal is important. Nutritional support of postoperative LCV patients has
not received a lot of attention; however, it is an area that needs more
investigation.
Future therapy
Current research is directed toward mechanisms to manage endotoxemia
and oxidant injury to the LC after ischemia and reperfusion. Research is
also required to determine methods to facilitate mucosal regeneration and
improve blood supply to the ischemic LC.
Recurrence of LCV can occur, and approximately 30% of horses that were
discharged after LCV had recurrent episodes of colic [4]. The major factor
influencing whether on not a horse had problems with abdominal pain after
surgery was having multiple episodes of colic before LCV surgery (17%
versus 50%) [3]. Although surgical methods to reduce the recurrence of LCV
exist (colopexy and LC resection), these procedures are usually not performed
at the first surgery. Many horses do not survive repeat LCV for either medical
or economic reasons. Investigation into nonsurgical methods to reduce LCV
recurrence, such as diet and management, are needed.
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Postoperative Management of The Large Colon Volvulus Patient

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Postoperative Management of The Large Colon Volvulus Patient

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Vet Clin Equine 20 (2004) 167–197

Postoperative management of the large

Prognosis, pre- and intraoperative considerations, and the importance

E-mail address: southwoo@vet.upenn.edu

63% of horses, and aspartate aminotransferase [AST] in 75% of horses), most

hematocrit (>50%) and TP (\4.5 g/dL) and fever to be associated with

severe or extensive than thought to be the case based on initial assessment.

rate, rectal temperature, gastrointestinal tract sounds, oral membrane color

infection, pneumonia, and placentitis or endometritis in broodmares. After

should also be monitored several times a week, particularly in horses that

24 to 48 hours after surgery; however, the hematocrit and TP should converge

the cardiovascular eﬀects of endotoxemia [15]. The ﬂuid rate can be

tration is aﬀected by albumin concentration. Extracellular electrolyte

Deficit ðmEqÞ ¼ Normal ðmEq=LÞ Measured ðmEq=LÞ BWT 0:3

where BWT is body weight (kilograms). Calcium should be given if calcium

Base Deficit 0:3 BWT ¼ HCO3 Deficit ðmEqÞ

hemoglobinuria [25]. In addition to potential complications, the beneﬁts of

factors and antithrombin III (ATIII); and to provide antibodies to endotoxin.

ðTPg TPrÞð0:05 BWTÞ=TPd

and it is unknown whether horses that are leukopenic require antimicrobials

doses up to 36,000 U/kg [54,55,58]. Moderate reversible neurologic signs

sodium salts, and because of the large range of molecular weights in

The author has routinely used heparin (40 U/kg administered IV

Free radical scavengers

superoxide dismutase, catalase, selenium, glutathione peroxidase, glutathi-

of endotoxin; however, treatment early in the course of endotoxemia was

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