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% shortterm 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: [email protected] 0749-0739/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.cveq.2003.12.004

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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

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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

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Fig. 2 (continued )

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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 pressure, 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

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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 hematocrit. A generalized lack of colonic viability or focal ischemic necrosis may be indicated by signs of moderate to severe abdominal pain, lack of gastrointestinal 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

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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.

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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

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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, pleuropneumonia). 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

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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 antimicrobials 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

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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 longterm (>72 hours) intravenous (IV) catheterization is recommended (Arrow, Arrow International, Reading, PA; Milacath, Mila International, Covington, 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

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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

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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 acidbase 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 hemodynamic 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

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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 endotoxemia 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 concentrations 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 recommended. Ionized calcium should be measured, because total calcium concen-

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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 administration, 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

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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 extravascular 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, Wilmington, 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

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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 concentration [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 protein 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 polysaccharide, 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 hyperimmune 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.

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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 aminoglycoside 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 gastrointestinal tract motility, which may be restored with administration of calcium [37]. These other reported complications are uncommonly recognized clinically 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 individual patient as well as for the surgical facility. Postoperative antimicrobials 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 parenteral antimicrobials (6.4 times increased risk), horses treated with parenteral 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,

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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 produced COX (COX-1), may inhibit repair of ischemic-injured intestine and

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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 administration 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 proinflammatory mediator (TNF and IL) responses of experimentally administered 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]. Nephrotoxicity has not been documented in experimental studies in horses, even with

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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 postoperative management of horses with LCV [44]. Pentoxifylline is administered 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 administration of endotoxin to horses and was also shown to inhibit endotoxininduced 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 pentoxifylline 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

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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 production of TF by monocytes and increase TF inhibitor, and inhibit plateletactivating 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 subcutaneously (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 administration. Reduced production of bradykinin and TXB2 were thought to be responsible for the findings in this study [64].

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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, alterations 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

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superoxide dismutase, catalase, selenium, glutathione peroxidase, glutathione, 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 measurements 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 cellto-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].

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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 endotoxin-induced leukopenia, hyperlactatemia, and coagulopathy in anesthetized 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 corticosteroids 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 exploratory 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 concentration [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

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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.

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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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