Ludovica Chiavaccini1 and Lauren R. Duffee2 1 Department of Comparative, Diagnostic and Population Medicine, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA 2 Massachusetts Veterinary Referral Hospital, Woburn, Massachusetts, USA “Colic” is a term used to describe abdominal pain in the horse. The underlying pathology typically occurs in the gastrointestinal tract but can also be caused by disease in the kidneys, bladder, or other viscera. Colic is a significant cause of morbidity and mortality in equine practice. Most horses with colic are treated with medical management, and only a minority of cases require surgical intervention. In a 1997 epidemiological study, approximately 11 colic cases occurred for every 100 horse‐years. While 75% of these were mild and resolved with no treatment or a single farm visit, 4% of all cases needed surgical intervention [1]. The percentage increases when considering horses hospitalized for colic. Of 1588 horses with colic presenting to a veterinary hospital in Denmark for inpatient care, 31% needed exploratory laparotomy [2]. Similarly, in another study on 649 horses hospitalized for colic, 28% received abdominal surgery [3]. Recent epidemiological studies have found an average survival to discharge rate of 42–54% for colic surgery [2,4]. Patients that present with colic that require surgical intervention represent a high‐risk population that necessitates careful preparation and intensive perioperative management. This chapter will focus on the anesthetic management of surgical colic cases, including the practical and theoretical aspects of preparing for an emergent exploratory laparotomy. After discussing the management concerns and anticipated anesthetic complications, the authors will describe the stabilization of the patient and selection of an appropriate anesthetic protocol. Endotoxemia in the colic horse presents a significant challenge to the anesthetist. Recent studies estimate that 30% of all horses with colic [5,6] and 55% of horses needing colic surgery [6] meet systemic inflammatory response syndrome (SIRS) criteria. The clinical effects of sepsis, often exacerbated during general anesthesia due to sympathetic suppression and the pharmacologic effects of anesthetic drugs, underlie many anticipated anesthetic complications encountered in horses undergoing colic surgery. Therefore, the anesthetist should understand the etiopathogenesis and the therapeutic strategies to manage the endotoxemic horse. Endotoxemia occurs when gram‐negative bacteria or their cell wall components, such as lipopolysaccharide (LPS), enter the bloodstream. With strangulating colic lesions, the impaired blood supply to the entrapped bowel leads to segments of ischemic gastrointestinal mucosa and consequent impairment of epithelial integrity that allow for translocation of these bacterial components [7,8]. LPS is bound by circulating LPS‐binding protein; this complex then binds to the CD14 protein on the surface of circulating macrophages. Activated macrophages then secrete numerous proinflammatory cytokines that initiate a signaling cascade, leading to the onset of SIRS [9,10]. Interleukin‐1 (IL‐1) induces fever, increases circulating neutrophils, reduces albumin synthesis, and increases acute phase protein production. Tumor necrosis factor‐α (TNFα) stimulates further IL‐1 production, neutrophil adhesion, and extravasation and plays a role in the coagulopathy seen during endotoxemia. Interleukin‐6 (IL‐6) leads to the differentiation of B‐lymphocytes into antibody‐producing cells and increases the production of acute phase proteins [7]. The release of epinephrine and norepinephrine into the systemic circulation is triggered by LPS, which increases cardiac output and causes tachycardia, pulmonary hypertension, arterial hypoxemia, and tachypnea. Splenic contraction contributes to hemoconcentration in dogs and, likely, in horses [11]. Myocardial dysfunction, characterized by biventricular dilation and reduced ejection fraction, is attributed to increased circulating TNFα [12]. The release of reactive oxygen species by neutrophils increases circulating inflammatory cytokines, like TNFα, and matrix metalloproteinases (MMPs), leading to endothelial glycocalyx degradation. Degradation of the glycocalyx increases vascular permeability to fluid and plasma proteins [12,13]. Circulating inflammatory mediators also result in vascular dysregulation and decreased systemic vascular resistance, leading to systemic hypotension [12]. Increased lactate concentrations, metabolic acidosis, and perfusion‐dependent oxygen consumption suggest disruptions in oxygen delivery and cellular metabolism, although the mechanism is not entirely understood [12]. Thus, septic shock has hypovolemic, cardiogenic, and distributive components, contributing to a state of hypoperfusion. Hyperglycemia first occurs due to increased hepatic gluconeogenesis, but glycogen depletion and inhibition of gluconeogenesis lead to hypoglycemia over time. Decreased capillary blood flow and pooling of blood in capillary beds lead to the characteristic congestion of mucous membranes, slow capillary refill time (CRT), and cold extremities commonly found on physical examination [14]. The microvascular clotting induced by acidosis and stagnant circulation, consumption of coagulation factors, and fibrinolysis results in coagulopathy that can evolve into disseminated intravascular coagulation (DIC) [15]. If left untreated, endotoxemia culminates in multiple organ dysfunction syndrome, with the kidney, liver, lung, and heart most vulnerable to failure [7]. No official consensus has defined the clinical features of SIRS in the horse. However, most clinicians have adopted the definition established for human patients [16]. A 2017 study determined the diagnostic criteria for SIRS in the horse through statistical modeling of physical examination and hematological variables. It was found that a heart rate (HR) > 52 beats/min, respiratory rate > 20 breaths/min, leukopenia < 5.0 × 109 cells/L or leukocytosis > 12.5 × 109 cells/L, and a rectal temperature < 37 °C or > 38.5 °C were associated with higher mortality [6]. Based on this definition, researchers found that 30 out of 55 surgical colic horses presenting for emergency laparotomy met the SIRS definition criteria and had almost sevenfold mortality risk than surgical colics that did not meet these criteria. There are several biomarkers used in human medicine to detect sepsis and SIRS. Recently, molecular biomarkers such as MMP‐9 [17], protein carbonyl content [18], serum amyloid A [19,20], soluble CD14 [21,22], adrenomedullin, and procalcitonin [23] have been studied in the horse. Treatment for patients with endotoxemia includes removing the source of infection (including LPS), fluid therapy and cardiovascular support, and inhibition of the inflammatory response. Administration of immunoglobulins against LPS with hyperimmunized J5 equine plasma helps accelerate the clearance of LPS and gram‐negative bacteria from the bloodstream [24,25]. Hyperimmunized plasma may also contain acute phase proteins that help inhibit the proinflammatory cytokine cascade, as it seems to reduce TNFα activity [26]. However, at present, there is conflicting evidence of the clinical efficacy and improved survival rate of endotoxemic horses treated with hyperimmunized plasma [27–29]. Polymyxin B is an antimicrobial that is effective against gram‐negative bacteria. Its utility lies in its ability to neutralize circulating endotoxin by binding to the lipid A region of LPS, forming a stable, covalently bound compound [30]. Polymyxin B also reduces circulating TNFα, is an antipyretic, and improves tachycardia [31]. However, its use may be limited due to its neurotoxic and nephrotoxic effects [32]. Administration of up to 6000 U/kg intravenously (IV) did not cause changes in adult horses’ γ‐glutamyl transferase (GGT):creatinine ratio [31,33]. In an in vitro endotoxemia model, pentoxifylline, a phosphodiesterase inhibitor, inhibited the activity of TNFα and IL‐6 [34]. Horses challenged with LPS after pentoxifylline administration (7.5 mg/kg bolus followed by a 3‐h infusion of 3 mg/kg/h) recorded significantly lower rectal temperatures and respiratory rates than the control group [35]. Additionally, when pentoxifylline (8 mg/kg IV) was combined with flunixin meglumine (1.1 mg/kg IV), horses had fewer cardiovascular changes after LPS administration [36]. Non‐steroidal anti‐inflammatory drugs (NSAIDs) are commonly utilized as a part of the treatment of endotoxemia due to their ability to reduce circulating prostaglandins levels [25]. Flunixin meglumine reduces clinical signs of endotoxemia and reduces the peripheral vascular effects of LPS [37]. The “antiendotoxic dose” (0.25 mg/kg IV) inhibits eicosanoid production without masking clinical signs of colic pain [38]. However, because flunixin meglumine has been shown to inhibit repair of the epithelial barrier in the ischemic bowel via the inhibition of both COX‐1 and COX‐2 isoenzymes [39], other COX‐2 selective NSAIDs, such as meloxicam (0.6 mg/kg IV) [40] and firocoxib, may become preferred alternatives. These NSAIDs cause less intestinal permeability to LPS than flunixin meglumine [41]. Glucocorticoids, such as dexamethasone and prednisolone, inhibit activation of nuclear factor κ‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling pathways. However, due to the suspected dysregulation of the hypothalamic–pituitary–adrenal axis, high cortisol levels in foals with sepsis [42], and conflicting results from human literature, they are not routinely used to manage the septic horse [25]. Ethyl pyruvate inhibits the formation of reactive oxygen species and has anti‐inflammatory properties [25,43]. Administration of ethyl pyruvate decreased production of TNFα, IL‐8, and COX‐2 expression in an in vitro experimental model [44]. In experimentally induced endotoxemia, ethyl pyruvate (150 mg/kg in 1 L of Lactated Ringer’s solution [LRS] infused over 1 h) significantly decreased pain scores and reduced proinflammatory cytokines compared to the control group that received flunixin meglumine (1.1 mg/kg IV) alone [45]. Despite the lack of detrimental effects of ethyl pyruvate in normal horses, it is not widely used in equine colic surgery. The anesthetist should familiarize themselves with the pertinent details of the case. The duration of clinical signs, diagnostics performed, and therapies performed by the referring veterinarian should be reviewed. The timeline and dosages of all medications should be listed. Prior surgical or anesthetic history should be reviewed if available. The anesthetist should perform a physical examination of the horse prior to induction of anesthesia. Evaluation of vital signs, auscultation of cardiopulmonary structures, and gastrointestinal borborygmi, pulse palpation, and visual examination of mucous membrane color and CRT provide essential information for the anesthetist. In addition, palpation of the ear tips and distal extremities provide insight into perfusion status, as cold limbs and ears are consistent with centralization of circulation seen with septic shock. The degree of pain and colic behavior should be evaluated in light of the sedative and analgesic agents already administered. Several pain scales can be used to evaluate the horse affected by colic [46–48]. While most horses can be violently painful with ischemic bowel lesions, draft breeds are more likely to behave stoically and mask disease severity within the abdomen. In the authors’ experience, horses that initially present with severe pain followed by a sudden decrease in intensity of colic signs are at high risk of gastric or intestinal rupture. The anesthetist should be aware of the findings on rectal palpation, the volume of nasogastric reflux, and abnormalities detected via abdominal ultrasound and abdominocentesis. Critical laboratory parameters to evaluate include packed cell volume (PCV) and total solids (TS), lactate, blood glucose, creatinine, complete blood count (CBC), and electrolytes (sodium, potassium, calcium, and magnesium). Hemoconcentration is common in horses with colic. However, a divergence of the PCV and TS, where the PCV is elevated in the face of reduced TS (e.g., PCV 60%, TS 3.4 g/dL), is suggestive of septic shock and more severe disease [13]. Lactate is an important biomarker of the severity of intestinal disease and may provide important prognostic information. Type A lactic acidosis occurs from increased lactate production following hypoperfusion and reduced oxygen delivery, as seen in colic horses due to dehydration, hypovolemia, and shock. Simultaneously, type B lactic acidosis may occur in septic horses due to reduced lactate clearance by the liver [49]. While single lactate values are unreliable prognostic indicators, sequentially increasing lactate values in the face of fluid resuscitation have been associated with increased mortality [50]. Comparison of peritoneal and peripheral lactate values can help diagnose a strangulating versus a non‐strangulating lesion. Horses with strangulating lesions have significantly higher peritoneal fluid lactate values than horses with non‐strangulating obstructions [51,52]. There is a significantly greater risk of ischemic bowel and mortality when the abdominal fluid has a higher lactate value than the peripheral blood [52–54]. Given the critical and emergent nature of the surgical colic and the high risk for morbidity, it is crucial to contemplate the potential problems facing the anesthetist. While the basic anesthetic principles of equine anesthesia remain, certain complications are more commonly observed in the horse undergoing exploratory laparotomy. Hypotension, defined as a systolic arterial pressure less than 90 mmHg (12 kPa) or a mean arterial pressure (MAP) less than 60 mmHg (8 kPa), is a complication commonly observed in horses undergoing emergency exploratory laparotomy. Hypotension has been recognized as a negative predictor of survival to anesthetic recovery [55,56]. Therefore, all horses undergoing colic surgery should have an arterial catheter placed for invasive blood pressure monitoring. This will provide continuous blood pressure measurement and will allow for waveform analysis. Evaluation of the arterial waveform and the plethysmograph waveform during mechanical ventilation can assist the anesthetist in evaluating the severity of the volume deficits and patient fluid responsiveness [57]. A more comprehensive discussion on waveform interpretation and fluid management of the horse undergoing colic surgery is provided later in this chapter. Many horses undergoing colic surgery arrive at induction dehydrated and hypovolemic, increasing the likelihood of hypotension after induction. Those horses that received prolonged medical management are more likely to be fully fluid resuscitated before induction. However, the violently painful colic patient often does not allow adequate fluid resuscitation before surgery. Endotoxemia and septic shock may also contribute to hypotension in the horse undergoing colic surgery. The vasomotor paralysis with endotoxemia can lead to significant vasodilation and subsequent hypotension [12]. Horses severely endotoxemic at the time of induction are likely to be hypotensive throughout the anesthetic event. Some horses may experience endotoxemic “showers” or episodes as the strangulating lesion is released and blood flow to the ischemic bowel resumes. As a severe drop in blood pressure can happen with surgical correction, the surgical and anesthetic teams should communicate to help anticipate and respond quickly to large swings in the patient’s cardiovascular stability. Iatrogenic cardiovascular depression is an important cause of intraoperative hypotension in colic patients. Horses presented for surgical colic are often sedated and premedicated with α2‐adrenergic receptor agonists like xylazine and detomidine. These agents cause bradycardia and eventually prolonged vasodilation with a significant reduction in the cardiac output [58,59]. Once the horse loses consciousness and the sympathetic drive is inhibited by anesthetic agents, the negative cardiovascular effects of these drugs can become readily apparent. Unfortunately, for the safety of the patient and surgical personnel, and given the lack of reliable sedative alternatives, α2‐adrenergic receptor agonists are a mainstay in equine anesthesia. It is well established that maintenance with inhalant anesthetics contributes significantly to hypotension through their vasodilative and negative inotropic effects [60,61]. Therefore, there is an emphasis on incorporating inhalant‐sparing agents in a balanced anesthetic protocol that helps limit the amount of inhalant anesthetic required to maintain a surgical plane of anesthesia. The reader is referred to the section entitled “Adjunct agents” in this chapter. Another critical factor contributing to hypotension is the compression of vasculature when the horse is placed in dorsal recumbency [62,63]. Tilting the table to Trendelenburg or reverse Trendelenburg positioning does not appear to have a significant effect on arterial blood pressure [64]. In the authors’ experience, the adverse effects of recumbency are more severe when the horse is not adequately fluid loaded. While dorsal recumbency is unavoidable in the horse undergoing colic surgery, precious time can be saved by starting to clip and surgically prepare the patient while it is standing or in lateral recumbency. Intermittent positive‐pressure ventilation (IPPV) is yet another contributing factor to hypotension. The positive intrathoracic pressures created with the inspiratory phase compromise venous return of blood to the heart [57,65]. The impairment involves the large veins returning to the right atrium and the pulmonary capillaries. It is reasonable to assume that the severity of the cardiovascular effects of IPPV increases with higher airway pressures and longer inspiratory times. However, there is conflicting evidence in the literature [66,67]. Therefore, the anesthetist must wisely balance the need for mechanical ventilation and its negative impact on cardiovascular function. The decision regarding which system to prioritize will vary from case to case and should be consistently re‐evaluated as the case progresses. Despite fluid administration and position changes, positive inotropes and vasopressors are often needed to maintain acceptable blood pressure in the horse undergoing colic surgery. Dobutamine can be used as an infusion (0.25–2 μg/kg/min) to increase cardiac output, stroke volume, and blood pressure [68,69]. In response to severe vasodilation, phenylephrine (0.25–1 μg/kg/min) or norepinephrine (0.1–1 μg/kg/min) can increase blood pressure through vasoconstriction, increasing the diastolic pressure and reducing venous blood pooling. Norepinephrine may be preferred over phenylephrine as a vasopressor as it may better preserve cardiac output [68,69]. Evaluation of intestinal perfusion demonstrated sustained blood flow through the small intestines, large intestines, and stomach with norepinephrine compared to phenylephrine infusion [69]. During the transition from the induction area to the operating table and from the table to the recovery area, ephedrine (0.05–0.1 mg/kg IV) can be a useful tool to provide both inotropic and vasomotor support, as it is a mixed β1‐ and α1‐adrenergic receptor agonist [70]. Ephedrine is effective as a single injection and has a 10–15‐min clinical effect. However, the pressure‐increasing effect of ephedrine is transient due to its indirect sympathomimetic activity, and it may become ineffective if used in infusion for a prolonged period [71]. In addition, the reader should be aware that ephedrine does cross the blood–brain barrier and may decrease the anesthetic plane of the horse. Adrenergic agent efficacy is reduced in the face of acidemia [72], and vasopressin may be required to increase systemic vascular resistance in this circumstance. Absolute or relative hypoxemia is a commonly encountered anesthetic complication in equine anesthesia [73]. In a recent retrospective study, horses undergoing colic surgery were over six times more likely to develop hypoxemia (defined as PaO2 less than 80 mmHg or 10.6 kPa) than horses undergoing elective procedures [74]. Despite the frequent occurrence of severe blood gas derangements, no study has established a clear association between hypoxemia and an increased risk of mortality in horses [73]. It is worth noting that the above‐mentioned retrospective study reported that 32.47% of horses undergoing a hypoxemic event during general anesthesia did not survive discharge from the hospital, compared to 15.49% of those that did not develop hypoxemia [74]. It appears that the gastrointestinal system can tolerate moderate hypoxemia. A recent study found that an arterial hemoglobin saturation with oxygen (SaO2) of less than 90% led to an initial increase in oxygen extraction to maintain cellular metabolism. However, tissue oxygenation markedly declined when the SaO2 decreased below 80% [75]. There is conflicting evidence on whether intraoperative hypoxemia increases the risk of surgical site infection in horses undergoing colic surgery. While one study found no link between low PaO2 and incisional complications [76], another study found that horses with PaO2 values less than 80 mmHg (10.6 kPa) and anesthesia times longer than 2 h had a greater risk for surgical site infections [77]. Finally, hypoxemia may be associated with higher risk of poor recovery after colic surgery [78]. The underlying cause for the reduced gas exchange in horses undergoing colic surgery is likely multifactorial but primarily due to ventilation–perfusion (V/Q) mismatch and atelectasis [73,79]. Atelectasis can be classified as either compression atelectasis or absorption atelectasis. By nature of the procedure, horses undergoing colic surgery are dorsally recumbent for the duration of surgery. In dorsal recumbency, the abdominal viscera impose significant pressure on the diaphragm [80–82]. This, combined with the reduced inspiratory muscle tone during general anesthesia, results in cranial displacement of the diaphragm causing compression atelectasis [83]. The abdominal distension that accompanies many colic cases exacerbates the compressive effects of dorsal recumbency. Therefore, horses undergoing surgery for large intestinal lesions are at higher risk of developing hypoxemia [74]. Exteriorizing the distended colon is often followed by significant improvements in the PaO2 [84]. Reverse Trendelenburg position failed to show a benefit on the PaO2 of horses positioned in dorsal recumbency [64,85,86]. The only exception may be in horses weighing more than 600 kg [86]. Several authors have investigated the effect of lower inspired oxygen fractions (FIO2) to reduce the formation of absorption atelectasis [87–90]. From the current body of literature, we can conclude that the use of a higher FIO2 in horses during inhalation anesthesia results in a higher PaO2, but also (and unsurprisingly) a greater alveolar–arterial difference (P(a‐a)O2 gradient) [91]. More evidence is needed to confirm or deny the benefit of reduced FIO2 in managing horses undergoing colic surgery. While a low V/Q ratio is likely the most significant contributor to hypoxemia in the dorsally recumbent horse, areas of increased alveolar dead space, and thus high V/Q ratios, also contribute to poor pulmonary gas exchange. Alveolar dead space increases with poor pulmonary perfusion, seen in reduced cardiac output states [92]. The combination of hypovolemia, cardiovascular side effects from sedatives and anesthetics, and septic shock all contribute to a state of hypoperfusion. Adding an inspiratory pause of 30% of the inspiratory time may improve dead space in dorsally recumbent horses, but its clinical value is still unclear [93]. The anesthetist should prepare to monitor the patient for the onset and progression of hypoxemia and gather the necessary equipment to intervene if hypoxemia arises. Pulse oximetry is a widely available and non‐invasive tool for measuring hemoglobin saturation and should be routinely used. Though there are species differences in the oxyhemoglobin dissociation curve [94], a SpO2 reading of 90% corresponds approximately to a PaO2 of 60 mmHg (8 kPa). As the SpO2 drops further, arterial oxygen content precipitously decreases, warranting intervention [73]. The pulse oximeter is a sensitive and valuable monitoring tool to detect hypoxemia when the horse is breathing room air (as occurs before connection to the anesthesia machine or during the recovery phase). However, when the animal is under general anesthesia and maintained with an FIO2 of 1.0 (100%), the pulse oximeter only signals if the problem is already severe. As a result, it is recommended to routinely perform serial arterial blood gas analysis in the horse undergoing colic surgery. General guidelines suggest an arterial blood sample should be taken 30 min after induction and then every 90–120 min in a stable case or every 45–60 min in a metabolically unstable case [95]. The PaO2 value obtained by blood gas analysis provides an objective measure of pulmonary gas exchange that can be tracked over time and used to evaluate the effectiveness of various interventions. Most treatments for hypoxemia aim to improve V/Q matching. A quick laparotomy incision and exteriorization of the colon reduce the compressive forces of the abdomen and limit the further development of compression atelectasis [84]. The open lung ventilation technique combines IPPV with intermittent alveolar recruitment maneuvers and positive end‐expiratory pressure (PEEP) [96,97]. In 30 warmblood horses anesthetized for colic surgery, 15 were mechanically ventilated with a 15–20 mL/kg tidal volume, 1:2 inspiratory to expiratory time (I:E) ratio and a peak inspiratory pressure (PIP) of 30–45 cmH2O, while 15 received similar ventilation with the addition of 15–25 cmH2O PEEP and intermittent alveolar recruitment maneuvers up to 80 cmH2O (open lung concept). Horses receiving open lung concept ventilation recorded significantly higher PaO2 values (300–450 mmHg; 40–60 kPa) compared to the control group (100–240 mmHg; 13.3–32 kPa) [98]. In an additional study performed on 24 warmblood horses anesthetized for colic surgery, the treatment group that received IPPV with 10 cmH2O PEEP and intermittent alveolar recruitment maneuvers recorded significantly higher PaO2 values and shorter recovery times than the control group [96]. Aerosolized albuterol can be utilized in the hypoxemic colic patient. An earlier study found a twofold increase in PaO2 within 20 min of a 2 μg/kg albuterol dose administered via the endotracheal tube in horses with an initial PaO2 less than 70 mmHg (9.3 kPa) [99]. However, the reader should be aware that the improvement in PaO2 is inconsistent [100]. The underlying mechanism is poorly understood and could be attributed to bronchodilation (via β2‐adrenergic stimulation), improved cardiac output (via β1‐adrenergic stimulation), or a combination of both effects. Finally, pulsed inhaled nitric oxide (NO) has shown promising results. Inhaled NO is delivered to the actively ventilated alveoli, causing selective pulmonary vasodilation and improving V/Q matching at its source [101,102]. An inhaled dose of 2000 ppm NO in nitrogen reduced the pulmonary shunt fraction and improved horses’ PaO2 [103,104]. Unfortunately, the delivery of inhaled NO is not widely available in most equine hospitals at this time. There is limited research on the occurrence of cardiac arrhythmias in horses undergoing colic surgery. Sinus tachycardia (HR > 55 beats/min) is the most common arrhythmia encountered in colic patients and has several underlying causes, including distension of the viscera, pain, and endotoxemia [7]. While hypovolemia and decreased cardiac return are common causes of sinus tachycardia in other species, the literature suggests that the HR in the anesthetized horse is less responsive to acute blood volume changes [105]. A 2014 study evaluated the cardiac rhythm in conscious colic horses over a 24‐h hospitalization period. Atrioventricular (AV) block and atrial premature complexes (APCs) occurred in both colic and healthy horses, although ventricular premature complexes (VPCs) only occurred in horses experiencing colic [106]. In a model of experimentally induced endotoxemia, VPCs were observed after the LPS injection [107]. Though not completely understood, VPCs are likely the result of increased sympathetic tone and circulating inflammatory cytokines [108]. Sporadic VPCs are self‐limiting and rarely require intervention, but in the case of runs of VPCs or multifocal VPCs, treatment with lidocaine should be initiated. Bradycardia and AV blocks are sometimes observed under general anesthesia in colic horses, most commonly at the beginning of the anesthetic event. They are usually attributed to α2‐adrenergic receptor agonist administration and are typically self‐limiting. If severe bradycardia (HR < 20 beats/min) is accompanied by hypotension, an anticholinergic like atropine (0.01–0.02 mg/kg IV), glycopyrrolate (0.005–0.01 mg/kg IV), or hyoscine N‐butylbromide (0.05–0.1 mg/kg IV) [109] can be administered. However, long‐lasting anticholinergics should generally be avoided in the horse due to the potential for impaired gastrointestinal motility [110]. Dobutamine can also be utilized as a positive chronotrope, although this requires higher dose rates (> 5 μg/kg/min) than are typically used for hemodynamic support [111]. An early study showed that one of 84 horses (1.2%) undergoing colic surgery developed postoperative myopathy [112]. In a 2016 retrospective analysis concerning mortality rates associated with equine anesthesia for elective and emergency cases, one horse was euthanized for postanesthetic myopathy/neuropathy, and nine horses had non‐fatal myopathy/neuropathy, accounting for 7% of fatal and 20% of non‐fatal recovery complications, respectively [113]. This study did not explore the relative risk of postanesthetic myopathy in emergency cases compared to elective cases. However, postoperative myopathy tends to occur with prolonged recumbency, typically combined with muscle hypoperfusion [114]. For this reason, horses undergoing colic surgery may be at higher risk of developing neuromyopathies compared to horses undergoing elective procedures. Prevention of postanesthetic myopathy and neuropathy is more effective than treatment. Horses undergoing prolonged anesthesia in a supine position should be placed on protective cushioned padding, the nose should be slightly elevated to minimize development of nasal edema, and the head, limbs, and pressure points should be properly padded. Proper positioning on the operating table and ensuring the hind limbs are not left in an extended position can help reduce the risk of peroneal and femoral nerve injury [112]. Postsurgical myopathy significantly hinders successful recovery, and such horses may need to be recovered with a sling. Treatment is mainly based on medical management and supportive care. In the worst cases, euthanasia may be the only remaining option. The time between the colic horse’s arrival to the hospital and the decision to proceed with colic surgery can be very short. Therefore, it should come as no surprise that thorough preparation by the anesthetist prior to the horse’s arrival is required to keep the process organized and efficient. An induction station or room should be designated as an emergency area reserved for patients with colic and, if possible, should be distinct from the area used for orthopedic cases to prevent contamination. This area can be set up ahead of time with everything needed (Box 62.1). The anesthesia machine should be left pressure checked, the inhalant anesthetic refilled, and the carbon dioxide absorbent should be fresh. The ventilator should be assembled, and a PEEP valve at hand. Positive inotropes and vasopressors should be ready in small fluid bags, attached to primed fluid sets, and assembled in volumetric pumps if available. A large bore fluid administration set and 5 L crystalloid fluid bags should be readily available. All material, including endotracheal tubes, catheters, fluids, arterial line supplies, etc., should be prepared to save valuable time once the horse arrives. Fluid administration should be started before anesthesia induction (or immediately after) to correct fluid, acid–base, and electrolyte derangements. In critically ill patients, the authors prefer to place at least one large‐gauge (10–14 gauge) jugular catheter per side before induction of anesthesia. A second jugular venous catheter can be used to maximize the fluid administration rate or to administer blood products, like hyperimmunized plasma. While not commonly used, the lateral thoracic vein may be another valuable access point for rapid administration of fluids during anesthesia. The lateral branch of the saphenous vein can be catheterized in the neonatal foal [115]. The anesthetist should address two questions when administering fluids: The type of fluids relies on the anesthetist’s final goal and a single fluid type alone is rarely used. For example, crystalloids can be used for tissue rehydration and correction of acid–base and electrolyte abnormalities. Synthetic colloids (e.g., 6% Hetastarch [HES]) can be used for increasing the colloid osmotic pressure (COP). Guidelines set by the Surviving Sepsis Campaign (SSC) in 2021 suggest that at least 30 mL/kg of IV isotonic crystalloid fluid should be given within the first 3 h of resuscitation in human patients with sepsis‐induced hypoperfusion or septic shock. The guidelines also caution against the use of saline for resuscitation, as the resulting hyperchloremic metabolic acidosis has been associated with increased mortality [116]. The prescribed volume corresponds to approximately 15 L for a 500 kg horse, which may be logistically difficult to achieve prior to anesthesia. Instead, small‐volume resuscitation using hypertonic saline solution (HSS), usually at concentrations between 7.2–7.5%, followed by a colloid can achieve similar or superior volume expansion utilizing much smaller volumes than crystalloids alone. The rationale involves using the high osmolality of HSS (2400 mOsm/L) to draw fluids from the extravascular space into the circulation, causing rapid volume expansion and restoring preload while improving cardiac output and perfusion [117,118]. Other effects of HSS beneficial to the horse undergoing colic surgery include protection against inflammation, injury, and impaired intestinal transit [119]. While beneficial, the effect of HSS is short‐lived because, as a crystalloid, it redistributes in the extravascular space within 60–120 min [120]. The addition of a colloid is intended to prolong the plasma expansion effects of HSS through the improvement of the COP [121–124]. Increased COP persisted for up to 24 h after administration of 8–10 mL/kg of HES in hypoproteinemic horses [124] and the effect was slightly longer in healthy horses [123]. More recent studies suggest that the plasma expansion effect of colloids is not a result of fluid resorption from the interstitial space but rather due to interaction with the non‐circulating portion of the intravascular fluid, the glycocalyx. Colloids bind to the glycocalyx increasing its COP and limiting the transendothelial flow of fluids [125]. For this reason, the effectiveness of colloids as plasma volume expanders is thought to be dependent on an intact glycocalyx. This means that under conditions of increased permeability such as sepsis, the plasma expansion effect of colloids is reduced. Controversies still exist regarding the clinical effectiveness of colloids versus crystalloids for fluid resuscitation in horses. It is known that in horses undergoing colic surgery, COP decreases proportionally with the decrease in total protein throughout anesthesia with the administration of 15–25 mL/kg/h of LRS [126]. In a recent clinical study comparing the effects of 6 mL/kg of pentastarch (10% HES) to an equal volume of LRS in horses undergoing elective surgical procedures, 10% HES improved hemodilution, corrected the decreased COP observed with LRS administration, and maintained better blood pressures through anesthesia [122]. However, an early study comparing resuscitation after experimentally induced endotoxemia using 5 mL/kg or 60 mL/kg of a balanced polyionic crystalloid solution, or 5 mL/kg of HSS followed by 10 mL/kg of 6% HES failed to show a difference in cardiovascular and pulmonary effects between the three treatments [127]. These findings corroborate the theory that the effectiveness of colloids as plasma expanders is less apparent in diseased horses than in healthy horses. In the 2016 SSC, a strong recommendation was issued against using starches for resuscitation, as they increased the risk of renal replacement therapy and death in adult patients with sepsis or septic shock [128]. But a recent human systemic review found little to no difference in the mortality rate in critically ill patients (including trauma, burns, and sepsis) using synthetic colloids or crystalloids for fluid volume resuscitation [129]. No strong evidence exists for horses undergoing colic surgery. In one report, long‐term postoperative mortality in horses undergoing emergency exploratory laparotomy was not statistically different following preoperative 10% HES administration versus HSS [130]. Other risks associated with the use of synthetic colloids are the potential for allergic reactions and coagulopathy. In an early study in healthy ponies receiving 6% HES, decreases in fibrinogen concentration, von Willebrand factor antigen, and factor VIII were reported; counterintuitively, reductions in both activated partial thromboplastin time and prothrombin time were also documented [131]. In healthy horses, tetrastarch (6% HES 130/0.4) showed fewer adverse effects and affected platelet function for a shorter period compared to hetastarch (6% HES 670/0.75) [123]. However, there is no mention of bleeding tendency or clinically relevant changes in coagulation parameters in any of the equine reports. The 2021 SSC suggested using albumin in patients that received a large volume of crystalloids instead of using crystalloids alone [128]. Little evidence exists on the use of natural colloids in horses. In one small study, 8 mL/kg of 5% equine albumin solution in 0.9% saline did not significantly change the COP of horses with colic compared to a control group [130]. The authors prefer to administer 2–4 mL/kg of HSS before or immediately after induction of general anesthesia, along with a balanced polyionic crystalloid solution, then add colloids (5–10 mL/kg of 6% HES or plasma), to reduce the total volume needed for resuscitation. For a long time, there was a tendency to treat horses undergoing colic surgery with very aggressive fluid therapy rates. The concept of fluid overload, while commonly recognized as an issue in human and small animal anesthesia, has been largely ignored in equine anesthesia. We now know that aggressive fluid therapy is associated with tissue edema (including pulmonary edema), impaired wound healing, compromised renal function, and increased mortality in septic and postoperative patients [132]. Muzzle and periorbital edema were observed in 83% of horses with experimentally induced endotoxemia that received high infusion rates of an isotonic polyionic crystalloid solution compared to none of the horses that received HSS–HES [127]. Moreover, a recent case‐control retrospective study suggested that larger volumes of fluids administered under anesthesia may be associated with developing postoperative reflux in horses undergoing colic surgery [133]. In human and small animal fluid therapy, the concept of Early Goal‐Directed Resuscitation has been embraced [134]. The idea behind it is the stepwise administration of fluids until normalization of perfusion indicators such as pulse rate and quality, CRT, central venous pressure (CVP), MAP, and urine output. Microvascular variables include pH, base excess/base deficit (BE/BD) systemic lactate, and central venous oxygen saturation (SvO2). While some of these variables can be easily assessed in the horse undergoing general anesthesia for exploratory laparotomy, others are not routinely measured. In addition, it is worth noting that some of these variables (e.g., CVP and urine output) are affected by general anesthesia and mechanical ventilation; hence, their clinical value is reduced in the anesthetized compared to the awake horse. The fluid therapy plan needs to account for: (1) the horse’s daily needs, (2) the hydration status, (3) the ongoing fluid losses, and (4) any acid–base derangement. In an adult horse, fluid requirements are usually estimated to be 2–4 mL/kg/h (or 40–60 mL/kg/day) [135]. The maintenance fluid requirement for a neonatal foal is higher than an adult and can be estimated at 3–5 mL/kg/h [136]. In equids, the gastrointestinal tract serves as a large reservoir of body water, accounting for approximately 20% of the total body water content [137]. As such, gastrointestinal derangement can cause significant and rapid water losses. Water losses through dehydration are estimated as percent dehydration. Physical examination parameters such as mucous membrane moisture, skin turgor, and relative position of the globe are used to estimate the degree of dehydration. Several charts and tables exist to estimate dehydration based on clinical parameters (Table 62.1). However, more recent findings have questioned the validity of such clinical and behavioral methods for assessing water losses [138,139]. In addition to these needs, any patient experiencing ongoing losses, such as nasogastric reflux, diarrhea, or third‐space losses, will require replacement of these volumes to maintain normal fluid balance. Metabolic acidosis occurs frequently in horses with gastrointestinal dysfunction. Severe acidosis can result in myocardial dysfunction, decreased cardiac output, and hypotension [140]. It also inhibits the binding of norepinephrine to adrenergic receptors [140,141]. Chloride deficient metabolic alkalosis can also be observed in horses experiencing abundant nasogastric reflux. Acid–base and electrolyte imbalances should be corrected before or during anesthesia. Metabolic acidosis can improve with administration of polyionic balanced crystalloid solutions. Sodium bicarbonate (NaHCO3) administration in the face of metabolic acidosis that is not caused by bicarbonate loss is controversial and is unlikely to improve survival [142]. However, if the total HCO3 is less than 12 mmol/L or BE is less than –11 mmol/L, bicarbonate therapy is indicated. The amount of NaHCO3 needed to correct acidosis can be calculated (Table 62.2). A quarter to half the calculated dose should be administered over 30 min to 1 h, and acid–base status should be reassessed. The authors prefer to correct pH to 7.2, to avoid overcorrection or side effects like paradoxical brain acidosis, reduced cardiac contractility, hypernatremia, and hyperosmolarity. In a study comparing electrolyte derangements in colic versus healthy horses, the colic group recorded significantly lower potassium, ionized calcium, and magnesium concentrations [143]. Hypocalcemia occurs in 53–86% of horses undergoing colic surgery [143–145]. Suspected underlying causes include endotoxemia, reduced feed intake, fluid therapy, and metabolic acidosis [145,146]. Hypocalcemia contributes to myocardial dysfunction and reduced vasomotor tone, requiring more aggressive vasopressor therapy than in normocalcemic patients [147]. Hypocalcemia can cause muscle weakness, tachycardia, hypotension and may contribute to postoperative ileus (POI) [148]. Calcium administration remains controversial. While some studies have demonstrated improved cardiac function with calcium supplementation in a rodent model of sepsis, others have shown increased mortality with no significant difference in cardiovascular performance [149–151]. Therefore, the authors usually advocate treatment when ionized calcium drops below 1–1.2 mmol/L. Calcium gluconate 10% can be administered at a dose ranging between 0.1 and 0.5 mL/kg (or calcium gluconate 23% at 0.05–0.2 mL/kg). Hypokalemia has been reported in 30% of horses presenting for colic surgery [144]. Horses with obstructive or ischemic bowel had significantly lower potassium values than the control group [143]. Potassium can be reduced due to anorexia, pain, gastrointestinal reflux, enterocolitis, and sodium‐induced diuresis [148,152]. Because potassium is an intracellular electrolyte, if potassium is low in the face of acidosis, the total deficit is likely to be severe. Hypokalemia can be treated with 0.04–0.08 mEq/kg/L (or adding 20–40 mEq of KCl in each L of balanced crystalloids solution). The dose should not exceed 0.5 mEq/kg/h. Guidelines for isotonic polyionic crystalloid solution administration and electrolyte correction are summarized in Table 62.2. Table 62.1 Estimation of dehydration of the horse based on clinical signs. Table 62.2 Recommendations for calculating isotonic polyionic crystalloid solution administration and electrolyte replacement.
62
Horses with Colic
Introduction
Endotoxemia and systemic inflammatory response syndrome
Preanesthetic considerations
Clinical history
Physical examination
Diagnostics
Anesthetic risks and anticipated complications
Hypotension
Impaired ventilation–perfusion matching
Arrhythmias
Postanesthetic myopathy and neuropathy
Preparation of the surgical area
Stabilization and fluid resuscitation
Clinical signs
Mild (4–6%)
Moderate (7–9%)
Severe (> 10%)
Capillary refill time
1–2 s
2–4 s
>4 s
Mucous membranes
Fair
Tacky
Dry
Skin tenting
2–3 s
3–5 s
>5 s
PCV (%)
40–50
50–65
>65
TP (g/dL)
6.5–7.5
7.5–8.5
>8.5
Factor
Formula
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