Introduction

This chapter aims to review anesthetic considerations for the management of surgical and diagnostic procedures in the neurologic equine patient as well as the short‐term management of neurologic conditions that may develop in the post‐anesthetic period. Increasing advancements in knowledge and imaging capabilities and the resulting expanded diagnostic and surgical options provide evolving challenges for the anesthetist. Willingness to explore these options in horses that may have previously been euthanized in combination with longer and more complex procedures increases the potential for complications significantly. An understanding of central nervous system physiology and pathophysiology and procedure‐specific complications and their management is therefore important. Communication between the diagnostic imaging, surgical, and anesthetic teams is key to ensure that positioning considerations (and needed positioning aids), surgical/anesthesia time, potential for blood loss, intracranial pressure (ICP) management, analgesia, recovery method, and any other unique challenges have been discussed prior to anesthesia.

General Considerations

Common causes of neurologic presentation in horses include developmental disorders (cervical vertebral malformation/instability), trauma to the brain or spinal cord, and infectious diseases (West Nile virus, equine protozoal myeloencephalitis, equine herpes myeloencephalopathy). Other diseases such as neoplasia, abscessation, vestibular, and cerebellar disease, as well as pharmacological or environmental toxicities may also be seen. Seizures may be observed concurrently or due to unexplained causes. Severity of other clinical signs can range from mild ataxia to recumbency and abnormal mentation, which further challenge anesthetic management.

Anesthetic management for the neurologic horse should focus on maintaining adequate cerebral perfusion pressures (CPPs), avoiding increased ICPs, minimizing ataxia and seizure activity, and managing other body systems (e.g. minimize myopathy) to maximize a favorable outcome. In addition to a detailed neurological evaluation, pre‐anesthetic assessment should include history, signalment, physical examination, and other diagnostic information available. Of particular interest to the anesthetist is the horse’s mentation, degree of ataxia, age, temperament, and ability to lie down and get back up, as this will help plan for anesthesia induction and recovery. For example, one might avoid or minimize sedation in an ataxic horse until it is positioned in the induction area to avoid worsening the ataxia with resulting immobility or inadvertent recumbency. If the horse is unable to stand, safely inducing anesthesia in the stall or trailer and the logistics of transporting the anesthetized animal to the imaging or operating room (i.e. cart, forklift) need to be outlined in advance. Availability of experienced personnel, method of transportation, and the ability to oxygenate and ventilate the horse during transport (using a demand valve or portable anesthesia machine) are important considerations; these should similarly be considered for recovery from anesthesia for a horse that is severely ataxic and has difficulty or is not capable of rising without assistance. Ideally, a padded stall set‐up for neurologic horses should be available and additional tools such as a sling or lift support (i.e. Anderson Sling, UC Davis Large Animal Lift) may be needed for the most severely affected animals. Less severely affected animals with documented ability to lay down and rise on their own often do well with less assistance.

Anesthetic Management for Conditions Affecting the Brain

When anesthetizing horses where brain trauma, neoplasia, inflammation, or abscessation is suspected, minimizing increases in ICP and maintaining CPPs is paramount. The brain has limited capacity for expansion within the calvarium, and an increase in tissue mass (from edema, abscessation, or tumor growth) will require a reduction of cerebral blood flow (CBF) and cerebrospinal fluid (CSF) in order to maintain ICP within normal values. As intracranial compliance is exceeded, ICP raises rapidly. Since CPP is determined by the difference between mean arterial pressure (MAP) and ICP (CPP = MAP − ICP), an increase in ICP will compromise CBF and CPP, leading to potential cerebral hypoxia and ischemia. In addition, elevated ICPs may lead to cerebral herniation and death (Drummond and Patel 2010).

Preventing increases in ICP or reducing ICP in cases where it is already elevated is a critical aspect in the anesthetic management of conditions affecting the brain. Brain tissue and the CSF can only be influenced by invasive procedures (removal of tumor mass, drainage of a subdural or extradural hematoma, CSF drainage from the cerebral ventricle), tissue edema can be addressed with the use of steroids and diuretics (discussed later in the chapter), but from an anesthesia perspective, CBF is where the most rapid changes can be achieved and therefore is typically the focus of management.

The venous side of the cerebral circulation is mostly passive, and venous drainage can be improved by maintaining the head and neck areas at a higher level than the heart, and by avoiding any compression or obstruction of the neck vessels. While head position has shown to have minimal effect in ICP of healthy awake standing horses (Brosnan et al. 2002a), it is particularly significant in anesthetized horses, where cerebral autoregulation may be disrupted and changes in hydrostatic gradients between the brain and the heart as a result of changing head position can significantly influence ICP (Brosnan et al. 2002b). Both dorsal and lateral recumbency were shown to cause intracranial hypertension in anesthetized horses, with dorsal recumbency causing the highest levels of intracranial hypertension (independent of head position) (Brosnan et al. 2002b). Therefore, when possible, lateral recumbency is favored during anesthesia of cases with suspected intracranial disease or trauma and special attention should be given to head and neck position. While intermittent positive pressure ventilation (IPPV) is routinely required to avoid hypoxemia and maintain carbon dioxide (CO₂) levels within normal limits (as discussed later in the chapter), the use of high positive end‐expiratory pressure (PEEP) should be avoided (Muench et al. 2005; Drummond and Patel 2010; Chen et al. 2019) as increases in central venous or intrathoracic pressures are associated with decreased cerebral venous drainage. High intrathoracic pressures also lead to a reduction in venous return, cardiac output, and MAPs, which in turn may impact the arterial side of the cerebral circulation, as discussed in the following text.

The arterial side of cerebral circulation represented by CBF is regulated by myogenic (autoregulation), chemical (cerebral metabolic rate [CMR], PaCO₂, and PaO₂), and neurogenic factors (Patel and Drummond 2010). In humans, CBF remains relatively constant for MAPs between 65 and 150 mmHg due to cerebral autoregulation (Lassen 1959; Drummond 1997; Rangel‐Castilla et al. 2008). When blood pressures fall below or rise above this range, CBF becomes directly dependent on systemic blood pressure. Cerebral autoregulation can be disrupted by intracranial disease/trauma and by anesthesia. Inhalant anesthetics have a dose‐dependent effect in cerebral autoregulation. With concentrations below the minimum alveolar concentration (1 MAC), cerebral autoregulation is maintained, but when concentrations rise above 1 MAC, cerebral vasodilation occurs, resulting in increase in CBF and cerebral volume. The pressure ranges that support autoregulation in the horse are not known, but autoregulation disruption by the effects of inhalant anesthetics at concentrations above 1 MAC have been shown (Brosnan et al. 2002b; Brosnan et al. 2003b). While ICP values in standing, awake horses are similar to what is described for other healthy animals (Brosnan et al. 2002a), that is not the case in laterally recumbent, isoflurane‐anesthetized horses (Brosnan et al. 2002b; Brosnan et al. 2003a,b). The significant intracranial hypertension described in isoflurane‐anesthetized horses suggests that horses are at a much higher risk of inadequate CPP and cerebral ischemia (Brosnan et al. 2002b). Inotropes and vasopressors, such as dobutamine, ephedrine, norepinephrine, and phenylephrine, do not have a direct effect on the cerebral circulation, but their effect on the systemic arterial pressure during anesthesia can help support CPP (Steiner et al. 2004).

CMR, PaCO_2, and PaO₂ further influence CBF. CMR is directly coupled with CBF and a decrease in CMR leads to a decrease in CBF. Reduction in brain function (as during sleep), with most anesthetic drugs (with the exception of ketamine and nitrous oxide) and hypothermia all lead to a decrease in CMR and CBF. Conversely, seizure activity is associated with significant increases in CMR and CBF (Madsen and Vorstrup 1991; Theodore et al. 1996).

CBF is very responsive to changes in PaCO₂, particularly within the 25–70 mmHg range. This is due to changes in cerebral pH caused by CO₂. As PaCO₂ rises, cerebral pH decreases, leading to cerebral vasodilation and increase in CBF (mediated in part by nitric oxide and prostaglandins). This is of particular concern during inhalant anesthesia, where CBF may be already increased. It is therefore important to control ventilation and maintain PaCO₂ levels at mid‐to‐lower end of the normal range (provided that appropriate MAP can be maintained). Hyperventilation (hypocapnia) should be avoided and limited to emergent situations where intracranial hypertension is severe and the risk of herniation is imminent. This is because while the response to changes in PaCO₂ is rapid, it is not sustained. Over a period of six to eight hours, cerebral pH starts to normalize and CBF returns to pre‐hyperventilation levels despite a high systemic arterial pH as bicarbonate is removed from the CSF and out across the blood brain barrier. Because the changes in CO₂ occur much faster than this equilibration process, if a patient has been hyperventilated for an extended period of time, acute normalization of CO₂ levels should be avoided as it could result in significant CSF acidosis and an acute increase in CBF and ICP. Hypoxemia, or a PaO₂ below 60 mmHg, also causes cerebral vasodilation leading to an increase in CBF (but not CMR) and should be avoided. Intranasal oxygen insufflation during induction and the use of a demand valve to supplement oxygen and support ventilation during transport to and from the operating room or computed tomography (CT)/magnetic resonance imaging (MRI) unit is recommended as is monitoring of PaO₂ and PaCO₂ during anesthesia. While a pulse oximeter and capnograph could be used in addition to arterial blood gases, it is important to remember that those monitoring modalities may not be as accurate in the horse. Pulse oximetry tends to underestimate hemoglobin saturation levels while the ET‐PaCO₂ differences can be as high as 15 mmHg in horses with normal lung function (Koenig et al. 2003).

Most injectable anesthetics, sedatives, and analgesic agents preserve cerebral autoregulation, decrease CMR and CBF, and do not increase ICP (Patel and Drummond 2010). Sedation of neurologic horses is routinely performed with alpha‐2 agonists as they provide reliable sedation, analgesia and help improve induction quality and reduce anesthetic requirements (Hubbell et al. 2010). Short‐acting alpha‐2 agonists, such as xylazine or dexmedetomidine, may be preferred to minimize duration of ataxia and cardiovascular effects. Opioids can be added to augment sedation. While effects are not well documented in horses, certain intravenous opioids (e.g. morphine and meperidine) have the potential to release histamine, which is a cerebral vasodilator and may cause an increase in CBF and CBV (Schregel et al. 1994). Hence, if utilized, slow administration is recommended. The use of acepromazine in patients with a history of seizures or undergoing procedures that can facilitate seizures (i.e. myelogram) remains controversial and is typically avoided. While there is no data in horses, phenothiazine tranquilizers have been historically associated with facilitation of seizure activity in humans (Shaw 1959; Logothetis 1967). A retrospective study in dogs with a history of seizures that received acepromazine did not show any evidence of epileptogenic activity (Tobias et al. 2006). Similarly, a study that evaluated the use of acepromazine as part of the premedication of dogs undergoing myelography reported no increase in seizure incidence when compared to dogs that did not receive acepromazine (Drynan et al. 2012). Acepromazine can however cause hypotension (Parry et al. 1982) and should be avoided in hypovolemic or systemically compromised horses.

Before being removed from the US market, thiopental used to be the preferred induction agent for horses with neurologic disease. While propofol is currently the induction agent of choice in small animals (and young foals) at risk of increased ICP, its use as an induction agent in the adult horse is limited as induction quality is not as good, and is associated with excitement, myoclonus, and paddling (Mama et al. 1995, 1996). However, induction quality can be significantly improved with the addition of guaifenesin. A guaifenesin‐propofol combination as described by Brosnan et al. (2011) can be used when intracranial hypertension is suspected. Ketamine is associated with increases in CMR and CBF; however, studies in humans indicate that when combined with other drugs such as benzodiazepines or propofol, the adverse effects on ICP are mostly eliminated (Strebel et al. 1995; Sakai et al. 2000). The combination of ketamine and propofol is an acceptable option and may have the benefit of better recovery quality then when ketamine is combined to a benzodiazepine (Wagner et al. 2002; Jarrett et al. 2018).

Maintenance of general anesthesia typically requires inhalant anesthetics. As described previously, inhalant anesthetics (isoflurane, sevoflurane, and desflurane) can disrupt cerebral autoregulation and cause dose‐dependent vasodilation at concentrations higher than 1 MAC. Therefore, it is recommended to avoid inhalant concentrations higher than 1 MAC if possible. A partial intravenous anesthesia technique may be considered such as the adjunctive use of propofol and/or dexmedetomidine continuous infusions to help reduce the inhalant anesthetic requirement (Marcilla et al. 2012; Villalba et al. 2014; Sacks et al. 2017; Tokushige et al. 2018). While there is no horse specific data regarding the effects of these anesthetic combinations on ICP and CPP, the use of dexmedetomidine infusions has been described in dogs undergoing craniotomies (Tayari and Bell 2019; Marquez‐Grados et al. 2020) and dexmedetomidine has been shown to inhibit the cerebrovascular dilation induced by isoflurane and sevoflurane in dogs (Ohata et al. 1999). Arterial blood gases and direct arterial blood pressures should be continuously monitored, and hypercapnia, hypoxemia, and hypotension should be prevented. The occurrence of Cushing’s response (hypertension and bradycardia) is a classical sign of severe intracranial hypertension and high risk of brain herniation in humans and in dogs (Doba and Reis 1972; Fodstad et al. 2006; Platt et al. 2001), but it has not been well described in the horse.

Additional strategies to reduce brain tissue edema and prevent secondary brain injury are also mostly based on data from human and small animal medicine. Early effective correction of hypotension is recommended. Fluid therapy should aim to maintain normovolemia and avoid reduction of serum osmolarity (Magdesian 2000; Pinto et al. 2006; Farrokh et al. 2019). Isotonic fluids such as Lactated Ringers (LRS) or normal saline are routinely used. LRS is slightly less osmolar than plasma but does not seem to negatively impact serum osmolality at typical rates. Normal saline may lead to hyperchloremic metabolic acidosis and if large volumes are required to re‐establish normovolemia, one may alternate saline and LRS to minimize this effect (Farrokh et al. 2019).

Osmotic diuretics are extensively used to reduce the volume of intra and extracellular fluid compartments in the brain as well as decrease the hematocrit and blood viscosity via plasma expansion (Knapp 2005). Early administration of osmotic diuretics, such as mannitol, is a cornerstone of intracranial hypertension management in humans (Carney et al. 2017; Farrokh et al. 2019), small animals (Sande and West 2010; DiFazio and Fletcher 2013), and horses (Feary et al. 2007) as it is fast acting and effective. Hypertonic saline is an alternative to mannitol as both seem to be equally effective in humans (Gu et al. 2019; Chen et al. 2020), with a recent study suggesting that hypertonic saline may have a more sustained effect on ICP (Shi et al. 2020). Hypertonic saline may be more practical to administer in the horse and have the additional benefit of improving circulating blood volume and perfusion in hypovolemic patients with intracranial hypertension (Fielding and Magdesian 2010; Mangat et al. 2020). It is also less likely to create dehydration and hypovolemia as its diuretic effect is not as pronounced. Also, the efficacy of mannitol, but not hypertonic saline, decreases with repeated dosing, which has encouraged studies in humans evaluating the potential use of hypertonic saline as a continuous infusion with promising results (Asehnoune et al. 2017; Mangat 2018). Electrolyte, acid–base status, and serum osmolality should be carefully monitored during osmotic diuretic therapy (Feary et al. 2007; Hoehne et al. 2021). Hypertonic saline tends to increase both sodium and chloride plasma levels and can lead to hyperchloremic metabolic acidosis, which in turn may have negative renal effects (Schmall et al. 1990; Fielding and Magdesian 2010; Sigmon et al. 2020). Although specific studies have not been performed in the horse, recommendations based on the human literature suggest that serum sodium concentrations above 155 mmol/l and serum osmolality above 320 mOsm/l should generally be avoided (Adelson et al. 2003; Fielding and Magdesian 2010; Alshayeb et al. 2011). Excessive brain cell shrinkage and development of hypernatremic encephalopathy are typical concerns in human and small animal medicine (Adrogue and Madias 2000; Guillaumin and DiBartola 2017), although this is not well documented in the horse (Mayhew 2009; Collins et al. 2018). Cases of refractory intracranial hypertension in humans seem to respond to hypertonic saline (Gu et al. 2019).

A combination of osmotic and loop diuretics (mannitol and furosemide) is sometimes used, with the idea that mannitol would create the osmotic gradient resulting in fluid being pulled out of the parenchyma into the intravascular space and furosemide would then remove the excess fluid from the intravascular space via diuresis, helping maintain the osmotic gradient (Todd et al. 2006). Furosemide, by inhibiting chloride channels may also slow down the normal volume‐restoring mechanism of neurons and glia, which regulates cell volume (Staub et al. 1994). Care should be taken to avoid dehydration and hypovolemia. There is some concern with the use of mannitol and other osmotic diuretics when intracranial bleeding is suspected as it may cause an increase in the intracerebral hemorrhage volume (Aminmansour et al. 2017). While the use of mannitol in patients with large intracranial hematomas has been described (Dastur and Yu 2017), other studies have shown that mannitol does not seem to be effective in reducing hemorrhage volume after a stroke and does not improve outcome (Wang et al. 2015).

The beneficial effects of using steroids to reduce brain tissue edema and increase blood brain barrier permeability in patients with brain tumors is well described in humans (Miller et al. 1977; Yeung et al. 1994; Wilkinson et al. 2006). Dexamethasone remains the mainstay of treatment of tumor edema (Shapiro et al. 1990; Dietrich et al. 2011) although other glucocorticoids such as prednisone, prednisolone, and methylprednisolone are also used (Dietrich et al. 2011). The recommendation is that, whenever possible, steroid therapy should be started 48 hours prior to anesthesia (although beneficial effects can be noticed within 24 hours) and be continued during anesthesia (Miller and Leech 1975; Miller et al. 1977; Bell et al. 1987). High doses of glucocorticoids were frequently used in the treatment of acute brain or spinal cord injuries in horses (Feary et al. 2007). While there may be a benefit in the neurological outcome of acute spinal cord injuries (Bracken et al. 1990; Bracken et al. 1992), the use of steroids in the treatment of traumatic brain injury in humans is not recommended as controlled trials have shown no benefit and even potential deleterious effects (Edwards et al. 2005). Based on this information and potential for side effects (e.g. laminitis) its use in the horse with head trauma is not currently recommended.

Dimethyl sulfoxide (DMSO) has been historically used as part of the treatment for traumatic brain and spinal cord injuries in horses (Reed 2007). The rationale for its use is based on the drug’s anti‐inflammatory and possible antioxidant properties (de la Torre et al. 1975; Rucker et al. 1981; Shi et al. 2001), but there are no studies evaluating if it is effective. Vitamin E and C have also been used for their antioxidant effects, but no evidence of benefit is available.

Anesthetic Considerations for Conditions Affecting the Neck

Suspected cervical vertebral stenotic myelopathy (CVSM) is likely the most common equine neurologic presentation for which anesthesia is required. A definitive CVSM diagnosis depends on myelography (and more recently a combination of myelography and computed tomography) to identify the exact location(s) of spinal cord compression (van Biervliet et al. 2004; Kristoffersen et al. 2014). This is particularly important if ventral cervical stabilization will be surgically attempted. Some lesions may be dynamic and are only seen when the neck is flexed (Kühnle et al. 2018). Several complications have been associated following myelography and include transient worsening of ataxia, delayed recovery from anesthesia, seizures, blindness, hyperesthesia, depression, fever, anaphylaxis, neuropathy, and myopathy (Stowater et al. 1978; Nyland et al. 1980; Mullen et al. 2015). Adverse reactions with different degrees of severity were reported in one‐third of the horses anesthetized for myelography in a multi‐center study, but only 2% of those required euthanasia (Mullen et al. 2015).

The severity of the horse’s neurologic status is an important consideration for the anesthetist as previously discussed. A higher grade of ataxia (grade 4) at presentation has been associated with an increased incidence of severe complications and deterioration of neurologic status post‐myelogram, while in less severe cases (grade 3 or less) the worsening of ataxia was typically transient (24–48 hours) and unlikely to affect outcome (Hubbell et al. 1988). A recent multi‐center study (Mullen et al. 2015) reported worsening of the neurologic status post‐myelogram in 25% of the study horses, but was not able to establish a correlation between the severity of neurologic status pre‐myelogram and an increased risk of adverse reactions.

Myelography is a relatively short procedure (typically less than one hour), but technical difficulties or additional imaging such as computed tomography can significantly increase anesthetic time and further impact recovery time and quality (Voulgaris and Hofmeister 2009; Clark‐Price 2013). Due to limited padding and the required positioning during the myelogram, a prolonged anesthetic time may increase the risk of myopathies and neuropathies (Johnston et al. 2004).

Administration of contrast solution into the CSF may significantly expand its volume and increase ICP. Typically, this is minimized by removal of a similar amount of CSF immediately prior to contrast administration and by administering the contrast slowly. Many of the complications associated with myelography seem to be related to the contrast media used; iohexol is preferred as it is associated with fewer adverse reactions than metrizamide (Widmer et al. 1998).

Induction of anesthesia is typically performed with ketamine combined with a benzodiazepine (midazolam or diazepam) or propofol. The ketamine‐propofol combination has been shown to provide better recovery quality than ketamine‐midazolam after a short period of general anesthesia (Jarrett et al. 2018). The decreased ataxia associated with this induction protocol may be particularly beneficial in neurologic horses after myelography. If the myelography can be completed in less than one hour, injectable agents may be used for maintenance of anesthesia. A combination of guaifenesin, ketamine, and xylazine (GKX) is commonly used. If guaifenesin is not available, it can be replaced with midazolam (Aarnes et al. 2018). For procedures >1 hour, inhalant anesthesia is preferred to avoid drug accumulation resulting in ataxia and prolonged recovery.

The jugular catheter is usually placed in the upper side to avoid being displaced during procedural positioning. It should be placed as low as possible on the neck as to not be occluded when the neck is flexed during the myelogram. (Figure 6.1) With the extreme position changes of the neck (Figures 6.2 and 6.3a,b), the endotracheal tube may also become bent or obstructed (Figure 6.4). Monitoring of the capnograph and changes in the sound of the ventilator (with certain machines if being used) will alert the anesthetist prior to this being observed on the radiographs. When inhalant anesthesia is used, direct arterial pressures should be continuously monitored. The arterial catheter is generally placed in the metatarsal artery to minimize interference with positioning during myelography and maintain accuracy. Dobutamine continuous infusion should be used as needed to maintain MAPs above 70 mmHg, and the upper limbs should be supported (Figure 6.5).

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